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Sample records for maternal obesity up-regulates

  1. Maternal obesity in Europe

    DEFF Research Database (Denmark)

    Devlieger, Roland; Benhalima, Katrien; Damm, Peter

    2016-01-01

    and offspring. These effects are often aggravated by the high incidence of abnormal glucose tolerance and excessive gestational weight gain found in this group. The main controversies around the management of the obese pregnant women are related to (1) the value of repeated weighing during pregnancy, (2......, the prevalence of maternal obesity varies from 7 to 25% and seems strongly related to social and educational inequalities. Obesity during pregnancy represents an important preventable risk factor for adverse pregnancy outcomes and is associated with negative long-term health outcomes for both mothers...

  2. Neonatal maternal separation up-regulates protein signalling for cell survival in rat hypothalamus.

    Science.gov (United States)

    Irles, Claudine; Nava-Kopp, Alicia T; Morán, Julio; Zhang, Limei

    2014-05-01

    We have previously reported that in response to early life stress, such as maternal hyperthyroidism and maternal separation (MS), the rat hypothalamic vasopressinergic system becomes up-regulated, showing enlarged nuclear volume and cell number, with stress hyperresponsivity and high anxiety during adulthood. The detailed signaling pathways involving cell death/survival, modified by adverse experiences in this developmental window remains unknown. Here, we report the effects of MS on cellular density and time-dependent fluctuations of the expression of pro- and anti-apoptotic factors during the development of the hypothalamus. Neonatal male rats were exposed to 3 h-daily MS from postnatal days 2 to 15 (PND 2-15). Cellular density was assessed in the hypothalamus at PND 21 using methylene blue staining, and neuronal nuclear specific protein and glial fibrillary acidic protein immunostaining at PND 36. Expression of factors related to apoptosis and cell survival in the hypothalamus was examined at PND 1, 3, 6, 9, 12, 15, 20 and 43 by Western blot. Rats subjected to MS exhibited greater cell-density and increased neuronal density in all hypothalamic regions assessed. The time course of protein expression in the postnatal brain showed: (1) decreased expression of active caspase 3; (2) increased Bcl-2/Bax ratio; (3) increased activation of ERK1/2, Akt and inactivation of Bad; PND 15 and PND 20 were the most prominent time-points. These data indicate that MS can induce hypothalamic structural reorganization by promoting survival, suppressing cell death pathways, increasing cellular density which may alter the contribution of these modified regions to homeostasis.

  3. Maternal Employment and Childhood Obesity

    DEFF Research Database (Denmark)

    Gwozdz, Wencke; Sousa-Poza, Alfonso; Reisch, Lucia

    2013-01-01

    The substantial increase in female employment rates in Europe over the past two decades has often been linked in political and public rhetoric to negative effects on child development, including obesity. We analyse this association between maternal employment and childhood obesity using rich...... on obesity's main drivers: calorie intake and physical activity. Our analysis provides little evidence for any association between maternal employment and childhood obesity, diet or physical activity....

  4. Maternal Employment and Childhood Obesity

    DEFF Research Database (Denmark)

    Gwozdz, Wencke; Sousa-Poza, Alfonso; Reisch, Lucia

    The substantial increase in female employment rates in Europe over the past two decades has often been linked in political and public rhetoric to negative effects on child development, including obesity. We analyse this association between maternal employment and childhood obesity using rich...... on obesity's main drivers: calorie intake and physical activity. Our analysis provides little evidence for any association between maternal employment and childhood obesity, diet or physical activity....

  5. Maternal obesity and prenatal programming.

    Science.gov (United States)

    Elshenawy, Summer; Simmons, Rebecca

    2016-11-05

    Obesity is a significant and increasing public health concern in the United States and worldwide. Clinical and epidemiological evidence clearly shows that genetic and environmental factors contribute to the increased susceptibility of humans to obesity and its associated comorbidities; the interplay of these factors is explained by the concept of epigenetics. The impact of maternal obesity goes beyond the newborn period; fetal programming during the critical window of pregnancy, can have long term detrimental effects on the offspring as well as future generations. Emerging evidence is uncovering a link between the clinical and molecular findings in the offspring with epigenetic changes in the setting of maternal obesity. Research targeted towards reducing the transgenerational propagation and developmental programming of obesity is vital in reducing the increasing rates of disease. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  6. Increased placental nutrient transport in a novel mouse model of maternal obesity with fetal overgrowth.

    Science.gov (United States)

    Rosario, Fredrick J; Kanai, Yoshikatsu; Powell, Theresa L; Jansson, Thomas

    2015-08-01

    To identify possible mechanisms linking obesity in pregnancy to increased fetal adiposity and growth, a unique mouse model of maternal obesity associated with fetal overgrowth was developed, and the hypothesis that maternal obesity causes up-regulation of placental nutrient transporter expression and activity was tested. C57BL/6J female mice were fed a control (C) or a high-fat/high-sugar (HF/HS) pelleted diet supplemented by ad libitum access to sucrose (20%) solution, mated, and studied at embryonic day 18.5. HF/HS diet increased maternal fat mass by 2.2-fold (P Maternal circulating insulin, leptin, and cholesterol were increased (P maternal obesity. © 2015 The Obesity Society.

  7. Maternal Obesity: Consequences and Prevention Strategies

    OpenAIRE

    Emre Yanikkerem; Selviye Mutlu

    2012-01-01

    Obesity is a medical condition in which excess body fat that it may have an adverse effect on health, leading to life expectancy and increased health problems. In keeping with the general international trend of rising prevalence of obesity, maternal obesity prevalence is rising. According to WHO, the prevalence of obesity in pregnancy ranges from 1.8 to 25.3%. Maternal obesity has been identified to be a risk factor for maternal and perinatal mortality. The aim of this article was reviewed in...

  8. Maternal androgen excess and obesity induce sexually dimorphic anxiety-like behavior in the offspring.

    Science.gov (United States)

    Manti, Maria; Fornes, Romina; Qi, Xiaojuan; Folmerz, Elin; Lindén Hirschberg, Angelica; de Castro Barbosa, Thais; Maliqueo, Manuel; Benrick, Anna; Stener-Victorin, Elisabet

    2018-03-22

    Maternal polycystic ovary syndrome (PCOS), a condition associated with hyperandrogenism, is suggested to increase anxiety-like behavior in the offspring. Because PCOS is closely linked to obesity, we investigated the impact of an adverse hormonal or metabolic maternal environment and offspring obesity on anxiety in the offspring. The obese PCOS phenotype was induced by chronic high-fat-high-sucrose (HFHS) consumption together with prenatal dihydrotestosterone exposure in mouse dams. Anxiety-like behavior was assessed in adult offspring with the elevated-plus maze and open-field tests. The influence of maternal androgens and maternal and offspring diet on genes implicated in anxiety were analyzed in the amygdala and hypothalamus with real-time PCR ( n = 47). Independent of diet, female offspring exposed to maternal androgens were more anxious and displayed up-regulation of adrenoceptor α 1B in the amygdala and up-regulation of hypothalamic corticotropin-releasing hormone ( Crh). By contrast, male offspring exposed to a HFHS maternal diet had increased anxiety-like behavior and showed up-regulation of epigenetic markers in the amygdala and up-regulation of hypothalamic Crh. Overall, there were substantial sex differences in gene expression in the brain. These findings provide novel insight into how maternal androgens and obesity exert sex-specific effects on behavior and gene expression in the offspring of a PCOS mouse model.-Manti, M., Fornes, R., Qi, X., Folmerz, E., Lindén Hirschberg, A., de Castro Barbosa, T., Maliqueo, M., Benrick, A., Stener-Victorin, E. Maternal androgen excess and obesity induce sexually dimorphic anxiety-like behavior in the offspring.

  9. Maternal Obesity, Inflammation, and Developmental Programming

    Directory of Open Access Journals (Sweden)

    Stephanie A. Segovia

    2014-01-01

    Full Text Available The prevalence of obesity, especially in women of child-bearing age, is a global health concern. In addition to increasing the immediate risk of gestational complications, there is accumulating evidence that maternal obesity also has long-term consequences for the offspring. The concept of developmental programming describes the process in which an environmental stimulus, including altered nutrition, during critical periods of development can program alterations in organogenesis, tissue development, and metabolism, predisposing offspring to obesity and metabolic and cardiovascular disorders in later life. Although the mechanisms underpinning programming of metabolic disorders remain poorly defined, it has become increasingly clear that low-grade inflammation is associated with obesity and its comorbidities. This review will discuss maternal metainflammation as a mediator of programming in insulin sensitive tissues in offspring. Use of nutritional anti-inflammatories in pregnancy including omega 3 fatty acids, resveratrol, curcumin, and taurine may provide beneficial intervention strategies to ameliorate maternal obesity-induced programming.

  10. Fetal Programming of Obesity: Maternal Obesity and Excessive Weight Gain

    Directory of Open Access Journals (Sweden)

    Seray Kabaran

    2014-10-01

    Full Text Available The prevalence of obesity is an increasing health problem throughout the world. Maternal pre-pregnancy weight, maternal nutrition and maternal weight gain are among the factors that can cause childhood obesity. Both maternal obesity and excessive weight gain increase the risks of excessive fetal weight gain and high birth weight. Rapid weight gain during fetal period leads to changes in the newborn body composition. Specifically, the increase in body fat ratio in the early periods is associated with an increased risk of obesity in the later periods. It was reported that over-nutrition during fetal period could cause excessive food intake during postpartum period as a result of metabolic programming. By influencing the fetal metabolism and tissue development, maternal obesity and excessive weight gain change the amounts of nutrients and metabolites that pass to the fetus, thus causing excessive fetal weight gain which in turn increases the risk of obesity. Fetal over-nutrition and excessive weight gain cause permanent metabolic and physiologic changes in developing organs. While mechanisms that affect these organs are not fully understood, it is thought that the changes may occur as a result of the changes in fetal energy metabolism, appetite control, neuroendocrine functions, adipose tissue mass, epigenetic mechanisms and gene expression. In this review article, the effects of maternal body weight and weight gain on fetal development, newborn birth weight and risk of obesity were evaluated, and additionally potential mechanisms that can explain the effects of fetal over-nutrition on the risk of obesity were investigated [TAF Prev Med Bull 2014; 13(5.000: 427-434

  11. Placental fatty acid transport in maternal obesity.

    Science.gov (United States)

    Cetin, I; Parisi, F; Berti, C; Mandò, C; Desoye, G

    2012-12-01

    Pregestational obesity is a significant risk factor for adverse pregnancy outcomes. Maternal obesity is associated with a specific proinflammatory, endocrine and metabolic phenotype that may lead to higher supply of nutrients to the feto-placental unit and to excessive fetal fat accumulation. In particular, obesity may influence placental fatty acid (FA) transport in several ways, leading to increased diffusion driving force across the placenta, and to altered placental development, size and exchange surface area. Animal models show that maternal obesity is associated with increased expression of specific FA carriers and inflammatory signaling molecules in placental cotyledonary tissue, resulting in enhanced lipid transfer across the placenta, dislipidemia, fat accumulation and possibly altered development in fetuses. Cell culture experiments confirmed that inflammatory molecules, adipokines and FA, all significantly altered in obesity, are important regulators of placental lipid exchange. Expression studies in placentas of obese-diabetic women found a significant increase in FA binding protein-4 expression and in cellular triglyceride content, resulting in increased triglyceride cord blood concentrations. The expression and activity of carriers involved in placental lipid transport are influenced by the endocrine, inflammatory and metabolic milieu of obesity, and further studies are needed to elucidate the strong association between maternal obesity and fetal overgrowth.

  12. Moderate and extreme maternal obesity.

    LENUS (Irish Health Repository)

    Abdelmaboud, M O

    2012-05-01

    The aim of this study was to investigate the prevalence of moderate and extreme obesity among an Irish obstetric population over a 10-year period, and to evaluate the obstetric features of such pregnancies. Of 31,869 women delivered during the years 2000-2009, there were 306 women in the study group, including 173 in the moderate or Class 2 obese category (BMI 35-39.9) and 133 in the extreme or Class 3 obese category (BMI > or = 40).The prevalence of obese women with BMI > or = 35 was 9.6 per 1000 (0.96%), with an upward trend observed from 2.1 per 1000 in the year 2000, to 11.8 per 1000 in the year 2009 (P = 0.001). There was an increase in emergency caesarean section (EMCS) risk for primigravida versus multigravid women, within both obese categories (P < 0.001). However, there was no significant difference in EMCS rates observed between Class 2 and Class 3 obese women, when matched for parity. The prevalence of moderate and extreme obesity reported in this population is high, and appears to be increasing. The increased rates of abdominal delivery, and the levels of associated morbidity observed, have serious implications for such women embarking on pregnancy.

  13. Voluntary exercise prevents colonic inflammation in high-fat diet-induced obese mice by up-regulating PPAR-γ activity

    International Nuclear Information System (INIS)

    Liu, Wei-Xin; Wang, Ting; Zhou, Feng; Wang, Ying; Xing, Jun-Wei; Zhang, Shen; Gu, Shou-Zhi; Sang, Li-Xuan; Dai, Cong; Wang, Hai-Lan

    2015-01-01

    Obesity is associated with increased colonic inflammation, which elevates the risk of colon cancer. Although exercise exerts anti-inflammatory actions in multiple chronic diseases associated with inflammation, it is unknown whether this strategy prevents colonic inflammation in obesity. We hypothesized that voluntary exercise would suppress colonic inflammation in high-fat diet (HFD)-induced obesity by modulation of peroxisome proliferator-activated receptor (PPAR)-γ. Male C57Bl/6J mice fed either a control diet (6.5% fat, CON) or a high-fat diet (24% fat, HFD) were divided into sedentary, voluntary exercise or voluntary exercise with PPAR-γ antagonist GW9662 (10 mg/kg/day). All interventions took place for 12 weeks. Compared with CON-sedentary group, HFD-sedentary mice gained significantly more body weight and exhibited metabolic disorders. Molecular studies revealed that HFD-sedentary mice had increased expression of inflammatory mediators and activation of nuclear factor (NF)-κB in the colons, which were associated with decreased expression and activity of PPAR-γ. Voluntary exercise markedly attenuated body weight gain, improved metabolic disorders, and normalized the expression of inflammatory mediators and activation of NF-κB in the colons in HFD-mice while having no effects in CON-animals. Moreover, voluntary exercise significantly increased expression and activity of PPAR-γ in the colons in both HFD- and CON-animals. However, all of these beneficial effects induced by voluntary exercise were abolished by GW9662, which inhibited expression and activity of PPAR-γ. The results suggest that decreased PPAR-γ activity in the colon of HFD-induced obesity may facilitate the inflammatory response and colon carcinogenesis. Voluntary exercise prevents colonic inflammation in HFD-induced obesity by up-regulating PPAR-γ activity. - Highlights: • Obesity down-regulates PPAR-γ in the colon. • Down-regulated colonic PPAR-γ may facilitate inflammatory

  14. Voluntary exercise prevents colonic inflammation in high-fat diet-induced obese mice by up-regulating PPAR-γ activity

    Energy Technology Data Exchange (ETDEWEB)

    Liu, Wei-Xin, E-mail: weixinliu@yahoo.com [Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning (China); Wang, Ting; Zhou, Feng; Wang, Ying; Xing, Jun-Wei; Zhang, Shen [Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning (China); Gu, Shou-Zhi [Department of Anatomy, Seirei Christopher College, Hamamatsu 433-8558 (Japan); Sang, Li-Xuan [Department of Cadre Ward II, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning (China); Dai, Cong [Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning (China); Wang, Hai-Lan [Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, Guangdong (China)

    2015-04-10

    Obesity is associated with increased colonic inflammation, which elevates the risk of colon cancer. Although exercise exerts anti-inflammatory actions in multiple chronic diseases associated with inflammation, it is unknown whether this strategy prevents colonic inflammation in obesity. We hypothesized that voluntary exercise would suppress colonic inflammation in high-fat diet (HFD)-induced obesity by modulation of peroxisome proliferator-activated receptor (PPAR)-γ. Male C57Bl/6J mice fed either a control diet (6.5% fat, CON) or a high-fat diet (24% fat, HFD) were divided into sedentary, voluntary exercise or voluntary exercise with PPAR-γ antagonist GW9662 (10 mg/kg/day). All interventions took place for 12 weeks. Compared with CON-sedentary group, HFD-sedentary mice gained significantly more body weight and exhibited metabolic disorders. Molecular studies revealed that HFD-sedentary mice had increased expression of inflammatory mediators and activation of nuclear factor (NF)-κB in the colons, which were associated with decreased expression and activity of PPAR-γ. Voluntary exercise markedly attenuated body weight gain, improved metabolic disorders, and normalized the expression of inflammatory mediators and activation of NF-κB in the colons in HFD-mice while having no effects in CON-animals. Moreover, voluntary exercise significantly increased expression and activity of PPAR-γ in the colons in both HFD- and CON-animals. However, all of these beneficial effects induced by voluntary exercise were abolished by GW9662, which inhibited expression and activity of PPAR-γ. The results suggest that decreased PPAR-γ activity in the colon of HFD-induced obesity may facilitate the inflammatory response and colon carcinogenesis. Voluntary exercise prevents colonic inflammation in HFD-induced obesity by up-regulating PPAR-γ activity. - Highlights: • Obesity down-regulates PPAR-γ in the colon. • Down-regulated colonic PPAR-γ may facilitate inflammatory

  15. Is Maternal Employment Related to Childhood Obesity?

    DEFF Research Database (Denmark)

    Gwozdz, Wencke

    2016-01-01

    Childhood obesity has been rising steadily in most parts of the world. Popular speculation attributes some of that increase to rising maternal employment. Employed mothers spend less time at home and thus less time with their children, whose diets and physical activity may suffer. Also, children...

  16. Asymmetric dimethylarginine (ADMA) elevation and arginase up-regulation contribute to endothelial dysfunction related to insulin resistance in rats and morbidly obese humans.

    Science.gov (United States)

    El Assar, Mariam; Angulo, Javier; Santos-Ruiz, Marta; Ruiz de Adana, Juan Carlos; Pindado, María Luz; Sánchez-Ferrer, Alberto; Hernández, Alberto; Rodríguez-Mañas, Leocadio

    2016-06-01

    The presence of insulin resistance (IR) is determinant for endothelial dysfunction associated with obesity. Although recent studies have implicated the involvement of mitochondrial superoxide and inflammation in the defective nitric oxide (NO)-mediated responses and subsequent endothelial dysfunction in IR, other mechanisms could compromise this pathway. In the present study, we assessed the role of asymmetric dimethylarginine (ADMA) and arginase with respect to IR-induced impairment of endothelium-dependent vasodilatation in human morbid obesity and in a non-obese rat model of IR. We show that both increased ADMA and up-regulated arginase are determinant factors in the alteration of the l-arginine/NO pathway associated with IR in both models and also that acute treatment of arteries with arginase inhibitor or with l-arginine significantly alleviate endothelial dysfunction. These results help to expand our knowledge regarding the mechanisms of endothelial dysfunction that are related to obesity and IR and establish potential therapeutic targets for intervention. Insulin resistance (IR) is determinant for endothelial dysfunction in human obesity. Although we have previously reported the involvement of mitochondrial superoxide and inflammation, other mechanisms could compromise NO-mediated responses in IR. We evaluated the role of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) and arginase with respect to IR-induced impairment of l-arginine/NO-mediated vasodilatation in human morbid obesity and in a non-obese rat model of IR. Bradykinin-induced vasodilatation was evaluated in microarteries derived from insulin-resistant morbidly obese (IR-MO) and non-insulin-resistant MO (NIR-MO) subjects. Defective endothelial vasodilatation in IR-MO was improved by l-arginine supplementation. Increased levels of ADMA were detected in serum and adipose tissue from IR-MO. Serum ADMA positively correlated with IR score and negatively with pD2 for bradykinin. Gene

  17. Maternal morbid obesity and obstetric outcomes.

    LENUS (Irish Health Repository)

    Farah, Nadine

    2012-02-01

    OBJECTIVE: The purpose of this retrospective cohort study was to review pregnancy outcomes in morbidly obese women who delivered a baby weighing 500 g or more in a large tertiary referral university hospital in Europe. METHODS: Morbid obesity was defined as a BMI > or =40.0 kg\\/m2 (WHO). Only women whose BMI was calculated at their first antenatal visit were included. The obstetric out-comes were obtained from the hospital\\'s computerised database. RESULTS: The incidence of morbid obesity was 0.6% in 5,824 women. Morbidly obese women were older and were more likely to be multigravidas than women with a normal BMI. The pregnancy was complicated by hypertension in 35.8% and diabetes mellitus in 20.0% of women. Obstetric interventions were high, with an induction rate of 42.1% and a caesarean section rate of 45.3%. CONCLUSIONS: Our findings show that maternal morbid obesity is associated with an alarmingly high incidence of medical complications and an increased level of obstetric interventions. Consideration should be given to developing specialised antenatal services for morbidly obese women. The results also highlight the need to evaluate the effectiveness of prepregnancy interventions in morbidly obese women.

  18. Pediatric Obesity: It's Time for Prevention before Conception Can Maternal Obesity Program Pediatric Obesity?

    OpenAIRE

    Zach Ferraro; Kristi B. Adamo

    2008-01-01

    Global increases in obesity have led public health experts to declare this disease a pandemic. Although prevalent in all ages, the dire consequences associated with maternal obesity have a pronounced impact on the long-term health of their children as a result of the intergenerational effects of developmental programming. Previously, fetal under-nutrition has been linked to the predisposition to pediatric obesity explained by the adiposity rebound and ‘catch-up’ growth that occurs when a chil...

  19. Oxidative stress and maternal obesity: feto-placental unit interaction.

    Science.gov (United States)

    Malti, N; Merzouk, H; Merzouk, S A; Loukidi, B; Karaouzene, N; Malti, A; Narce, M

    2014-06-01

    To determine oxidative stress markers in maternal obesity during pregnancy and to evaluate feto-placental unit interaction, especially predictors of fetal metabolic alterations. 40 obese pregnant women (prepregnancy BMI > 30 kg/m²) were compared to 50 control pregnant women. Maternal, cord blood and placenta samples were collected at delivery. Biochemical parameters (total cholesterol and triglycerides) and oxidative stress markers (malondialdehyde, carbonyl proteins, superoxide anion expressed as reduced Nitroblue Tetrazolium, nitric oxide expressed as nitrite, reduced glutathione, catalase, superoxide dismutase) were assayed by biochemical methods. Maternal, fetal and placental triglyceride levels were increased in obese group compared to control. Maternal malondialdehyde, carbonyl proteins, nitric oxide and superoxide anion levels were high while reduced glutathione concentrations and superoxide dismutase activity were low in obesity. In the placenta and in newborns of these obese mothers, variations of redox balance were also observed indicating high oxidative stress. Maternal and placental interaction constituted a strong predictor of fetal redox variations in obese pregnancies. Maternal obesity compromised placental metabolism and antioxidant status which strongly impacted fetal redox balance. Oxidative stress may be one of the key downstream mediators that initiate programming of the offspring. Maternal obesity is associated with metabolic alterations and dysregulation of redox balance in the mother-placenta - fetus unit. These perturbations could lead to maternal and fetal complications and should be carefully considered. Copyright © 2014 Elsevier Ltd. All rights reserved.

  20. Effects of Maternal Obesity on Fetal Programming: Molecular Approaches

    Science.gov (United States)

    Neri, Caterina; Edlow, Andrea G.

    2016-01-01

    Maternal obesity has become a worldwide epidemic. Obesity and a high-fat diet have been shown to have deleterious effects on fetal programming, predisposing offspring to adverse cardiometabolic and neurodevelopmental outcomes. Although large epidemiological studies have shown an association between maternal obesity and adverse outcomes for offspring, the underlying mechanisms remain unclear. Molecular approaches have played a key role in elucidating the mechanistic underpinnings of fetal malprogramming in the setting of maternal obesity. These approaches include, among others, characterization of epigenetic modifications, microRNA expression, the gut microbiome, the transcriptome, and evaluation of specific mRNA expression via quantitative reverse transcription polmerase chain reaction (RT-qPCR) in fetuses and offspring of obese females. This work will review the data from animal models and human fluids/cells regarding the effects of maternal obesity on fetal and offspring neurodevelopment and cardiometabolic outcomes, with a particular focus on molecular approaches. PMID:26337113

  1. Maternal obesity and neurodevelopmental and psychiatric disorders in offspring

    Science.gov (United States)

    Edlow, Andrea G.

    2017-01-01

    There is a growing body of evidence from both human epidemiologic and animal studies that prenatal and lactational exposure to maternal obesity and high-fat diet are associated with neurodevelopmental and psychiatric disorders in offspring. These disorders include cognitive impairment, autism spectrum disorders, attention deficit hyperactivity disorder, cerebral palsy, anxiety and depression, schizophrenia, and eating disorders. This review synthesizes human and animal data linking maternal obesity and high-fat diet consumption to abnormal fetal brain development and neurodevelopmental and psychiatric morbidity in offspring. In addition, it highlights key mechanisms by which maternal obesity and maternal diet might impact fetal and offspring neurodevelopment, including neuroinflammation; increased oxidative stress, dysregulated insulin, glucose, and leptin signaling; dysregulated serotonergic and dopaminergic signaling; and perturbations in synaptic plasticity. Finally, the review summarizes available evidence regarding investigational therapeutic approaches to mitigate the harmful effects of maternal obesity on fetal and offspring neurodevelopment. PMID:27684946

  2. Does maternal obesity have an influence on feeding behavior of obese children?

    Science.gov (United States)

    Cebeci, A N; Guven, A

    2015-12-01

    Although the pathogenesis of childhood obesity is multi factorial, maternal obesity and parenting have major roles. The aim of this study was to evaluate the influence of maternal obesity on feeding practices toward their obese school children. Obese children and adolescents referred to the pediatric endocrinology department were enrolled consecutively. Height and weight of all children and their mothers were measured. Maternal feeding practices were measured using an adapted version of the Child Feeding Questionnaire (CFQ). Answers were compared between obese (Body Mass Index [BMI] ≥ 30 kg/m2) and non-obese mothers. A total of 491 obese subjects (292 girls, mean age 12.0 ± 2.8 years) and their mothers participated in this study. A direct correlation between children's BMI and their mothers' BMI was found (Pobese in the study, only half of them consider themselves as obese. No difference were found in the scores of the subscales "perceived responsibility", "restriction", "concern for child's weight" and "monitoring" between obese and non-obese mothers. Child's BMI-SDS positively correlated with mothers' personal weight perception, concern for child's weight and restriction after adjustment for child's age (P obesity increases mothers' concern and food restriction behavior. While mothers of obese children have a high prevalence of obesity, maternal obesity was found to have no significant influence on feeding behavior of obese school children.

  3. Maternal obesity and infant mortality: a meta-analysis.

    Science.gov (United States)

    Meehan, Sean; Beck, Charles R; Mair-Jenkins, John; Leonardi-Bee, Jo; Puleston, Richard

    2014-05-01

    Despite numerous studies reporting an elevated risk of infant mortality among women who are obese, the magnitude of the association is unclear. A systematic review and meta-analysis was undertaken to assess the association between maternal overweight or obesity and infant mortality. Four health care databases and gray literature sources were searched and screened against the protocol eligibility criteria. Observational studies reporting on the relationship between maternal overweight and obesity and infant mortality were included. Data extraction and risk of bias assessments were performed. Twenty-four records were included from 783 screened. Obese mothers (BMI ≥30) had greater odds of having an infant death (odds ratio 1.42; 95% confidence interval, 1.24-1.63; P obese (BMI >35) (odds ratio 2.03; 95% confidence interval, 1.61-2.56; P obese mothers and that this risk may increase with greater maternal BMI or weight; however, residual confounding may explain these findings. Given the rising prevalence of maternal obesity, additional high-quality epidemiologic studies to elucidate the actual influence of elevated maternal mass or weight on infant mortality are needed. If a causal link is determined and the biological basis explained, public health strategies to address the issue of maternal obesity will be needed. Copyright © 2014 by the American Academy of Pediatrics.

  4. Pediatric Obesity: It's Time for Prevention before Conception Can Maternal Obesity Program Pediatric Obesity?

    Directory of Open Access Journals (Sweden)

    Zach Ferraro

    2008-01-01

    Full Text Available Global increases in obesity have led public health experts to declare this disease a pandemic. Although prevalent in all ages, the dire consequences associated with maternal obesity have a pronounced impact on the long-term health of their children as a result of the intergenerational effects of developmental programming. Previously, fetal under-nutrition has been linked to the predisposition to pediatric obesity explained by the adiposity rebound and ‘catch-up’ growth that occurs when a child born to a nutrient deprived mother is exposed to the obesogenic environment of present day. Given the recent increase in maternal overweight/obesity (OW/OB our attention has shifted from nutrient restriction to overabundance and excess during pregnancy. Consideration must now be given to interventions that could mitigate pregravid body mass index (BMI, attenuate gestational weight gain (GWG and reduce postpartum weight retention (PPWR in an attempt to prevent the downstream signaling of pediatric obesity and halt the intergenerational cycle of weight related disease currently plaguing our world. Thus, this paper will briefly review current research that best highlights the proposed mechanisms responsible for the development of child OW/OB and related sequalae (e.g. type II diabetes (T2D and cardiovascular disease (CVD resulting from maternal obesity.

  5. Prevention and management of maternal obesity in pregnancy

    OpenAIRE

    E. Alexopoulou; N. Giannousi; I. K. Thanasas

    2017-01-01

    Nowadays obesity is one of the most important nutritional problems with features contemporary epidemic which concerns not only the developed but also the developing countries. Obesity during pregnancy associate with maternal and perinatal risks that make the management of obesity, before and during pregnancy imperative. The best and most effective treatment of obesity in pregnancy is prevention. A healthy diet and regular exercise of pregnant woman is crucial for the normal dev...

  6. Maternal obesity and obstetric outcomes in a tertiary referral center

    Directory of Open Access Journals (Sweden)

    Gitana Ramonienė

    2017-01-01

    Conclusions: Maternal obesity is significantly associated with an increased risk of gestational hypertension, preeclampsia, gestational diabetes, dystocia, labor induction, failed induction of labor, large-for-gestational-age newborns and cesarean delivery.

  7. Intergenerational impact of maternal obesity and postnatal feeding practices on pediatric obesity

    OpenAIRE

    Thompson, Amanda L.

    2013-01-01

    The postnatal feeding practices of obese and overweight mothers may place their children at particular risk for the development of obesity through shared biology and family environments. This paper reviews the feeding practices of obese mothers, describes potential mechanisms linking maternal feeding behaviors to child obesity risk, and highlights potential avenues for intervention. This review documents that supporting breastfeeding, improving the food choices of obese women, and encouraging...

  8. Relationship Between Maternal Obesity And Increased Risk Of ...

    African Journals Online (AJOL)

    Introduction: The incidence of obesity has risen over the past several decades and in spite of advancement in modern medicine, it remains a risk factor for maternal morbidity and mortality. Objective: To determine the association between obesity (increased body mass index) and increased risk of preeclampsia. The possible ...

  9. Adolescent obesity and maternal and paternal sensitivity and monitoring.

    Science.gov (United States)

    Neal Davis, R; Ashba, Jacqueline; Appugliese, Danielle P; Kaciroti, Niko; Corwyn, Robert F; Bradley, Robert H; Lumeng, Julie C

    2011-06-01

    To determine if adolescent obesity is associated with parenting characterized by lower sensitivity and lower monitoring of adolescent activities. We used data from 744 adolescents in the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development. Height and weight were measured at age 15½ years and obesity defined as body mass index ≥ 95th percentile for age and sex. Maternal and paternal sensitivity were assessed by direct observation of a parent-adolescent interaction task. Maternal and paternal monitoring were assessed by parent report. Lower sensitivity and lower monitoring were each defined as the lowest quartiles. Two separate multivariate logistic regression models were created to evaluate, individually for mothers and fathers, associations of sensitivity and monitoring with adolescent obesity, controlling for adolescent sex and race, family income-to-needs ratio, and parental obesity. Fourteen percent of the adolescents were obese. Lower sensitivity was associated with adolescent obesity in the maternal parenting model (adjusted odds ratio [AOR] 2.36, 95% confidence interval [CI] 1.44-3.86, n = 709), but not paternal parenting model (AOR = 0.79, 95% CI 0.38-1.63, n = 460). Neither maternal nor paternal monitoring was associated with adolescent obesity (AOR = 1.03, 95% CI 0.63-1.68; AOR = 1.07, 95% CI 0.52-2.22, respectively). Lower maternal sensitivity, measured by direct observation of parent-adolescent interactions, was associated with adolescent obesity. Efforts to prevent and treat childhood obesity, both at the practitioner level and the community level, may be enhanced by educating parents that their reactions to their children's behaviors may have consequences related to obesity.

  10. Effects of maternal obesity on placental function and fetal development

    Science.gov (United States)

    Howell, Kristy R.; Powell, Theresa L.

    2017-01-01

    Obesity has reached epidemic proportions and pregnancies in obese mothers have increased risk for complications including gestational diabetes, hypertensive disorders, preterm birth and caesarian section. Children born to obese mothers are at increased risk of obesity and metabolic disease and are susceptible to develop neuropsychiatric and cognitive disorders. Changes in placental function not only play a critical role in the development of pregnancy complications but may also be involved in linking maternal obesity to long-term health risks in the infant. Maternal adipokines i.e., interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), leptin and adiponectin link maternal nutritional status and adipose tissue metabolism to placental function. Adipokines and metabolic hormones have direct impact on placental function by modulating placental nutrient transport. Nutrient delivery to the fetus is regulated by a complex interaction between insulin signaling, cytokine profile and insulin responsiveness, which is modulated by adiponectin and IL-1β. In addition, obese pregnant women are at risk for hypertension and preeclampsia with reduced placental vascularity and blood flow, which would restrict placental nutrient delivery to the developing fetus. These sometimes opposing signals regulating placental function may contribute to the diversity of short and long-term outcomes observed in pregnant obese women. This review focuses on the changes in adipokines and obesity-related metabolic hormones, how these factors influence placental function and fetal development to contribute to long-term metabolic and behavioral consequences of children born to obese mothers. PMID:27864335

  11. Maternal immunization with ovalbumin prevents neonatal allergy development and up-regulates inhibitory receptor FcγRIIB expression on B cells

    Directory of Open Access Journals (Sweden)

    Duarte Alberto JS

    2010-03-01

    Full Text Available Abstract Background Preconception allergen immunization prevents neonatal allergen sensitization in mice by a complex interaction between regulatory cells/factors and antibodies. The present study assessed the influence of maternal immunization with ovalbumin (OVA on the immune response of 3 day-old and 3 week-old offspring immunized or non-immunized with OVA and evaluated the effect of IgG treatment during fetal development or neonatal period. Results Maternal immunization with OVA showed increased levels of FcγRIIb expression in splenic B cells of neonates, which were maintained for up to 3 weeks and not affected by additional postnatal OVA immunization. Maternal immunization also exerted a down-modulatory effect on both IL-4 and IFN-γ-secreting T cells and IL-4 and IL-12- secreting B cells. Furthermore, immunized neonates from immunized mothers showed a marked inhibition of antigen-specifc IgE Ab production and lowered Th2/Th1 cytokine levels, whereas displaying enhanced FcγRIIb expression on B cells. These offspring also showed reduced antigen-specific proliferative response and lowered B cell responsiveness. Moreover, in vitro evaluation revealed an impairment of B cell activation upon engagement of B cell antigen receptor by IgG from OVA-immunized mice. Finally, in vivo IgG transference during pregnancy or breastfeeding revealed that maternal Ab transference was able to increase regulatory cytokines, such as IL-10, in the prenatal stage; yet only the postnatal treatment prevented neonatal sensitization. None of the IgG treatments induced immunological changes in the offspring, as it was observed for those from OVA-immunized mothers. Conclusion Maternal immunization upregulates the inhibitory FcγRIIb expression on offspring B cells, avoiding skewed Th2 response and development of allergy. These findings contribute to the advancement of prophylactic strategies to prevent allergic diseases in early life.

  12. Maternal employment and childhood obesity--a European perspective.

    Science.gov (United States)

    Gwozdz, Wencke; Sousa-Poza, Alfonso; Reisch, Lucia A; Ahrens, Wolfgang; Eiben, Gabriele; M Fernandéz-Alvira, Juan; Hadjigeorgiou, Charalampos; De Henauw, Stefaan; Kovács, Eva; Lauria, Fabio; Veidebaum, Toomas; Williams, Garrath; Bammann, Karin

    2013-07-01

    The substantial increase in female employment rates in Europe over the past two decades has often been linked in political and public rhetoric to negative effects on child development, including obesity. We analyse this association between maternal employment and childhood obesity using rich objective reports of various anthropometric and other measures of fatness from the IDEFICS study of children aged 2-9 in 16 regions of eight European countries. Based on such data as accelerometer measures and information from nutritional diaries, we also investigate the effects of maternal employment on obesity's main drivers: calorie intake and physical activity. Our analysis provides little evidence for any association between maternal employment and childhood obesity, diet or physical activity. Copyright © 2013 Elsevier B.V. All rights reserved.

  13. The impact of maternal obesity during pregnancy on offspring immunity.

    Science.gov (United States)

    Wilson, Randall M; Messaoudi, Ilhem

    2015-12-15

    In the United States, approximately 64% of women of childbearing age are either overweight or obese. Maternal obesity during pregnancy is associated with a greater risk for adverse maternal-fetal outcomes. Adverse health outcomes for the offspring can persist into adulthood, increasing the incidence of several chronic conditions including cardiovascular disease, diabetes, and asthma. Since these diseases have a significant inflammatory component, these observations are indicative of perturbation of the normal development and maturation of the immune system of the offspring in utero. This hypothesis is strongly supported by data from several rodent studies. Although the mechanisms of these perturbations are not fully understood, it is thought that increased placental inflammation due to obesity may directly affect neonatal development through alterations in nutrient transport. In this review we examine the impact of maternal obesity on the neonatal immune system, and potential mechanisms for the changes observed. Published by Elsevier Ireland Ltd.

  14. Impact of maternal prenatal psychosocial stress and maternal obesity on infant microbiota

    NARCIS (Netherlands)

    Browne, P.D.; Berg, E. van den; Weerth, C. de; Browne, P.D.; Claassen, E.; Cabena, M.D.

    2017-01-01

    The prenatal period is a critical window of development for all major physiological systems in the human body. During pregnancy, maternal prenatal psychosocial stress (PNS) and maternal obesity are identified as risk factors for infant and child health. Several possible mechanisms have been

  15. Relationships between pediatric obesity and maternal emotional states and attitudes.

    Science.gov (United States)

    Akay, Aynur Pekcanlar; Ozturk, Yesim; Avcil, Sibel Nur; Kavurma, Canem; Tufan, Evren

    2015-01-01

    The goal of this study was to investigate depression and anxiety levels of mothers whose child (7-11 years) and adolescent (12-18 years) offspring had obesity, as well as those mothers' attitudes toward their children and their family relationships. This is a cross-sectional, case-control study of 100 dyads. All mothers completed the Beck Depression Inventory, the State-Trait Anxiety Inventory, the Parental Attitude Research Instrument, and the Family Assessment Device. Maternal state anxiety in the group with obesity was significantly higher than controls (p = 0.03). As measured by Family Assessment Device, affective involvement (p = 0.05) and behavior control (p = 0.00) scores were significantly higher for those with obesity. Obesity and adolescence have independent effects on maternal state anxiety; affective involvement domain of family function is affected by both obesity and its interaction with adolescence, while behavior control domain is singularly affected by obesity. Our results may demonstrate that, for the mothers of children who have obesity, this condition may have an adverse effect on their lives and their family relationships. Pediatric obesity and developmental stage of offspring may have different effects on maternally reported psychometric variables. Cross-sectional design may hinder causal explanations. Further studies with longitudinal designs are needed. © The Author(s) 2015.

  16. Intergenerational impact of maternal obesity and postnatal feeding practices on pediatric obesity.

    Science.gov (United States)

    Thompson, Amanda L

    2013-10-01

    The postnatal feeding practices of obese and overweight mothers may place their children at increased risk for the development of obesity through shared biology and family environments. This article reviews the feeding practices of obese mothers, describes the potential mechanisms linking maternal feeding behaviors to child obesity risk, and highlights the potential avenues of intervention. Strategies important for improving the quality of the eating environment and preventing the intergenerational transmission of obesity include supporting breastfeeding, improving the food choices of obese women, and encouraging the development of feeding styles that are responsive to hunger and satiety cues. © 2013 International Life Sciences Institute.

  17. Intergenerational impact of maternal obesity and postnatal feeding practices on pediatric obesity

    Science.gov (United States)

    Thompson, Amanda L.

    2014-01-01

    The postnatal feeding practices of obese and overweight mothers may place their children at particular risk for the development of obesity through shared biology and family environments. This paper reviews the feeding practices of obese mothers, describes potential mechanisms linking maternal feeding behaviors to child obesity risk, and highlights potential avenues for intervention. This review documents that supporting breastfeeding, improving the food choices of obese women, and encouraging the development of feeding styles that are responsive to hunger and satiety cues are important for improving the quality of the eating environment and preventing the intergenerational transmission of obesity. PMID:24147925

  18. Maternal Exposure of Rats to Isoflurane during Late Pregnancy Impairs Spatial Learning and Memory in the Offspring by Up-Regulating the Expression of Histone Deacetylase 2.

    Science.gov (United States)

    Luo, Foquan; Hu, Yan; Zhao, Weilu; Zuo, Zhiyi; Yu, Qi; Liu, Zhiyi; Lin, Jiamei; Feng, Yunlin; Li, Binda; Wu, Liuqin; Xu, Lin

    2016-01-01

    Increasing evidence indicates that most general anesthetics can harm developing neurons and induce cognitive dysfunction in a dose- and time-dependent manner. Histone deacetylase 2 (HDAC2) has been implicated in synaptic plasticity and learning and memory. Our previous results showed that maternal exposure to general anesthetics during late pregnancy impaired the offspring's learning and memory, but the role of HDAC2 in it is not known yet. In the present study, pregnant rats were exposed to 1.5% isoflurane in 100% oxygen for 2, 4 or 8 hours or to 100% oxygen only for 8 hours on gestation day 18 (E18). The offspring born to each rat were randomly subdivided into 2 subgroups. Thirty days after birth, the Morris water maze (MWM) was used to assess learning and memory in the offspring. Two hours before each MWM trial, an HDAC inhibitor (SAHA) was given to the offspring in one subgroup, whereas a control solvent was given to those in the other subgroup. The results showed that maternal exposure to isoflurane impaired learning and memory of the offspring, impaired the structure of the hippocampus, increased HDAC2 mRNA and downregulated cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) mRNA, N-methyl-D-aspartate receptor 2 subunit B (NR2B) mRNA and NR2B protein in the hippocampus. These changes were proportional to the duration of the maternal exposure to isoflurane and were reversed by SAHA. These results suggest that exposure to isoflurane during late pregnancy can damage the learning and memory of the offspring rats via the HDAC2-CREB -NR2B pathway. This effect can be reversed by HDAC2 inhibition.

  19. Maternal obesity and sex-specific differences in placental pathology.

    Science.gov (United States)

    Leon-Garcia, Sandra M; Roeder, Hilary A; Nelson, Katharine K; Liao, Xiaoyan; Pizzo, Donald P; Laurent, Louise C; Parast, Mana M; LaCoursiere, D Yvette

    2016-02-01

    Adverse effects of obesity have been linked to inflammation in various tissues, but studies on placental inflammation and obesity have demonstrated conflicting findings. We sought to investigate the influence of pregravid obesity and fetal sex on placental histopathology while controlling for diabetes and hypertension. Placental histopathology focusing on inflammatory markers of a cohort of normal weight (BMI = 20-24.9) and obese (BMI ≥ 30) patients was characterized. Demographic, obstetric and neonatal variables were assessed. 192 normal and 231 obese women were included. Placental characteristics associated with obesity and fetal sex independent of diabetes and hypertension were placental disc weight >90(th) percentile, decreased placental efficiency, chronic villitis (CV), fetal thrombosis, and normoblastemia. Additionally, female fetuses of obese mothers had higher rates of CV and fetal thrombosis. Increasing BMI increased the risk of normoblastemia and CV. The final grade and extent of CV was significantly associated with obesity and BMI, but not fetal gender. Finally, CV was less common in large-for-gestation placentas. Maternal obesity results in placental overgrowth and fetal hypoxia as manifested by normoblastemia; it is also associated with an increased incidence of CV and fetal thrombosis, both more prevalent in female placentas. We have shown for the first time that the effect of maternal obesity on placental inflammation is independent of diabetes and hypertension, but significantly affected by fetal sex. Our data also point to the intriguing possibility that CV serves to normalize placental size, and potentially fetal growth, in the setting of maternal obesity. Copyright © 2015. Published by Elsevier Ltd.

  20. Impact of maternal obesity on very preterm infants.

    Science.gov (United States)

    Khalak, Rubia; Rijhsinghani, Asha; McCallum, Sarah E

    2017-05-01

    Infants born at less than  34 weeks' gestational age are at higher risk for morbidity and mortality. Data are limited on the impact of maternal obesity on the very preterm infant. This study reviewed whether maternal obesity further increases the intensive care needs of very preterm infants of less than 34 weeks' gestation. Maternal and neonatal data for live-born singleton births of 23 0/7 to 33 6/7 weeks' gestation delivering in upstate New York were reviewed. BMI categorization followed the National Institutes of Health BMI classification that subdivides obesity into three ascending BMI groups. Records were obtained on 1,224 women, of whom 31.6% were classified with obesity. Despite similar mean gestational age (31 to 31.6 weeks, P = 0.57) and birth weight (1,488 to 1,569 g, P = 0.51) of the infants in the BMI categories, delivery room (DR) resuscitation was more common for infants of women with level III obesity (63.2%, P = 0.04) with a trend toward the continued need for assisted ventilation (54.7%, P = 0.06). Preterm infants of women with level III obesity were more likely to require DR resuscitation with a trend to continued need for ventilatory support beyond 6 hours of age. This could impact utilization of DR resources at delivering hospitals. © 2017 The Obesity Society.

  1. Maternal obesity surgery : effects in women, spouses and offspring

    OpenAIRE

    Berglind, Daniel

    2014-01-01

    Introduction: Bariatric surgery is an important treatment for the worldwide increasing epidemic of obesity. However, the effects of such surgery on offspring epigenetic profile and effects on objectively measured physical activity and sedentary behavior in women undergoing bariatric surgery and family members are essentially unknown. Aim: The aim of this thesis was to investigate possible effects of maternal weight loss after bariatric surgery and effects on differences in maternal gest...

  2. Prevention and management of maternal obesity in pregnancy

    Directory of Open Access Journals (Sweden)

    E. Alexopoulou

    2017-03-01

    Full Text Available Nowadays obesity is one of the most important nutritional problems with features contemporary epidemic which concerns not only the developed but also the developing countries. Obesity during pregnancy associate with maternal and perinatal risks that make the management of obesity, before and during pregnancy imperative. The best and most effective treatment of obesity in pregnancy is prevention. A healthy diet and regular exercise of pregnant woman is crucial for the normal development of pregnancy. Moreover every obese pregnant woman should be informed about the importance of calorie - intake regulation and weight reduction both before and after pregnancy. Additional therapeutic options are bariatric surgical procedures that a woman can have before pregnancy and anticoagulation therapy during pregnancy. This article attempts brief review on the current scientific knowledge that exists about the role of nutrition and physical activity in controlling the weight of obese pregnant women and its beneficial contribution to the health of both the mother and the newborn.

  3. Disrupted Prenatal Maternal Cortisol, Maternal Obesity, and Childhood Wheeze. Insights into Prenatal Programming

    Science.gov (United States)

    Fisher, Kate; Chiu, Yueh-Hsiu Mathilda; Wright, Robert O.; Fein, Rebecca; Cohen, Sheldon; Coull, Brent A.

    2013-01-01

    Rationale: Exploring prenatal factors influencing childhood wheeze may inform programming mechanisms. Objectives: We examined associations among prenatal maternal cortisol profiles, maternal obesity, and repeated wheeze up to age 2 years (n = 261). Methods: Salivary cortisol was collected five times per day over 3 days at 29.0 ± 4.9 weeks gestation. Mothers were categorized as obese (body mass index ≥ 30 kg/m2) versus nonobese (body mass index cortisol metrics (level at each time point, morning rise, diurnal and afternoon slopes) and obesity on wheeze adjusting for covariates. Linear mixed models were implemented to examine associations between cortisol trajectories and wheezing. Interactions between maternal cortisol and obesity were considered. Measurements and Main Results: Mothers were primarily minority (56.5% Hispanic, 24.1% African American), 61% had less than or equal to 12 years of education, 34% were obese, and 8.4% of children had repeated wheeze. An interquartile range increase in mean log cortisol at bedtime (odds ratio, 2.2; 95% confidence interval, 1.09–4.09) and maternal obesity (odds ratio, 3.43; 95% confidence interval, 1.26–9.35) were independently associated with wheeze. Linear mixed models revealed an association between a flatter afternoon slope (slower decline in log cortisol per hour) and repeated wheeze in children of obese mothers (children with [−0.017 change] and without [−0.061 change] wheeze [P = 0.009 for time × wheeze interaction]), but not in children of nonobese mothers (with [−0.050 change] and without [−0.061 change] wheeze [P = 0.51]). Conclusions: Maternal prenatal cortisol disruption and obesity were independently associated with children’s wheeze. Obese women with adverse cortisol profiles were most likely to have children with repeated wheeze. PMID:23590260

  4. Maternal employment and childhood obesity : a European perspective

    OpenAIRE

    Gwozdz, Wencke; Sousa-Posa, Alfonso; Reisch, Lucia A.; Ahrens, Wolfgang; Henauw, Stefaan de; Eiben, Gabriele; Fernandez-Alvira, Juan M.; Hadjigeorgiou, Charalampos; Kovacs, Eva; Lauria, Fabio; Veidebaum, Toomas; Williams, Garrath; Bammann, Karin

    2013-01-01

    The substantial increase in female employment rates in Europe over the past two decades has often been linked in political and public rhetoric to negative effects on child development, including obesity. We analyse this association between maternal employment and childhood obesity using rich objective reports of various anthropometric and other measures of fatness from the IDEFICS study of children aged 2-9 in 16 regions of eight European countries. Based on such data as accelerometer measure...

  5. Maternal obesity, caesarean delivery and caesarean delivery on maternal request: a cohort analysis from China.

    Science.gov (United States)

    Zhou, Yubo; Blustein, Jan; Li, Hongtian; Ye, Rongwei; Zhu, Liping; Liu, Jianmeng

    2015-05-01

    To quantify the association between maternal obesity and caesarean delivery, particularly caesarean delivery on maternal request (CDMR), a fast-growing component of caesarean delivery in many nations. We followed 1,019,576 nulliparous women registered in the Perinatal Healthcare Surveillance System during 1993-2010. Maternal body mass index (BMI, kg/m(2) ), before pregnancy or during early pregnancy, was classified as underweight (obese (≥27.5), consistent with World Health Organization guidelines for Asian people. The association between maternal obesity and overall caesarean and its subtypes was modelled using log-binomial regression. During the 18-year period, 404,971 (39.7%) caesareans and 93,927 (9.2%) CDMRs were identified. Maternal obesity was positively associated with overall caesarean and CDMR. Adjusted risk ratios for overall caesarean in the four ascending BMI categories were 0.96 [95% confidence interval (CI) 0.94, 0.97], 1.00 (Reference), 1.16 [95% CI 1.14, 1.18], 1.39 [95% CI 1.43, 1.54], and for CDMR were 0.95 [95% CI 0.94, 0.96], 1.00 (Reference), 1.20 [95% CI 1.18, 1.22], 1.48 [95% CI 1.433, 1.54]. Positive associations were consistently found in women residing in southern and northern provinces and in subgroups stratified by year of delivery, urban or rural residence, maternal age, education, level of delivering hospital, and birthweight. In a large Chinese cohort study, maternal obesity was associated with an increased risk of caesarean delivery and its subtypes, including CDMR. Given the rising global prevalence of obesity, and in view of the growth of CDMR, it seems likely that caesarean births will increase, unless there are changes in obstetrical practice. © 2015 John Wiley & Sons Ltd.

  6. Maternal Obesity: Risks for Developmental Delays in Early Childhood.

    Science.gov (United States)

    Duffany, Kathleen O'Connor; McVeigh, Katharine H; Kershaw, Trace S; Lipkind, Heather S; Ickovics, Jeannette R

    2016-02-01

    To assess the risk for neurodevelopmental delays for children of mothers who were obese (≥200 pounds) prior to pregnancy, and to characterize delays associated with maternal obesity among children referred to and found eligible to receive Early Intervention Program services. We conducted a retrospective cohort study (N = 541,816) using a population-based New York City data warehouse with linked birth and Early Intervention data. Risks for children suspected of a delay and 'significantly delayed', with two moderate or one severe delay, were calculated. Among the group of children eligible by delay for Early Intervention, analyses assessed risk for being identified with a moderate-to-severe delay across each of five functional domains as well as risks for multiple delays. Children of mothers who were obese were more likely to be suspected of a delay (adjusted RR 1.19 [CI 1.15-1.22]) and borderline association for 'significantly delayed' (adjusted RR 1.01 [CI 1.00-1.02). Among children eligible by delay, children of mothers who were obese evidenced an increased risk for moderate-to-severe cognitive (adjusted RR 1.04 [CI 1.02-1.07]) and physical (adjusted RR 1.04 [CI 1.01-1.08]) delays and for global developmental delay (adjusted RR 1.05 [CI 1.01-1.08]). Maternal obesity is associated with increased risk of developmental delay in offspring. Among children with moderate or severe delays, maternal obesity is associated with increased risk of cognitive and physical delays as well as with increased risk for global developmental delay. While causation remains uncertain, this adds to the growing body of research reporting an association between maternal obesity and neurodevelopmental delays in offspring.

  7. Maternal obesity and rate of cesarean delivery in Djibouti.

    Science.gov (United States)

    Minsart, Anne-Frederique; N'guyen, Thai-Son; Dimtsu, Hirut; Ratsimanresy, Rachel; Dada, Fouad; Ali Hadji, Rachid

    2014-11-01

    To calculate the prevalence of maternal obesity and to determine the relation between obesity and cesarean delivery in an urban hospital in Djibouti. In an observational cohort study, all women who had a live birth or stillbirth between October 2012 and November 2013 were considered for inclusion. Body mass index (BMI, calculated as weight in kilograms divided by the square of height in meters) was calculated throughout pregnancy, and women with a BMI of at least 30.0 were deemed to be obese. Multivariate logistic regression analyses were used to evaluate the relation between cesarean and obesity. Overall, 100 (24.8%) of 404 women were obese before 14 weeks of pregnancy, as were 112 (25.2%) of 445 before 22 weeks, and 200 (43.2%) of 463 at delivery. Obesity before 22 weeks was associated with a 127% excess risk of cesarean delivery (adjusted odds ratio 2.27; 95% CI 1.07-4.82; P=0.032). Similar trends were found when the analyses were limited to the subgroup of women without a previous cesarean delivery or primiparae. Prevalence of maternal obesity is high in Djibouti City and is related to an excess risk of cesarean delivery, even after controlling for a range of medical and socioeconomic variables. Copyright © 2014 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved.

  8. The role of family and maternal factors in childhood obesity.

    Science.gov (United States)

    Gibson, Lisa Y; Byrne, Susan M; Davis, Elizabeth A; Blair, Eve; Jacoby, Peter; Zubrick, Stephen R

    2007-06-04

    To investigate the relationship between a child's weight and a broad range of family and maternal factors. Cross-sectional data from a population-based prospective study, collected between January 2004 and December 2005, for 329 children aged 6-13 years (192 healthy weight, 97 overweight and 40 obese) and their mothers (n=265) recruited from a paediatric hospital endocrinology department and eight randomly selected primary schools in Perth, Western Australia. Height, weight and body mass index (BMI) of children and mothers; demographic information; maternal depression, anxiety, stress and self-esteem; general family functioning; parenting style; and negative life events. In a multilevel model, maternal BMI and family structure (single-parent v two-parent families) were the only significant predictors of child BMI z scores. Childhood obesity is not associated with adverse maternal or family characteristics such as maternal depression, negative life events, poor general family functioning or ineffective parenting style. However, having an overweight mother and a single-parent (single-mother) family increases the likelihood of a child being overweight or obese.

  9. Maternal obesity in Africa: a systematic review and meta-analysis.

    Science.gov (United States)

    Onubi, Ojochenemi J; Marais, Debbi; Aucott, Lorna; Okonofua, Friday; Poobalan, Amudha S

    2016-09-01

    Maternal obesity is emerging as a public health problem, recently highlighted together with maternal under-nutrition as a 'double burden', especially in African countries undergoing social and economic transition. This systematic review was conducted to investigate the current evidence on maternal obesity in Africa. MEDLINE, EMBASE, Scopus, CINAHL and PsycINFO were searched (up to August 2014) and identified 29 studies. Prevalence, associations with socio-demographic factors, labour, child and maternal consequences of maternal obesity were assessed. Pooled risk ratios comparing obese and non-obese groups were calculated. Prevalence of maternal obesity across Africa ranged from 6.5 to 50.7%, with older and multiparous mothers more likely to be obese. Obese mothers had increased risks of adverse labour, child and maternal outcomes. However, non-obese mothers were more likely to have low-birthweight babies. The differences in measurement and timing of assessment of maternal obesity were found across studies. No studies were identified either on the knowledge or attitudes of pregnant women towards maternal obesity; or on interventions for obese pregnant women. These results show that Africa's levels of maternal obesity are already having significant adverse effects. Culturally adaptable/sensitive interventions should be developed while monitoring to avoid undesired side effects. © The Author 2015. Published by Oxford University Press on behalf of Faculty of Public Health.

  10. Maternal Obesity, Gestational Weight Gain, and Asthma in Offspring.

    Science.gov (United States)

    Polinski, Kristen J; Liu, Jihong; Boghossian, Nansi S; McLain, Alexander C

    2017-11-09

    Obesity is common among women of childbearing age; intrauterine exposure to maternal obesity or gestational weight gain may influence the development of asthma in early childhood. We examined the relationships of maternal obesity and gestational weight gain with asthma in offspring. We used data from the Early Childhood Longitudinal Study-Birth Cohort, which has a nationally representative sample of children followed from birth in 2001 through age 4 (n = 6,450). Asthma was based on parental report of a medical professional's diagnosis. We used generalized estimating equation binomial models to compute adjusted odds ratios (ORs) of childhood asthma with maternal obesity and 4 measures of gestational weight gain. Compared with children of normal-weight mothers, children of obese mothers had increased risk of asthma (adjusted OR, 1.63; 95% confidence interval [CI], 1.26-2.12) by age 4, and children born to overweight mothers had similar risk (adjusted OR, 1.25; 95% CI, 0.99-1.59). Extreme-low weight gain (gain (≥25 kg) were associated with increased risk of asthma; however, the following measures were not significant predictors of asthma: meeting gestational weight gain recommendations of the Institute of Medicine, total gestational weight gain, and weekly rate of weight gain in the second and third trimesters. Extreme-low or extreme-high gestational weight gain and maternal obesity are risk factors for early childhood asthma, further evidence of the long-term impact of intrauterine exposure on children and the need to target preconception care to improve child health indicators.

  11. Maternal Obesity: Lifelong Metabolic Outcomes for Offspring from Poor Developmental Trajectories During the Perinatal Period.

    Science.gov (United States)

    Zambrano, Elena; Ibáñez, Carlos; Martínez-Samayoa, Paola M; Lomas-Soria, Consuelo; Durand-Carbajal, Marta; Rodríguez-González, Guadalupe L

    2016-01-01

    The prevalence of obesity in women of reproductive age is increasing in developed and developing countries around the world. Human and animal studies indicate that maternal obesity adversely impacts both maternal health and offspring phenotype, predisposing them to chronic diseases later in life including obesity, dyslipidemia, type 2 diabetes mellitus, and hypertension. Several mechanisms act together to produce these adverse health effects including programming of hypothalamic appetite-regulating centers, increasing maternal, fetal and offspring glucocorticoid production, changes in maternal metabolism and increasing maternal oxidative stress. Effective interventions during human pregnancy are needed to prevent both maternal and offspring metabolic dysfunction due to maternal obesity. This review addresses the relationship between maternal obesity and its negative impact on offspring development and presents some maternal intervention studies that propose strategies to prevent adverse offspring metabolic outcomes. Copyright © 2016 IMSS. Published by Elsevier Inc. All rights reserved.

  12. A study of association of obesity with maternal complications

    International Nuclear Information System (INIS)

    Iqbal, N.; Rahim, S.; Azhar, I.A.

    2013-01-01

    To determine the association of obesity with maternal complications. Methodology: A prospective cohort study was conducted at Gynae Unit lll Jinnah Hospital Lahore, from 21st May 2011 to 20th Nov.2011 All women fulfilling the inclusion were included in this study. Two groups were made, Group l was allotted to obese pregnant women and Group ll was allotted to non-obese pregnant women. Demographic data included age, parity, duration of pregnancy and maternal complications i-e urinary tract infection , instrumental vaginal delivery and post-partum haemorrhage were recorded and analyzed by SPSS -version 13. Results: The results of this study revealed that demographics like age parity and duration of pregnancy were almost similar in both groups , common age was 25.21 +- 2.73 in group-A and 26.34 +- 3.56 years in group -B . Comparison of maternal complications revealed that 22.23 % in group-A and 10.70% in group -B had urinary tract infection, relative risk was 2.087, instrumental delivery in group -A was 14.42% and in group-B was 4.19% relative risk was 3.44 while post-partum haemorrhage was 9.77% in group -A and 3.26% in group -B , relative risk was 3.00. Conclusion: The frequency of maternal complications is higher among obese pregnant women so it is recommended that every pregnant woman who presents with increased BMI should be sort out for maternal complications. (author)

  13. Maternal Super Obesity and Neonatal Morbidity after Term Cesarean Delivery.

    Science.gov (United States)

    Smid, Marcela C; Vladutiu, Catherine J; Dotters-Katz, Sarah K; Manuck, Tracy A; Boggess, Kim A; Stamilio, David M

    2016-10-01

    Objective To estimate the association between maternal super obesity (body mass index [BMI] ≥ 50 kg/m(2)) and neonatal morbidity among neonates born via cesarean delivery (CD). Methods Retrospective cohort of singleton neonates delivered via CD ≥ 37 weeks in the Maternal-Fetal Medicine Unit Cesarean Registry. Maternal BMI at delivery was stratified as 18.5 to 29.9 kg/m(2), 30 to 39.9 kg/m(2), 40 to 49.9 kg/m(2), and ≥ 50 kg/m(2). Primary outcomes included acute (5-minute Apgar score neonatal injury, and/or transient tachypnea of the newborn) and severe (grade 3 or 4 intraventricular hemorrhage, necrotizing enterocolitis, seizure, respiratory distress syndrome, hypoxic ischemic encephalopathy, meconium aspiration, ventilator support ≥ 2 days, sepsis and/or neonatal death) neonatal morbidity. Odds of neonatal morbidity were estimated for each BMI category adjusting for clinical and operative characteristics. Results Of 41,262 maternal-neonatal dyads, 36% of women were nonobese, 49% had BMI of 30 to 39.9 kg/m(2), 12% had BMI of 40 to 49.9 kg/m(2), and 3% were super obese. Compared with nonobese women, super obese women had twofold odds of acute (5 vs. 10%; adjusted odds ratio [aOR]: 1.81, 95% confidence interval [CI]: 1.59-2.73) and severe (3 vs. 6%; aOR: 2.08; 95% CI: 1.59-2.73) neonatal morbidity. Conclusion Among term infants delivered via CD, maternal super obesity is associated with increased risk of neonatal morbidity. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

  14. Dietary patterns of obese children: Maternal perceptions and experiences

    Directory of Open Access Journals (Sweden)

    Marina Linhares Bezerra CAMPOS

    Full Text Available ABSTRACT Objective: To understand maternal perceptions and experiences regarding the eating habits of obese children aged five to nine years. Methods: This is a qualitative research, and semi-structured interviews and discourse analysis were used to interpret narratives of 13 women from the city of Fortaleza, Ceará state, Brazil. Results: These women described the eating habits of their obese children in terms of how they eat and mentioned: eating fast, eating in front of the television, secret eating, eating large amounts of food, and the consumption of processed foods that are high in fat, sugars, and sodium. Conclusion: Seeing the mother and her obese child as a unit that needs support and guidance is a big step to plant the seeds to reap the rewards, i.e., exerting important impacts on the lives of these families and on the current scenario of childhood obesity.

  15. Prenatal Exposure to Maternal Obesity Alters Anxiety and Stress Coping Behaviors in Aged Mice.

    Science.gov (United States)

    Balsevich, Georgia; Baumann, Valentin; Uribe, Andres; Chen, Alon; Schmidt, Mathias V

    2016-01-01

    There is growing evidence that maternal obesity and prenatal exposure to a high-fat diet program fetal development to regulate the physiology and behavior of the offspring in adulthood. Yet the extent to which the maternal dietary environment contributes to adult disease vulnerability remains unclear. In the current study we tested whether prenatal exposure to maternal obesity increases the offspring's vulnerability to stress-related psychiatric disorders. We used a mouse model of maternal diet-induced obesity to investigate whether maternal obesity affects the response to adult chronic stress exposure in young adult (3-month-old) and aged adult (12-month-old) offspring. Long-lasting, delayed impairments to anxiety-like behaviors and stress coping strategies resulted on account of prenatal exposure to maternal obesity. Although maternal obesity did not change the offspring's behavioral response to chronic stress per se, we demonstrate that the behavioral outcomes induced by prenatal exposure to maternal obesity parallel the deleterious effects of adult chronic stress exposure in aged male mice. We found that the glucocorticoid receptor (GR, Nr3c1) is upregulated in various hypothalamic nuclei on account of maternal obesity. In addition, gene expression of a known regulator of the GR, FKBP51, is increased specifically within the paraventricular nucleus. These findings indicate that maternal obesity parallels the deleterious effects of adult chronic stress exposure, and furthermore identifies GR/FKBP51 signaling as a novel candidate pathway regulated by maternal obesity. © 2015 S. Karger AG, Basel.

  16. Maternal obesity (Class I-III), gestational weight gain and maternal leptin levels during and after pregnancy : a prospective cohort study

    OpenAIRE

    Carlhäll, Sara; Bladh, Marie; Brynhildsen, Jan; Claesson, Ing-Marie; Josefsson, Ann; Sydsjö, Gunilla; Thorsell, Annika; Blomberg, Marie

    2016-01-01

    Background Maternal obesity is accompanied by maternal and fetal complications during and after pregnancy. The risks seem to increase with degree of obesity. Leptin has been suggested to play a role in the development of obesity related complications. Whether maternal leptin levels differ between obese and morbidly obese women, during and after pregnancy, have to our knowledge not been previously described. Neither has the association between maternal leptin levels and gestational weight gain...

  17. Early Maternal Employment and Childhood Obesity among Economically Disadvantaged Families in the USA

    Science.gov (United States)

    Coley, Rebekah Levine; Lombardi, Caitlin McPherran

    2012-01-01

    Research indicates a link between maternal employment and children's risk of obesity, but little prior work has addressed maternal employment during children's infancy. This study examined the timing and intensity of early maternal employment and associations with children's later overweight and obesity in a sample of low-income families in…

  18. Dietary Proteins, Developmental Programming, and Potential Implication in Maternal Obesity

    Directory of Open Access Journals (Sweden)

    Alireza Jahan-mihan

    2017-08-01

    Full Text Available Background: Proteins are known mainly based on their metabolic and nutritional functions including protein synthesis and a source of energy. In spite of various physiological properties attributed to proteins, their functions have neither been addressed by assessing quality of proteins nor by nutrition and dietetic practices. Methods: Studies were included if they were randomized animal studies, clinical trials and systematic reviews/meta-analysis published in English language. Results: The effect of maternal diet in general and dietary proteins in particular during development on health of offspring has been well-studied. Protein content as well as source of protein in the diet consumed during pregnancy and lactation influenced the risk of metabolic syndrome characteristics in offspring. Both high and low protein diets showed detrimental effects on health of offspring. Moreover, comparison of maternal casein-based diet with soy protein-based diet showed more favorable effect on body weight, body composition, blood pressure, and glucose metabolism in offspring. However, the role of maternal dietary proteins in developing the risk of metabolic syndrome characteristics in offspring in gestational obesity is still unclear and needs further study. Conclusions: Dietary proteins are determining factors in developmental programming. Both quantity and source of proteins in maternal diet influenced the development of metabolic syndrome characteristics in offspring. However, whether they have the same function in presence of gestational obesity is still unclear and needs further study.

  19. Maternal obesity and Caesarean delivery in sub-Saharan Africa.

    Science.gov (United States)

    Cresswell, Jenny A; Campbell, Oona M R; De Silva, Mary J; Slaymaker, Emma; Filippi, Veronique

    2016-07-01

    To quantify maternal obesity as a risk factor for Caesarean delivery in sub-Saharan Africa. Multivariable logistic regression analysis using 31 nationally representative cross-sectional data sets from the Demographic and Health Surveys (DHS). Maternal obesity was a risk factor for Caesarean delivery in sub-Saharan Africa; a clear dose-response relationship (where the magnitude of the association increased with increasing BMI) was observable. Compared to women of optimal weight, overweight women (BMI 25-29 kg/m(2) ) were significantly more likely to deliver by Caesarean (OR: 1.54; 95% CI: 1.33, 1.78), as were obese women (30-34.9 kg/m(2) (OR: 2.39; 95%CI: 1.96-2.90); 35-39.9 kg/m(2) (OR: 2.47 95%CI: 1.78-3.43)) and morbidly obese women (BMI ≥40 kg/m(2) OR: 3.85; 95% CI: 2.46-6.00). BMI is projected to rise substantially in sub-Saharan Africa over the next few decades and demand for Caesarean sections already exceeds available capacity. Overweight women should be advised to lose weight prior to pregnancy. Furthermore, culturally appropriate prevention strategies to discourage further population-level rises in BMI need to be designed and implemented. © 2016 The Authors. Tropical Medicine & International Health Published by John Wiley & Sons Ltd.

  20. The role of maternal obesity in the risk of neuropsychiatric disorders

    OpenAIRE

    Heidi Michelle Rivera; Kelly J Christiansen; Elinor L Sullivan; Elinor L Sullivan

    2015-01-01

    Recent evidence indicates that perinatal exposure to maternal obesity, metabolic disease, including diabetes and hypertension, and unhealthy maternal diet has a long-term impact on offspring behavior and physiology. During the past three decades, the prevalence of both obesity and neuropsychiatric disorders has rapidly increased. Epidemiologic studies provide evidence that maternal obesity and metabolic complications increase the risk of attention deficit hyperactivity disorder, autism spectr...

  1. Maternal obesity in early pregnancy and risk of adverse outcomes.

    Science.gov (United States)

    Bautista-Castaño, Inmaculada; Henriquez-Sanchez, Patricia; Alemán-Perez, Nestor; Garcia-Salvador, Jose J; Gonzalez-Quesada, Alicia; García-Hernández, Jose A; Serra-Majem, Luis

    2013-01-01

    To assess the role of the health consequences of maternal overweight and obesity at the start of pregnancy on gestational pathologies, delivery and newborn characteristics. A cohort of pregnant women (n = 6.558) having delivered at the Maternal & Child University Hospital of Gran Canaria (HUMIGC) in 2008 has been studied. Outcomes were compared using multivariate analyses controlling for confounding variables. Compared to normoweight, overweight and obese women have greater risks of gestational diabetes mellitus (RR = 2.13 (95% CI: 1.52-2.98) and (RR = 2.85 (95% CI: 2.01-4.04), gestational hypertension (RR = 2.01 (95% CI: 1.27-3.19) and (RR = 4.79 (95% CI: 3.13-7.32) and preeclampsia (RR = 3.16 (95% CI: 1.12-8.91) and (RR = 8.80 (95% CI: 3.46-22.40). Obese women have also more frequently oligodramnios (RR = 2.02 (95% CI: 1.25-3.27), polyhydramnios. (RR = 1.76 (95% CI: 1.03-2.99), tearing (RR = 1.24 (95% CI: 1.05-1.46) and a lower risk of induced deliveries (RR = 0.83 (95% CI: 0.72-0.95). Both groups have more frequently caesarean section (RR = 1.36 (95% CI: 1.14-1.63) and (RR = 1.84 (95% CI: 1.53-2.22) and manual placenta extraction (RR = 1.65 (95% CI: 1.28-2.11) and (RR = 1.77 (95% CI: 1.35-2.33). Newborns from overweight and obese women have higher weight (pApgar 1 min was significantly higher in newborns from normoweight mothers: 8.65 (95% CI: 8.62-8.69) than from overweight: 8.56 (95% CI: 8.50-8.61) or obese mothers: 8.48 (95% CI: 8.41-8.54). Obesity and overweight status at the beginning of pregnancy increase the adverse outcomes of the pregnancy. It is important to promote the normalization of bodyweight in those women who intend to get pregnant and to provide appropriate advice to the obese women of the risks of obesity at the start of the pregnancy.

  2. Childhood obesity is associated with maternal smoking in pregnancy.

    Science.gov (United States)

    Toschke, André Michael; Koletzko, Berthold; Slikker, William; Hermann, Monika; von Kries, Rüdiger

    2002-08-01

    Overweight and obesity are major public health issues. Childhood obesity often persists throughout adulthood. Recently a higher prevalence of obesity in adults whose mothers smoked during pregnancy was reported. The aim of this study was to assess whether this association is also detectable in pre-school children in a different setting and to identify the critical period for intrauterine exposure to inhaled smoke products in pregnancy. We analysed questionnaire data on early feeding and lifestyle factors of 8,765 German children aged 5.00 to 6.99 years. Obesity was defined as a body mass index >97th percentile. The prevalence estimates for obesity were: mother never smoked 2.8% (95% CI 2.4%-3.2%), smoked after pregnancy only 1.6% (95%CI 0.4%-4.1%), smoked throughout pregnancy 6.2% (95% CI 4.5%-8.3%), smoked before pregnancy, but not throughout 4.5% (95%CI 3.6%-5.7%). These associations could not be explained by confounding due to a number of constitutional, sociodemographic and lifestyle factors. The unadjusted/adjusted odds ratios were: smoked during pregnancy: 2.32 (95% CI 1.63%-3.30%)/1.92 (95% CI 1.29%-2.86%); smoked before, but not throughout pregnancy: 1.67 (95%CI 1.26%-2.22%)/1.74 (95%CI 1.29%-2.34%). the association of maternal smoking in pregnancy and obesity was also detectable in children at school entry. Since smoking after pregnancy was not associated with childhood obesity, intrauterine exposure rather than family lifestyle factors associated with smoking appears to be instrumental. There appears to be a role for early intrauterine exposure.

  3. The impact of maternal obesity on inflammatory processes and consequences for later offspring health outcomes.

    Science.gov (United States)

    Segovia, S A; Vickers, M H; Reynolds, C M

    2017-10-01

    Obesity is a global epidemic, affecting both developed and developing countries. The related metabolic consequences that arise from being overweight or obese are a paramount global health concern, and represent a significant burden on healthcare systems. Furthermore, being overweight or obese during pregnancy increases the risk of offspring developing obesity and other related metabolic complications in later life, which can therefore perpetuate a transgenerational cycle of obesity. Obesity is associated with a chronic state of low-grade metabolic inflammation. However, the role of maternal obesity-mediated alterations in inflammatory processes as a mechanism underpinning developmental programming in offspring is less understood. Further, the use of anti-inflammatory agents as an intervention strategy to ameliorate or reverse the impact of adverse developmental programming in the setting of maternal obesity has not been well studied. This review will discuss the impact of maternal obesity on key inflammatory pathways, impact on pregnancy and offspring outcomes, potential mechanisms and avenues for intervention.

  4. Association between Maternal Obesity and Autism Spectrum Disorder in Offspring: A Meta-Analysis

    Science.gov (United States)

    Li, Ya-Min; Ou, Jian-Jun; Liu, Li; Zhang, Dan; Zhao, Jing-Ping; Tang, Si-Yuan

    2016-01-01

    As the link between maternal obesity and risk of autism among offspring is unclear, the present study assessed this association. A systematic search of an electronic database was performed to identify observational studies that examined the association between maternal obesity and autism. The outcome measures were odds ratios comparing offspring…

  5. Maternal diagnosis of obesity and risk of cerebral palsy in the child.

    Science.gov (United States)

    Crisham Janik, Mary D; Newman, Thomas B; Cheng, Yvonne W; Xing, Guibo; Gilbert, William M; Wu, Yvonne W

    2013-11-01

    To examine the association between maternal hospital diagnoses of obesity and risk of cerebral palsy (CP) in the child. For all California hospital births from 1991-2001, we linked infant and maternal hospitalization discharge abstracts to California Department of Developmental Services records of children receiving services for CP. We identified maternal hospital discharge diagnoses of obesity (International Classification of Diseases, 9th edition 646.1, 278.00, or 278.01) and morbid obesity (International Classification of Diseases, 9th edition 278.01), and performed logistic regression to explore the relationship between maternal obesity diagnoses and CP. Among 6.2 million births, 67 200 (1.1%) mothers were diagnosed with obesity, and 7878 (0.1%) with morbid obesity; 8798 (0.14%) children had CP. A maternal diagnosis of obesity (relative risk [RR] 1.30, 95% CI 1.09-1.55) or morbid obesity (RR 2.70, 95% CI 1.89-3.86) was associated with increased risk of CP. In multivariable analysis adjusting for maternal race, age, education, prenatal care, insurance status, and infant sex, both obesity (OR 1.27, 95% CI 1.06-1.52) and morbid obesity (OR 2.56, 95% CI 1.79-3.66) remained independently associated with CP. On stratified analyses, the association of obesity (RR 1.72, 95% CI 1.25-2.35) or morbid obesity (RR 3.79, 95% CI 2.35-6.10) with CP was only significant among women who were hospitalized prior to the birth admission. Adjusting for potential comorbidities and complications of obesity did not eliminate this association. Maternal obesity may confer an increased risk of CP in some cases. Further studies are needed to confirm this finding. Copyright © 2013 Mosby, Inc. All rights reserved.

  6. Prenatal Exposure to Maternal Obesity Alters Anxiety and Stress Coping Behaviors in Aged Mice

    OpenAIRE

    Balsevich, G.; Baumann, V.; Uribe, A.; Chen, A.; Schmidt, M.

    2016-01-01

    Background: There is growing evidence that maternal obesity and prenatal exposure to a high-fat diet program fetal development to regulate the physiology and behavior of the offspring in adulthood. Yet the extent to which the maternal dietary environment contributes to adult disease vulnerability remains unclear. In the current study we tested whether prenatal exposure to maternal obesity increases the offspring's vulnerability to stress-related psychiatric disorders. Methods: We used a mouse...

  7. Maternal obesity in early pregnancy and risk of adverse outcomes.

    Directory of Open Access Journals (Sweden)

    Inmaculada Bautista-Castaño

    Full Text Available To assess the role of the health consequences of maternal overweight and obesity at the start of pregnancy on gestational pathologies, delivery and newborn characteristics.A cohort of pregnant women (n = 6.558 having delivered at the Maternal & Child University Hospital of Gran Canaria (HUMIGC in 2008 has been studied. Outcomes were compared using multivariate analyses controlling for confounding variables.Compared to normoweight, overweight and obese women have greater risks of gestational diabetes mellitus (RR = 2.13 (95% CI: 1.52-2.98 and (RR = 2.85 (95% CI: 2.01-4.04, gestational hypertension (RR = 2.01 (95% CI: 1.27-3.19 and (RR = 4.79 (95% CI: 3.13-7.32 and preeclampsia (RR = 3.16 (95% CI: 1.12-8.91 and (RR = 8.80 (95% CI: 3.46-22.40. Obese women have also more frequently oligodramnios (RR = 2.02 (95% CI: 1.25-3.27, polyhydramnios. (RR = 1.76 (95% CI: 1.03-2.99, tearing (RR = 1.24 (95% CI: 1.05-1.46 and a lower risk of induced deliveries (RR = 0.83 (95% CI: 0.72-0.95. Both groups have more frequently caesarean section (RR = 1.36 (95% CI: 1.14-1.63 and (RR = 1.84 (95% CI: 1.53-2.22 and manual placenta extraction (RR = 1.65 (95% CI: 1.28-2.11 and (RR = 1.77 (95% CI: 1.35-2.33. Newborns from overweight and obese women have higher weight (p<0.001 and a greater risk of being macrosomic (RR = 2.00 (95% CI: 1.56-2.56 and (RR = 2.74 (95% CI: 2.12-3.54. Finally, neonates from obese mother have a higher risk of being admitted to special care units (RR = 1.34 (95% CI: 1.01-1.77. Apgar 1 min was significantly higher in newborns from normoweight mothers: 8.65 (95% CI: 8.62-8.69 than from overweight: 8.56 (95% CI: 8.50-8.61 or obese mothers: 8.48 (95% CI: 8.41-8.54.Obesity and overweight status at the beginning of pregnancy increase the adverse outcomes of the pregnancy. It is important to promote the normalization of bodyweight in those women who intend to get pregnant and to

  8. Maternal work and children's diet, activity, and obesity.

    Science.gov (United States)

    Datar, Ashlesha; Nicosia, Nancy; Shier, Victoria

    2014-04-01

    Mothers' work hours are likely to affect their time allocation towards activities related to children's diet, activity and well-being. For example, mothers who work more may be more reliant on processed foods, foods prepared away from home and school meal programs for their children's meals. A greater number of work hours may also lead to more unsupervised time for children that may, in turn, allow for an increase in unhealthy behaviors among their children such as snacking and sedentary activities such as TV watching. Using data on a national cohort of children, we examine the relationship between mothers' average weekly work hours during their children's school years on children's dietary and activity behaviors, BMI and obesity in 5th and 8th grade. Our results are consistent with findings from the literature that maternal work hours are positively associated with children's BMI and obesity especially among children with higher socioeconomic status. Unlike previous papers, our detailed data on children's behaviors allow us to speak directly to affected behaviors that may contribute to the increased BMI. We show that children whose mothers work more consume more unhealthy foods (e.g. soda, fast food) and less healthy foods (e.g. fruits, vegetables, milk) and watch more television. Although they report being slightly more physically active, likely due to organized physical activities, the BMI and obesity results suggest that the deterioration in diet and increase in sedentary behaviors dominate. Copyright © 2014 Elsevier Ltd. All rights reserved.

  9. Do Maternal Caregiver Perceptions of Childhood Obesity Risk Factors and Obesity Complications Predict Support for Prevention Initiatives Among African Americans?

    Science.gov (United States)

    Alexander, Dayna S; Alfonso, Moya L; Cao, Chunhua; Wright, Alesha R

    2017-07-01

    Objectives African American maternal caregiver support for prevention of childhood obesity may be a factor in implementing, monitoring, and sustaining children's positive health behaviors. However, little is known about how perceptions of childhood obesity risk factors and health complications influence caregivers' support of childhood obesity prevention strategies. The objective of this study was to determine if childhood obesity risk factors and health complications were associated with maternal caregivers' support for prevention initiatives. Methods A convenience sample of maternal caregivers (N = 129, ages 22-65 years) completed the childhood obesity perceptions (COP) survey. A linear regression was conducted to determine whether perceptions about childhood obesity risk factors and subsequent health complications influenced caregivers' support for prevention strategies. Results Caregivers' perceptions of childhood obesity risk factors were moderate (M = 3.4; SD = 0.64), as were their perceptions of obesity-related health complications (M = 3.3; SD = 0.75); however, they perceived a high level of support for prevention strategies (M = 4.2; SD = 0.74). In the regression model, only health complications were significantly associated with caregiver support (β = 0.348; p obesity prevention efforts should emphasize health complications by providing education and strategies that promote self-efficacy and outcome expectations among maternal caregivers.

  10. The renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet

    Science.gov (United States)

    Glastras, Sarah J.; Chen, Hui; Tsang, Michael; Teh, Rachel; McGrath, Rachel T.; Zaky, Amgad; Chen, Jason; Wong, Muh Geot; Pollock, Carol A.; Saad, Sonia

    2017-01-01

    Aims/Hypothesis Developmental programming induced by maternal obesity influences the development of chronic disease in offspring. In the present study, we aimed to determine whether maternal obesity exaggerates obesity-related kidney disease. Methods Female C57BL/6 mice were fed high-fat diet (HFD) for six weeks prior to mating, during gestation and lactation. Male offspring were weaned to normal chow or HFD. At postnatal Week 8, HFD-fed offspring were administered one dose streptozotocin (STZ, 100 mg/kg i.p.) or vehicle control. Metabolic parameters and renal functional and structural changes were observed at postnatal Week 32. Results HFD-fed offspring had increased adiposity, glucose intolerance and hyperlipidaemia, associated with increased albuminuria and serum creatinine levels. Their kidneys displayed structural changes with increased levels of fibrotic, inflammatory and oxidative stress markers. STZ administration did not potentiate the renal effects of HFD. Though maternal obesity had a sustained effect on serum creatinine and oxidative stress markers in lean offspring, the renal consequences of maternal obesity were overwhelmed by the powerful effect of diet-induced obesity. Conclusion Maternal obesity portends significant risks for metabolic and renal health in adult offspring. However, diet-induced obesity is an overwhelming and potent stimulus for the development of CKD that is not potentiated by maternal obesity. PMID:28225809

  11. The renal consequences of maternal obesity in offspring are overwhelmed by postnatal high fat diet.

    Directory of Open Access Journals (Sweden)

    Sarah J Glastras

    Full Text Available Developmental programming induced by maternal obesity influences the development of chronic disease in offspring. In the present study, we aimed to determine whether maternal obesity exaggerates obesity-related kidney disease.Female C57BL/6 mice were fed high-fat diet (HFD for six weeks prior to mating, during gestation and lactation. Male offspring were weaned to normal chow or HFD. At postnatal Week 8, HFD-fed offspring were administered one dose streptozotocin (STZ, 100 mg/kg i.p. or vehicle control. Metabolic parameters and renal functional and structural changes were observed at postnatal Week 32.HFD-fed offspring had increased adiposity, glucose intolerance and hyperlipidaemia, associated with increased albuminuria and serum creatinine levels. Their kidneys displayed structural changes with increased levels of fibrotic, inflammatory and oxidative stress markers. STZ administration did not potentiate the renal effects of HFD. Though maternal obesity had a sustained effect on serum creatinine and oxidative stress markers in lean offspring, the renal consequences of maternal obesity were overwhelmed by the powerful effect of diet-induced obesity.Maternal obesity portends significant risks for metabolic and renal health in adult offspring. However, diet-induced obesity is an overwhelming and potent stimulus for the development of CKD that is not potentiated by maternal obesity.

  12. Does maternal psychopathology increase the risk of pre-schooler obesity? A systematic review.

    Science.gov (United States)

    Benton, Pree M; Skouteris, Helen; Hayden, Melissa

    2015-04-01

    The preschool years may be a critical period for child obesity onset; however, literature examining obesity risk factors to date has largely focused on school-aged children. Several links have been made between maternal depression and childhood obesity risks; however, other types of maternal psychopathology have been widely neglected. The aim of the present review was to systematically identify articles that examined relationships between maternal psychopathology variables, including depressive and anxiety symptoms, self-esteem and body dissatisfaction, and risks for pre-schooler obesity, including weight outcomes, physical activity and sedentary behaviour levels, and nutrition/diet variables. Twenty articles meeting review criteria were identified. Results showed positive associations between maternal depressive symptoms and increased risks for pre-schooler obesity in the majority of studies. Results were inconsistent depending on the time at which depression was measured (i.e., antenatal, postnatal, in isolation or longitudinally). Anxiety and body dissatisfaction were only measured in single studies; however, both were linked to pre-schooler obesity risks; self-esteem was not measured by any studies. We concluded that maternal depressive symptoms are important to consider when assessing risks for obesity in preschool-aged children; however, more research is needed examining the impact of other facets of maternal psychopathology on obesity risk in pre-schoolers. Copyright © 2014 Elsevier Ltd. All rights reserved.

  13. Maternal Pre-Gravid Obesity Changes Gene Expression Profiles Towards Greater Inflammation and Reduced Insulin Sensitivity in Umbilical Cord

    Science.gov (United States)

    Thakali, Keshari M.; Saben, Jessica; Faske, Jennifer B.; Lindsey, Forrest; Gomez-Acevedo, Horacio; Lowery, Curtis L.; Badger, Thomas M.; Andres, Aline; Shankar, Kartik

    2014-01-01

    Background Maternal obesity is associated with unfavorable outcomes, which may be reflected in the as yet undiscovered gene expression profiles of the umbilical cord (UC). Methods UCs from 12 lean (pre-gravid BMI obese (OW/OB, pre-gravid BMI ≥25) women without gestational diabetes were collected for gene expression analysis using Human Primeview microarrays (Affymetrix). Metabolic parameters were assayed in mother’s plasma and cord blood. Results Although offspring birth weight and adiposity (at 2-wk) did not differ between groups, expression of 232 transcripts was affected in UC from OW/OB compared to those of lean mothers. GSEA analysis revealed an up-regulation of genes related to metabolism, stimulus and defense response and inhibitory to insulin signaling in the OW/OB group. We confirmed that EGR1, periostin, and FOSB mRNA expression was induced in UCs from OW/OB moms, while endothelin receptor B, KFL10, PEG3 and EGLN3 expression was decreased. Messenger RNA expression of EGR1, FOSB, MEST and SOCS1 were positively correlated (pmaternal obesity and changes in UC gene expression profiles favoring inflammation and insulin resistance, potentially predisposing infants to develop metabolic dysfunction later on in life. PMID:24819376

  14. Teratology Public Affairs Committee position paper: maternal obesity and pregnancy.

    Science.gov (United States)

    Scialli, Anthony R

    2006-02-01

    Compared to normal-weight women, obese women have an increased risk of infertility and pregnancy complications. The most consistently described pregnancy complications are hypertensive disorders, gestational diabetes mellitus, thromboembolic events, and cesarean section. Fetal and neonatal complications may include congenital malformations, macrosomia, and shoulder dystocia. The literature suggests that women with a body mass index (BMI) >or=30 have approximately double the risk of having a child with a neural tube defect (NTD) compared to normal-weight women, and the increased risk associated with higher maternal body weight does not appear to be modified by folic acid supplementation. The Public Affairs Committee of the Teratology Society supports the public health initiatives identified by the U.S. Food and Drug Administration in 2004 and the research initiatives identified by the National Institutes of Health in 2004. The Public Affairs Committee recommends that clinicians counsel women about appropriate caloric intake and exercise and that health-care providers educate parents about appropriate childhood nutrition. Breast-feeding should be encouraged based on evidence of a protective effect against childhood obesity, as well as other health advantages. Birth Defects Research (Part A), 2006. (c) 2006 Wiley-Liss, Inc.

  15. Genetic Evidence for Causal Relationships Between Maternal Obesity-Related Traits and Birth Weight

    DEFF Research Database (Denmark)

    Tyrrell, Jessica; Richmond, Rebecca C; Palmer, Tom M

    2016-01-01

    IMPORTANCE: Neonates born to overweight or obese women are larger and at higher risk of birth complications. Many maternal obesity-related traits are observationally associated with birth weight, but the causal nature of these associations is uncertain. OBJECTIVE: To test for genetic evidence...... of causal associations of maternal body mass index (BMI) and related traits with birth weight. DESIGN, SETTING, AND PARTICIPANTS: Mendelian randomization to test whether maternal BMI and obesity-related traits are potentially causally related to offspring birth weight. Data from 30,487 women in 18 studies...

  16. Maternal Obesity Is Associated with Alterations in the Gut Microbiome in Toddlers

    Science.gov (United States)

    Galley, Jeffrey D.; Bailey, Michael; Kamp Dush, Claire; Schoppe-Sullivan, Sarah; Christian, Lisa M.

    2014-01-01

    Children born to obese mothers are at increased risk for obesity, but the mechanisms behind this association are not fully delineated. A novel possible pathway linking maternal and child weight is the transmission of obesogenic microbes from mother to child. The current study examined whether maternal obesity was associated with differences in the composition of the gut microbiome in children in early life. Fecal samples from children 18–27 months of age (n = 77) were analyzed by pyro-tag 16S sequencing. Significant effects of maternal obesity on the composition of the gut microbiome of offspring were observed among dyads of higher socioeconomic status (SES). In the higher SES group (n = 47), children of obese (BMI≥30) versus non-obese mothers clustered on a principle coordinate analysis (PCoA) and exhibited greater homogeneity in the composition of their gut microbiomes as well as greater alpha diversity as indicated by the Shannon Diversity Index, and measures of richness and evenness. Also in the higher SES group, children born to obese versus non-obese mothers had differences in abundances of Faecalibacterium spp., Eubacterium spp., Oscillibacter spp., and Blautia spp. Prior studies have linked some of these bacterial groups to differences in weight and diet. This study provides novel evidence that maternal obesity is associated with differences in the gut microbiome in children in early life, particularly among those of higher SES. Among obese adults, the relative contribution of genetic versus behavioral factors may differ based on SES. Consequently, the extent to which maternal obesity confers measureable changes to the gut microbiome of offspring may differ based on the etiology of maternal obesity. Continued research is needed to examine this question as well as the relevance of the observed differences in gut microbiome composition for weight trajectory over the life course. PMID:25409177

  17. Maternal obesity is associated with alterations in the gut microbiome in toddlers.

    Directory of Open Access Journals (Sweden)

    Jeffrey D Galley

    Full Text Available Children born to obese mothers are at increased risk for obesity, but the mechanisms behind this association are not fully delineated. A novel possible pathway linking maternal and child weight is the transmission of obesogenic microbes from mother to child. The current study examined whether maternal obesity was associated with differences in the composition of the gut microbiome in children in early life. Fecal samples from children 18-27 months of age (n = 77 were analyzed by pyro-tag 16S sequencing. Significant effects of maternal obesity on the composition of the gut microbiome of offspring were observed among dyads of higher socioeconomic status (SES. In the higher SES group (n = 47, children of obese (BMI≥30 versus non-obese mothers clustered on a principle coordinate analysis (PCoA and exhibited greater homogeneity in the composition of their gut microbiomes as well as greater alpha diversity as indicated by the Shannon Diversity Index, and measures of richness and evenness. Also in the higher SES group, children born to obese versus non-obese mothers had differences in abundances of Faecalibacterium spp., Eubacterium spp., Oscillibacter spp., and Blautia spp. Prior studies have linked some of these bacterial groups to differences in weight and diet. This study provides novel evidence that maternal obesity is associated with differences in the gut microbiome in children in early life, particularly among those of higher SES. Among obese adults, the relative contribution of genetic versus behavioral factors may differ based on SES. Consequently, the extent to which maternal obesity confers measureable changes to the gut microbiome of offspring may differ based on the etiology of maternal obesity. Continued research is needed to examine this question as well as the relevance of the observed differences in gut microbiome composition for weight trajectory over the life course.

  18. Maternal obesity is associated with alterations in the gut microbiome in toddlers.

    Science.gov (United States)

    Galley, Jeffrey D; Bailey, Michael; Kamp Dush, Claire; Schoppe-Sullivan, Sarah; Christian, Lisa M

    2014-01-01

    Children born to obese mothers are at increased risk for obesity, but the mechanisms behind this association are not fully delineated. A novel possible pathway linking maternal and child weight is the transmission of obesogenic microbes from mother to child. The current study examined whether maternal obesity was associated with differences in the composition of the gut microbiome in children in early life. Fecal samples from children 18-27 months of age (n = 77) were analyzed by pyro-tag 16S sequencing. Significant effects of maternal obesity on the composition of the gut microbiome of offspring were observed among dyads of higher socioeconomic status (SES). In the higher SES group (n = 47), children of obese (BMI≥30) versus non-obese mothers clustered on a principle coordinate analysis (PCoA) and exhibited greater homogeneity in the composition of their gut microbiomes as well as greater alpha diversity as indicated by the Shannon Diversity Index, and measures of richness and evenness. Also in the higher SES group, children born to obese versus non-obese mothers had differences in abundances of Faecalibacterium spp., Eubacterium spp., Oscillibacter spp., and Blautia spp. Prior studies have linked some of these bacterial groups to differences in weight and diet. This study provides novel evidence that maternal obesity is associated with differences in the gut microbiome in children in early life, particularly among those of higher SES. Among obese adults, the relative contribution of genetic versus behavioral factors may differ based on SES. Consequently, the extent to which maternal obesity confers measureable changes to the gut microbiome of offspring may differ based on the etiology of maternal obesity. Continued research is needed to examine this question as well as the relevance of the observed differences in gut microbiome composition for weight trajectory over the life course.

  19. Obesity Disrupts the Rhythmic Profiles of Maternal and Fetal Progesterone in Rat Pregnancy.

    Science.gov (United States)

    Crew, Rachael C; Mark, Peter J; Clarke, Michael W; Waddell, Brendan J

    2016-09-01

    Maternal obesity increases the risk of abnormal fetal growth, but the underlying mechanisms remain unclear. Because steroid hormones regulate fetal growth, and both pregnancy and obesity markedly alter circadian biology, we hypothesized that maternal obesity disrupts the normal rhythmic profiles of steroid hormones in rat pregnancy. Obesity was established by cafeteria (CAF) feeding for 8 wk prior to mating and throughout pregnancy. Control (CON) animals had ad libitum access to chow. Daily profiles of plasma corticosterone, 11-dehydrocorticosterone, progesterone, and testosterone were measured at Days 15 and 21 of gestation (term = 23 days) in maternal (both days) and fetal (Day 21) plasma. CAF mothers exhibited increased adiposity relative to CON and showed fetal and placental growth restriction. There was no change, however, in total fetal or placental mass due to slightly larger litter sizes in CAF. Nocturnal declines in progesterone were observed in maternal (39% lower) and fetal (45% lower) plasma in CON animals, but these were absent in CAF animals. CAF mothers were hyperlipidemic at both days of gestation, but this effect was isolated to the dark period at Day 21. CAF maternal testosterone was slightly lower at Day 15 (8%) but increased above CON by Day 21 (16%). Despite elevated maternal testosterone, male fetal testosterone was suppressed by obesity on Day 21. Neither maternal nor fetal glucocorticoid profiles were affected by obesity. In conclusion, obesity disrupts rhythmic profiles of maternal and fetal progesterone, preventing the normal nocturnal decline. Obesity subtly changed testosterone profiles but did not alter maternal and fetal glucocorticoids. © 2016 by the Society for the Study of Reproduction, Inc.

  20. Increased chemerin concentrations in fetuses of obese mothers and correlation with maternal insulin sensitivity.

    Science.gov (United States)

    Barker, Gillian; Lim, Ratana; Rice, Gregory E; Lappas, Martha

    2012-11-01

    The aim of this study was to determine the effect of maternal obesity and gestational diabetes mellitus (GDM) on (i) the circulating concentrations of chemerin in cord and maternal plasma, and (ii) gene expression and release of chemerin from human placenta and adipose tissue. Chemerin concentrations were measured in maternal and cord plasma from 62 normal glucose tolerant women (NGT) and 69 women with GDM at the time of term elective Caesarean section. Placenta and adipose tissue expression and release of chemerin was measured from 22 NGT and 22 GDM women. There was no effect of maternal obesity or GDM on maternal chemerin concentrations. Chemerin concentrations were significantly higher in cord plasma from women with maternal obesity. Cord chemerin concentrations in NGT women negatively correlated with the concentrations of maternal insulin sensitivity. There was no effect of GDM on maternal and cord chemerin concentrations, and on the release of chemerin from placenta and adipose tissue. At the time of term Caesarean section, preexisting maternal obesity, and its associated insulin resistance, is associated with higher cord plasma chemerin concentrations.

  1. Maternal pre-pregnancy obesity and risk for inattention and negative emotionality in children.

    Science.gov (United States)

    Rodriguez, Alina

    2010-02-01

    This study aimed to replicate and extend previous work showing an association between maternal pre-pregnancy adiposity and risk for attention deficit hyperactivity disorder (ADHD) symptoms in children. A Swedish population-based prospective pregnancy-offspring cohort was followed up when children were 5 years old (N = 1,714). Mothers and kindergarten teachers rated children's ADHD symptoms, presence and duration of problems, and emotionality. Dichotomized outcomes examined difficulties of clinical relevance (top 15% of the distribution). Analyses adjusted for pregnancy (maternal smoking, depressive symptoms, life events, education, age, family structure), birth outcomes (birth weight, gestational age, infant sex) and concurrent variables (family structure, maternal depressive symptoms, parental ADHD symptoms, and child overweight) in an attempt to rule out confounding. Maternal pre-pregnancy overweight and obesity predicted high inattention symptom scores and obesity was associated with a two-fold increase in risk of difficulties with emotion intensity and emotion regulation according to teacher reports. Means of maternal ratings were unrelated to pre-pregnancy body mass index (BMI). Presence and duration of problems were associated with both maternal over and underweight according to teachers. Despite discrepancies between maternal and teacher reports, these results provide further evidence that maternal pre-pregnancy overweight and obesity are associated with child inattention symptoms and extend previous work by establishing a link between obesity and emotional difficulties. Maternal adiposity at the time of conception may be instrumental in programming child mental health, as prenatal brain development depends on maternal energy supply. Possible mechanisms include disturbed maternal metabolic function. If maternal pre-pregnancy obesity is a causal risk factor, the potential for prevention is great.

  2. Cord blood chemerin: differential effects of gestational diabetes mellitus and maternal obesity

    NARCIS (Netherlands)

    van Poppel, M.N.M.; Zeck, W.; Ulrich, D.; Schest, E.C.; Hirschmugl, B.; Lang, U.; Wadsack, C.; Desoye, G.

    2014-01-01

    Objective Chemerin is a novel adipokine implicated in inflammation and obesity. We hypothesized that foetal chemerin would be elevated in gestational diabetes mellitus (GDM) and correlate with foetal and maternal adiposity. Design Observational, longitudinal study. Subjects and measurements Foetal

  3. Maternal obesity influences the relationship between location of neonate fat mass and total fat mass.

    Science.gov (United States)

    Hull, H R; Thornton, J; Paley, C; Navder, K; Gallagher, D

    2015-08-01

    It is suggested that maternal obesity perpetuates offspring obesity to future generations. To determine whether location of neonate fat mass (FM: central vs. peripheral) is related to total neonate FM and whether maternal obesity influences this relationship. Neonate body composition and skin-fold thicknesses were assessed in healthy neonates (n = 371; 1-3 days old). Linear regression models examined the relationship between total FM and location of FM (central vs. peripheral). Location of FM was calculated by skin-folds: peripheral was the sum of (biceps and triceps)/2 and central was represented by the subscapular skin-fold. A significant interaction was found for location of FM and maternal obesity. Holding all predictors constant, in offspring born to non-obese mothers, a 0.5 mm increase in central FM predicted a 15 g greater total FM, whereas a 0.5 mm increase in peripheral FM predicted a 66 g greater total FM. However, in offspring born to obese mothers, a 0.5 mm increase in central FM predicted a 56 g total FM, whereas a 0.5 mm increase in peripheral FM predicted a 14 g greater total FM. The relationship between total FM and location of FM is influenced by maternal obesity. © 2014 The Authors. Pediatric Obesity © 2014 World Obesity.

  4. Prenatal exposure to very severe maternal obesity is associated with adverse neuropsychiatric outcomes in children.

    Science.gov (United States)

    Mina, T H; Lahti, M; Drake, A J; Räikkönen, K; Minnis, H; Denison, F C; Norman, J E; Reynolds, R M

    2017-01-01

    Prenatal maternal obesity has been linked to adverse childhood neuropsychiatric outcomes, including increased symptoms of attention deficit hyperactivity disorder (ADHD), internalizing and externalizing problems, affective disorders and neurodevelopmental problems but few studies have studied neuropsychiatric outcomes among offspring born to very severely obese women or assessed potential familial confounding by maternal psychological distress. We evaluated neuropsychiatric symptoms in 112 children aged 3-5 years whose mothers had participated in a longitudinal study of obesity in pregnancy (50 very severe obesity, BMI ⩾40 kg/m2, obese class III and 62 lean, BMI 18.5-25 kg/m2). The mothers completed the Conners' Hyperactivity Scale, Early Symptomatic Syndrome Eliciting Neurodevelopmental Clinical Examination Questionnaire (ESSENCE-Q), Child's Sleep Habits Questionnaire (CSHQ), Strengths and Difficulties Questionnaire (SDQ), and Child Behavior Checklist (CBCL) to assess child neuropsychiatric symptoms. Covariates included child's sex, age, birthweight, gestational age, socioeconomic deprivation levels, maternal age, parity, smoking status during pregnancy, gestational diabetes and maternal concurrent symptoms of anxiety and depression assessed using State Anxiety of Spielberger State-Trait Anxiety Index (STAI) and General Health Questionnaire (GHQ), respectively. Children exposed to prenatal maternal very severe obesity had significantly higher scores in the Conners' Hyperactivity Scale; ESSENCE-Q; total sleep problems in CSHQ; hyperactivity, conduct problems and total difficulties scales of the SDQ; higher externalizing and total problems, anxious/depressed, aggressive behaviour and other problem syndrome scores and higher DSM-oriented affective, anxiety and ADHD problems in CBCL. Prenatal maternal very severe obesity remained a significant predictor of child neuropsychiatric problems across multiple scales independent of demographic factors, prenatal factors and

  5. Maternal obesity and vitamin D sufficiency are associated with cord blood vitamin D insufficiency.

    Science.gov (United States)

    Josefson, Jami L; Feinglass, Joseph; Rademaker, Alfred W; Metzger, Boyd E; Zeiss, Dinah M; Price, Heather E; Langman, Craig B

    2013-01-01

    An inverse relationship between total serum 25-hydroxyvitamin D (25-OH D) and increased adiposity has been established in children, adolescents, and adults. However, the relationship between neonatal adiposity and vitamin D status has not been reported. Both maternal obesity and vitamin D deficiency in pregnancy are common and are associated with adverse pregnancy outcomes. The aim of the study was to determine the relationship between vitamin D levels in mothers and newborns, as influenced by maternal obesity, and evaluate these associations with neonatal adiposity. Sixty-one maternal-neonatal pairs participated in this cross-sectional study at an academic medical center. Mothers had a prepregnancy body mass index that was normal or obese. Maternal and cord blood sera were assayed for 25-OH D, and neonatal body composition was measured by air displacement plethysmography. Mothers had similar and sufficient levels of 25-OH D when measured at 36-38 wk gestation, irrespective of body mass index category (normal weight, 46.05, vs. obese, 49.84 ng/ml; P = not significant). However, cord blood 25-OH D was higher in neonates of normal-weight mothers compared to neonates of obese mothers (27.45 vs. 20.81 ng/ml; P = 0.02). The variance in cord blood 25-OH D was explained by four factors: maternal 25-OH D level, the presence of maternal obesity, maternal age, and neonatal adiposity (r(2) = 0.66). Obese women transfer less 25-OH D to offspring than normal-weight women, despite similar serum levels. Cord blood 25-OH D levels directly correlate to neonatal percentage body fat. These novel findings underscore the evolving relationships between maternal obesity, vitamin D nutritional status, and adiposity in the neonatal period that may influence subsequent childhood and adulthood vitamin D-dependent processes.

  6. Effects of maternal obesity on fetal weight and obstetric outcomes in ...

    African Journals Online (AJOL)

    Background: Maternal weight is one of the factors that influence obstetric outcome. Women therefore should enter pregnancy with a weight within the normal body mass index category, and stay within the recommended gestational weight gain guidelines for optimal outcome. The limited data on maternal obesity and its ...

  7. Maternal obesity, environmental factors, cesarean delivery and breastfeeding as determinants of overweight and obesity in children: results from a cohort.

    Science.gov (United States)

    Portela, Daniel S; Vieira, Tatiana O; Matos, Sheila Ma; de Oliveira, Nelson F; Vieira, Graciete O

    2015-04-15

    Overweight and obesity are a public health problem with a multifactorial aetiology. The objective of this study was to evaluate risk factors for overweight and obesity in children at 6 years of age, including type of delivery and breastfeeding. This study relates to a cohort of 672 mother-baby pairs who have been followed from birth up to 6 years of age. The sample included mothers and infants seen at all ten maternity units in a large Brazilian city. Genetic, socioeconomic, demographic variables and postnatal characteristics were analyzed. The outcome analyzed was overweight and/or obesity defined as a body mass index greater than or equal to +1 z-score. The sample was stratified by breastfeeding duration, and a descriptive analysis was performed using a hierarchical logistic regression. P-values of obesity among the children were 15.6% and 12.9%, respectively. Among the subset of breastfed children, factors associated with the outcome were maternal overweight and/or obesity (PR 1.92; 95% confidence interval "95% CI" 1.15-3.24) and lower income (PR 0.50; 95% CI 0.29-0.85). Among children who had not been breastfed or had been breastfed for shorter periods (less than 12 months), predictors were mothers with lower levels of education (PR 0.39; 95% CI 0.19-0.78), working mothers (PR 1.83; 95% CI 1.05-3.21), caesarean delivery (PR 1.98; 95% CI 1.14 - 3.50) and maternal obesity (PR 3.05; 95% CI 1.81 - 5.25). Maternal obesity and caesarean delivery were strongly associated with childhood overweight and/or obesity. Lower family income and lower levels of education were identified as protective factors. Breastfeeding duration appeared to modify the association between overweight/obesity and the other predictors studied.

  8. Genetic evidence for causal relationships between maternal obesity-related traits and birth weight

    NARCIS (Netherlands)

    A.W.R. Tyrrell; R.C. Richmond (Rebecca C.); T.M. Palmer (Tom); B. Feenstra (Bjarke); J. Rangarajan (Janani); S. Metrustry (Sarah); A. Cavadino (Alana); L. Paternoster (Lavinia); L.L. Armstrong (Loren L.); N.M.G. De Silva (N. Maneka G.); A.R. Wood (Andrew); M. Horikoshi (Momoko); F. Geller (Frank); R. Myhre (Ronny); J.P. Bradfield (Jonathan); E. Kreiner-Møller (Eskil); I. Huikari (Ille); J.N. Painter (Jodie N.); J.J. Hottenga (Jouke Jan); C. Allard (Catherine); D. Berry (Diane); L. Bouchard (Luigi); S. Das (Shikta); D.M. Evans (David); H. Hakonarson (Hakon); M.G. Hayes (M. Geoffrey); J. Heikkinen (Jani); A. Hofman (Albert); B.A. Knight (Bridget); P.A. Lind (Penelope); M.I. McCarthy (Mark); G. Mcmahon (George); S.E. Medland (Sarah Elizabeth); M. Melbye (Mads); A.P. Morris (Andrew); M. Nodzenski (Michael); C. Reichetzeder (Christoph); S.M. Ring (Susan); S. Sebert (Sylvain); V. Sengpiel (Verena); T.I.A. Sørensen (Thorkild); G.A.H.M. Willemsen (Gonneke); E.J.C. de Geus (Eco); N.G. Martin (Nicholas); T.D. Spector (Timothy); C. Power (Christine); M.-R. Jarvelin (Marjo-Riitta); H. Bisgaard (Hans); S.F.A. Grant (Struan); C. Nohr (Christian); V.W.V. Jaddoe (Vincent); B. Jacobsson (Bo); J.C. Murray (Jeffrey C.); B. Hocher (Berthold); A.T. Hattersley (Andrew); D.M. Scholtens (Denise M.); G.D. Smith; M.-F. Hivert (Marie-France); J.F. Felix (Janine); E. Hypponen (Elina); W.L. Lowe Jr. (William); T.M. Frayling (Timothy); D.A. Lawlor (Debbie); R.M. Freathy (Rachel)

    2016-01-01

    textabstractIMPORTANCE Neonates born to overweight or obese women are larger and at higher risk of birth complications. Many maternal obesity-related traits are observationally associated with birth weight, but the causal nature of these associations is uncertain. OBJECTIVE To test for genetic

  9. Maternal obesity during pregnancy and cardiovascular development and disease in the offspring

    NARCIS (Netherlands)

    R. Gaillard (Romy)

    2015-01-01

    textabstractMaternal obesity during pregnancy is an important public health problem in Western countries. Currently, obesity prevalence rates in pregnant women are estimated to be as high as 30 %. In addition, approximately 40 % of women gain an excessive amount of weight during pregnancy in Western

  10. Childhood Health Consequences of Maternal Obesity during Pregnancy: A Narrative Review

    NARCIS (Netherlands)

    R. Gaillard (Romy); S.M.S. Santos (Susana); L. Duijts (Liesbeth); J.F. Felix (Janine)

    2016-01-01

    textabstractBackground: Obesity is a major public health problem among women of reproductive age. In a narrative review, we examined the influence of maternal obesity during pregnancy on fetal outcomes and childhood adiposity, cardio-metabolic, respiratory and cognitive-related health outcomes. We

  11. Maternal obesity and post-natal high fat diet disrupt hepatic circadian rhythm in rat offspring

    Science.gov (United States)

    Offspring of obese (Ob) rat dams gain greater body wt and fat mass when fed high-fat diet (HFD) as compared to controls. Alterations of diurnal circadian rhythm are known to detrimentally impact metabolically active tissues such as liver. We sought to determine if maternal obesity (MOb) leads to p...

  12. The Effects of Maternal Obesity on Neonates, Infants, Children, Adolescents, and Adults.

    Science.gov (United States)

    Hemond, Joni; Robbins, Riann B; Young, Paul C

    2016-03-01

    With the increasing prevalence of obesity, including among women of childbearing age, there is increasing concern regarding the short-term and long-term effects on the offspring of women who are overweight and obese. In this paper we report the results of our review of the recent literature suggesting important adverse short-term and long-term consequences of maternal obesity on their children.

  13. Maternal obesity during pregnancy and cardiovascular development and disease in the offspring.

    Science.gov (United States)

    Gaillard, Romy

    2015-11-01

    Maternal obesity during pregnancy is an important public health problem in Western countries. Currently, obesity prevalence rates in pregnant women are estimated to be as high as 30%. In addition, approximately 40% of women gain an excessive amount of weight during pregnancy in Western countries. An accumulating body of evidence suggests a long-term impact of maternal obesity and excessive weight gain during pregnancy on adiposity, cardiovascular and metabolic related health outcomes in the offspring in fetal life, childhood and adulthood. In this review, we discuss results from recent studies, potential underlying mechanisms and challenges for future epidemiological studies.

  14. Maternal depression and socio-economic status moderate the parenting style/child obesity association.

    Science.gov (United States)

    Topham, Glade L; Page, Melanie C; Hubbs-Tait, Laura; Rutledge, Julie M; Kennedy, Tay S; Shriver, Lenka; Harrist, Amanda W

    2010-08-01

    The purpose of the study was to test the moderating influence of two risk factors, maternal depression and socio-economic status (SES), on the association between authoritarian and permissive parenting styles and child obesity. Correlational, cross-sectional study. Parenting style was measured with the Parenting Styles and Dimensions Questionnaire (PSDQ). Maternal depression was measured using the Center for Epidemiologic Studies Depression Scale (CES-D). BMI-for-age percentile was used to categorize children by weight status (children with BMI-for-age > or = 95th percentile were classified as obese). SES was computed from parent education and occupational status using the four-factor Hollingshead index. Rural public schools in a mid-western state in the USA. One hundred and seventy-six mothers of first-grade children (ninety-one boys, eighty-five girls) enrolled in rural public schools. Both maternal depression and SES were found to moderate the permissive parenting style/child obesity association, but not the authoritarian/child obesity association. For depressed mothers, but not for non-depressed mothers, more permissive parenting was predictive of child obesity. Similarly more permissive parenting was predictive of child obesity among higher SES mothers, but not for lower SES mothers. Maternal depression and SES interact with permissive parenting style to predict child obesity. Future research should examine the relationship among these variables using a longitudinal design.

  15. Lower levels of maternal capital in early life predict offspring obesity in adulthood.

    Science.gov (United States)

    Gillette, Meghan T; Lohman, Brenda J; Neppl, Tricia K

    2017-05-01

    As of 2013, 65% of the world's population lived in countries where overweight/obesity kills more people than being underweight. Evolutionary perspectives provide a holistic understanding of both how and why obesity develops and its long-term implications. To test whether the maternal capital hypothesis, an evolutionary perspective, is viable for explaining the development of obesity in adulthood. Restricted-use data from the National Longitudinal Study of Adolescent Health (Add Health; n = 11 403) was analysed using logistic regressions. The sample included adolescents and their biological mothers. The odds of obesity in adulthood increased by 22% for every standard deviation increase in lack of maternal capital (Exp (B) = 1.22, p obese in adulthood, even after controlling for other factors in infancy, adolescence and adulthood. The results showed that those whose mothers had lower capital were more prone to later life disease (specifically, obesity). The maternal capital perspective is useful for explaining how and why early life characteristics (including maternal resources) predict obesity in adulthood. Implications of the findings are discussed.

  16. Trajectories of maternal weight from before pregnancy through postpartum and associations with childhood obesity.

    Science.gov (United States)

    Leonard, Stephanie A; Rasmussen, Kathleen M; King, Janet C; Abrams, Barbara

    2017-11-01

    Background: Prepregnancy body mass index [BMI (in kg/m 2 )], gestational weight gain, and postpartum weight retention may have distinct effects on the development of child obesity, but their combined effect is currently unknown. Objective: We described longitudinal trajectories of maternal weight from before pregnancy through the postpartum period and assessed the relations between maternal weight trajectories and offspring obesity in childhood. Design: We analyzed data from 4436 pairs of mothers and their children in the National Longitudinal Survey of Youth 1979 (1981-2014). We used latent-class growth modeling in addition to national recommendations for prepregnancy BMI, gestational weight gain, and postpartum weight retention to create maternal weight trajectory groups. We used modified Poisson regression models to assess the associations between maternal weight trajectory group and offspring obesity at 3 age periods (2-5, 6-11, and 12-19 y). Results: Our analysis using maternal weight trajectories based on either latent-class results or recommendations showed that the risk of child obesity was lowest in the lowest maternal weight trajectory group. The differences in obesity risk were largest after 5 y of age and persisted into adolescence. In the latent-class analysis, the highest-order maternal weight trajectory group consisted almost entirely of women who were obese before pregnancy and was associated with a >2-fold increase in the risk of offspring obesity at ages 6-11 y (adjusted RR: 2.39; 95% CI: 1.97, 2.89) and 12-19 y (adjusted RR: 2.74; 95% CI: 2.13, 3.52). In the analysis with maternal weight trajectory groups based on recommendations, the risk of child obesity was consistently highest for women who were overweight or obese at the beginning of pregnancy. Conclusion: These findings suggest that high maternal weight across the childbearing period increases the risk of obesity in offspring during childhood, but high prepregnancy BMI has a stronger

  17. Maternal Obesity and Impaired Fetal and Infant Survival-One More Piece Added to the Puzzle

    DEFF Research Database (Denmark)

    Nohr, Ellen A

    2016-01-01

    The association between maternal obesity and increased risks of stillbirth and infant mortality is well documented, but it has often been questioned whether the association is driven by obesity per se or by unmeasured factors such as insulin resistance or genes. In this issue of the Journal, Lindam...... et al. compared the body mass indices (weight (kg)/height (m)(2)) of women who had stillbirths and infant deaths with those of their sisters or of population controls. Significant excess risks of both outcomes were observed in obese women (body mass index ≥30), and associations were strongest when...... sister controls were used. Although this careful analysis adds to the existing evidence of a causal relationship between maternal obesity and impaired fetal and infant survival, a biological pathway has not yet been established. Additionally, we are in urgent need of effective tools to reduce obesity...

  18. Maternal obesity in singleton versus twin gestations: a population-based matched case-control study.

    Science.gov (United States)

    Lucovnik, Miha; Blickstein, Isaac; Verdenik, Ivan; Trojner-Bregar, Andreja; Tul, Natasa

    2015-04-01

    To examine the impact of pre-pregnancy obesity on adverse outcomes in twin compared to singleton pregnancies. Dichorionic twin gestations with maternal body mass index >30 were matched to three singleton controls. Both obese groups were matched (1:3) with non-obese controls. Rates of preeclampsia, gestational diabetes, cesarean section, and preterm birth were compared. One hundred eighty-nine dichorionic twin pregnancies in obese mothers were matched to 567 twin pregnancies in non-obese mothers, and to 567 singleton pregnancies in obese mothers. The latter were matched to 1701 non-obese mothers with singletons. Preeclampsia was more common in obese mothers with both twins and singletons (odds ratio (OR) 3.95, 95% confidence interval (CI) 2.18-7.16 and OR 6.53, 95% CI 3.75-11.4, respectively) as was gestational diabetes (OR 4.35, 95% CI 2.18-8.69; OR 5.53 95% CI 3.60-8.50). Obese mothers with singletons were more likely to deliver abdominally, but the cesarean rates were obesity independent in twins. Obese mothers were more likely to deliver at Obesity-attributable adverse outcomes are lower in twins compared to singletons. Obesity increases the risk of preterm birth regardless of plurality.

  19. Maternal Obesity: A Global Health Problem and It's Implications on Maternal and Fetal Health

    Directory of Open Access Journals (Sweden)

    Anjum Hashmi

    2010-12-01

    Conclusion: Obese women are at increased risk of pregnancy induced obesity and associated with an increased risk of hypertension, gestational diabetes mellitus, thromboembolic disease and urinary tract infection.

  20. What is common becomes normal: the effect of obesity prevalence on maternal perception.

    Science.gov (United States)

    Binkin, N; Spinelli, A; Baglio, G; Lamberti, A

    2013-05-01

    This analysis investigates the poorly-known effect of local prevalence of childhood obesity on mothers' perception of their children's weight status. In 2008, a national nutritional survey of children attending the third grade of elementary school was conducted in Italy. Children were measured and classified as underweight, normal weight, overweight and obese, using the International Obesity Task Force cut-offs for body mass index (BMI). A parental questionnaire included parental perception of their child's weight status (underweight, normal, a little overweight and a lot overweight). Regions were classified by childhood obesity prevalence (maternal perception and regional obesity prevalence, and maternal and child characteristics were examined using bivariate and logistic regression analyses. Complete data were available for 37 590 children, of whom 24% were overweight and 12% obese. Mothers correctly identified the status of 84% of normal weight, 52% of overweight and 14% of obese children. Among overweight children, factors associated with underestimation of the child's weight included lower maternal education (adjusted odds ratio, aOR, 1.9; 95% confidence interval (CI) 1.6-2.4), residence in a high-obesity region (aOR 2.2; 95% CI 1.9-2.6), male gender (aOR 1.4; 95% CI 1.2-1.6) and child's BMI. Higher regional obesity prevalence is associated with lower maternal perception, suggesting that what is common has a greater likelihood of being perceived as normal. As perception is a first step to change, it may be harder to intervene in areas with high-obesity prevalence where intervention is most urgent. Copyright © 2011 Elsevier B.V. All rights reserved.

  1. The role of maternal obesity in the risk of neuropsychiatric disorders

    Science.gov (United States)

    Rivera, Heidi M.; Christiansen, Kelly J.; Sullivan, Elinor L.

    2015-01-01

    Recent evidence indicates that perinatal exposure to maternal obesity, metabolic disease, including diabetes and hypertension, and unhealthy maternal diet has a long-term impact on offspring behavior and physiology. During the past three decades, the prevalence of both obesity and neuropsychiatric disorders has rapidly increased. Epidemiologic studies provide evidence that maternal obesity and metabolic complications increase the risk of attention deficit hyperactivity disorder (ADHD), autism spectrum disorders, anxiety, depression, schizophrenia, eating disorders (food addiction, anorexia nervosa, and bulimia nervosa), and impairments in cognition in offspring. Animal models of maternal high-fat diet (HFD) induced obesity also document persistent changes in offspring behavior and impairments in critical neural circuitry. Animals exposed to maternal obesity and HFD consumption display hyperactivity, impairments in social behavior, increased anxiety-like and depressive-like behaviors, substance addiction, food addiction, and diminished cognition. During development, these offspring are exposed to elevated levels of nutrients (fatty acids, glucose), hormones (leptin, insulin), and inflammatory factors (C-reactive protein, interleukin, and tumor necrosis factor). Such factors appear to permanently change neuroendocrine regulation and brain development in offspring. In addition, inflammation of the offspring brain during gestation impairs the development of neural pathways critical in the regulation of behavior, such as serotoninergic, dopaminergic, and melanocortinergic systems. Dysregulation of these circuits increases the risk of mental health disorders. Given the high rates of obesity in most developed nations, it is critical that the mechanisms by which maternal obesity programs offspring behavior are thoroughly characterized. Such knowledge will be critical in the development of preventative strategies and therapeutic interventions. PMID:26150767

  2. The role of maternal obesity in the risk of neuropsychiatric disorders

    Directory of Open Access Journals (Sweden)

    Heidi Michelle Rivera

    2015-06-01

    Full Text Available Recent evidence indicates that perinatal exposure to maternal obesity, metabolic disease, including diabetes and hypertension, and unhealthy maternal diet has a long-term impact on offspring behavior and physiology. During the past three decades, the prevalence of both obesity and neuropsychiatric disorders has rapidly increased. Epidemiologic studies provide evidence that maternal obesity and metabolic complications increase the risk of attention deficit hyperactivity disorder, autism spectrum disorders, anxiety, depression, schizophrenia, eating disorders (food addiction, anorexia nervosa, and bulimia nervosa, and cognition in offspring. Animal models of maternal high-fat diet induced obesity also document persistent changes in offspring behavior and impairments in critical neural circuitry. Animals exposed to maternal obesity and high-fat diet consumption display impairments in hyperactivity, social behavior, increased anxiety-like and depressive-like behaviors, substance addiction, food addiction, and diminished cognition. During development, these offspring are exposed to elevated levels of nutrients (fatty acids, glucose, hormones (leptin, insulin, and inflammatory factors (C-reactive protein, interleukin, and tumor necrosis factor. Such factors appear to permanently change neuroendocrine regulation and brain development in offspring. In addition, inflammation of the offspring brain during gestation impairs the development of neural pathways critical in the regulation of behavior, such as serotoninergic, dopaminergic, and melanocortinergic. Dysregulation of these circuits increases the risk of mental health disorders. Given the high rates of obesity in most developed nations, it is critical that the mechanisms by which maternal obesity programs offspring behavioral are thoroughly characterized. Such knowledge will be critical in the development of preventative strategies and therapeutic interventions.

  3. Programming Body Composition in Offspring by Maternal Obesity Is Associated with Increased Adipogenesis and Decreased WNT/ Beta-Catenin Signaling in the Adipose Tissue

    Science.gov (United States)

    Maternal obesity during pregnancy significantly influences the risk of obesity in the offspring. We recently demonstrated that maternal obesity at conception programs obesity in the offspring. Obese dam offspring when weaned on high-fat diets gain significantly greater body weight/adiposity (via NMR...

  4. Maternal immigrant status and high birth weight: implications for childhood obesity.

    Science.gov (United States)

    El-Sayed, Abdulrahman M; Galea, Sandro

    2011-01-01

    Childhood obesity, a growing epidemic, is associated with greater risk of several chronic diseases in adulthood. Children of immigrant mothers are at higher risk for obesity than children of non-immigrant mothers. High birth weight is the most important neonatal predictor of childhood obesity in the general population. To understand the etiology of obesity in children of immigrant mothers, we assessed the relation between maternal immigrant status and risk for high birth weight. Data about all births in Michigan (N = 786,868) between 2000-2005 were collected. We used bivariate chi-square tests and multivariate logistic regression models to assess the relation between maternal immigrant status and risk for neonatal high birth weight. The prevalence of high birth weight among non-immigrant mothers was 10.6%; the prevalence among immigrant mothers was 8.0% (P maternal age, education, marital status, parity, and tobacco use, children of immigrant mothers had lower odds (odds ratio = 0.69, 95% confidence interval = 0.67-0.70) of high birth weight compared to those of non-immigrant mothers. Although maternal immigrant status has been shown to be associated with greater childhood obesity, surprisingly, children of immigrant mothers have lower risk of high birth weight than children of non-immigrant mothers. This suggests that factors in early childhood, potentially cultural or behavioral factors, may play a disproportionately important role in the etiology of childhood obesity in children of immigrant vs non-immigrant mothers.

  5. Maternal obesity, gestational diabetes, breastfeeding and childhood overweight at age 2 years.

    Science.gov (United States)

    Bider-Canfield, Z; Martinez, M P; Wang, X; Yu, W; Bautista, M P; Brookey, J; Page, K A; Buchanan, T A; Xiang, A H

    2017-04-01

    Maternal obesity, excessive gestational weight gain (EGWG), gestational diabetes mellitus (GDM) and breastfeeding are four important factors associated with childhood obesity. The objective of the study was to assess the interplay among these four factors and their independent contributions to childhood overweight in a cohort with standard clinical care. The cohort included 15 710 mother-offspring pairs delivered in 2011. Logistic regression was used to assess associations between maternal exposures and childhood overweight (body mass index >85th percentile) at age 2 years. Mothers with pre-pregnancy obesity or overweight were more likely to have EGWG, GDM and less likely to breastfeed ≥6 months. Mothers with GDM had 40-49% lower EGWG rates and similar breastfeeding rates compared with mothers without GDM. Analysis adjusted for exposures and covariates revealed an adjusted odds ratio (95% confidence interval) associated with childhood overweight at age 2 years of 2.34 (2.09-2.62), 1.50 (1.34-1.68), 1.23 (1.12-1.35), 0.95 (0.83-1.10) and 0.76 (0.69-0.83) for maternal obesity, overweight, EGWG, GDM and breastfeeding ≥6 months vs. maternal pre-pregnancy obesity or overweight and EGWG were independently associated with an increased risk, and breastfeeding ≥6 months was associated with a decreased risk of childhood overweight at age 2 years. © 2016 World Obesity Federation.

  6. Effects of maternal obesity on early and long-term outcomes for offspring

    Directory of Open Access Journals (Sweden)

    Stirrat LI

    2014-03-01

    Full Text Available Laura I Stirrat,1,2 Rebecca M Reynolds2,3 1Medical Research Council Centre for Reproductive Health, Queens Medical Research Institute, University of Edinburgh, Edinburgh, UK; 2Tommy's Centre for Maternal and Fetal Health, Queens Medical Research Institute, University of Edinburgh, Edinburgh, UK; 3Endocrinology Unit, University/British Heart Foundation Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, Edinburgh, UK Abstract: The prevalence of maternal obesity has increased significantly in recent years, and obesity is currently the most common comorbidity of pregnancy. Pregnancies of obese women are often defined as "high-risk" for the purposes of clinical care, with many well documented risks to the mother and developing baby. Maternal physiology and metabolism is dysregulated in the context of obesity, which may contribute to some of the adverse outcomes during pregnancy. Furthermore, maternal obesity has been hypothesized to cause harmful effects for the developing baby through "early life programming." This review will examine evidence from human studies for outcomes of offspring from obese women during pregnancy, during labor, during the neonatal period, and later in life. Keywords: pregnancy, short-term, physiology, metabolism, early life programming, neonatal complications, adverse intrauterine environment

  7. Maternal obesity modulates intracellular lipid turnover in the human term placenta.

    Science.gov (United States)

    Hirschmugl, B; Desoye, G; Catalano, P; Klymiuk, I; Scharnagl, H; Payr, S; Kitzinger, E; Schliefsteiner, C; Lang, U; Wadsack, C; Hauguel-de Mouzon, S

    2017-02-01

    Obesity before pregnancy is associated with impaired metabolic status of the mother and the offspring later in life. These adverse effects have been attributed to epigenetic changes in utero, but little is known about the role of placental metabolism and its contribution to fetal development. We examined the impact of maternal pre-pregnancy obesity on the expression of genes involved in placental lipid metabolism in lean and obese women. Seventy-three lean and obese women with healthy pregnancy were recruited at term elective cesarean delivery. Metabolic parameters were measured on maternal venous blood samples. Expression of 88 genes involved in lipid metabolism was measured in whole placenta tissue. Proteins of genes differently expressed in response to maternal obesity were quantified, correlated with maternal parameters and immunolocalized in placenta sections. Isolated primary trophoblasts were used for in vitro assays. Triglyceride (TG) content was increased in placental tissue of obese (1.10, CI 1.04-1.24 mg g -1 , Pwomen. Among target genes examined, six showed positive correlation (Pobese vs lean women. CGI-58 protein levels correlated positively with maternal insulin levels and pre-pregnancy body mass index (R=0.63, Ptreatment of cultured trophoblast cells. Pre-gravid obesity significantly modifies the expression of placental genes related to transport and storage of neutral lipids. We propose that the upregulation of CGI-58, a master regulator of TG hydrolysis, contributes to the turnover of intracellular lipids in placenta of obese women, and is tightly regulated by metabolic factors of the mother.

  8. Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4+CD25+ regulatory T cells

    International Nuclear Information System (INIS)

    Jin, Yulan; Purohit, Sharad; Chen, Xueqin; Yi, Bing; She, Jin-Xiong

    2012-01-01

    Highlights: ► This is the first study to provide direct evidence of the role of Stat5b in NOD mice. ► Over-expression of wild type Stat5b transgene protects NOD mice against diabetes. ► This protection may be mediated by the up-regulation of CD4 + CD25 + Tregs. -- Abstract: The signal transducers and activators of transcription (STAT) family of proteins play a critical role in cytokine signaling required for fine tuning of immune regulation. Previous reports showed that a mutation (L327M) in the Stat5b protein leads to aberrant cytokine signaling in the NOD mice. To further elaborate the role of Stat5b in diabetes, we established a NOD transgenic mouse that over-expresses the wild type Stat5b gene. The incidences of spontaneous diabetes as well as cyclophosphamide-induced diabetes were significantly reduced and delayed in the Stat5b transgenic NOD mice compared to their littermate controls. The total cell numbers of CD4 + T cells and especially CD8 + T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. Consistent with these findings, CD4 + and CD8 + T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl. Furthermore, the number and proportion of CD4 + CD25 + regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4 + CD25 + regulatory T cells.

  9. Maternal obesity alters immune cell frequencies and responses in umbilical cord blood samples.

    Science.gov (United States)

    Wilson, Randall M; Marshall, Nicole E; Jeske, Daniel R; Purnell, Jonathan Q; Thornburg, Kent; Messaoudi, Ilhem

    2015-06-01

    Maternal obesity is one of the several key factors thought to modulate neonatal immune system development. Data from murine studies demonstrate worse outcomes in models of infection, autoimmunity, and allergic sensitization in offspring of obese dams. In humans, children born to obese mothers are at increased risk for asthma. These findings suggest a dysregulation of immune function in the children of obese mothers; however, the underlying mechanisms remain poorly understood. The aim of this study was to examine the relationship between maternal body weight and the human neonatal immune system. Umbilical cord blood samples were collected from infants born to lean, overweight, and obese mothers. Frequency and function of major innate and adaptive immune cell populations were quantified using flow cytometry and multiplex analysis of circulating factors. Compared to babies born to lean mothers, babies of obese mothers had fewer eosinophils and CD4 T helper cells, reduced monocyte and dendritic cell responses to Toll-like receptor ligands, and increased plasma levels of IFN-α2 and IL-6 in cord blood. These results support the hypothesis that maternal obesity influences programming of the neonatal immune system, providing a potential link to increased incidence of chronic inflammatory diseases such as asthma and cardiovascular disease in the offspring. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  10. Maternal obesity and breastfeeding intention, initiation, intensity and duration: a systematic review.

    Science.gov (United States)

    Turcksin, Rivka; Bel, Sarah; Galjaard, Sander; Devlieger, Roland

    2014-04-01

    This systematic review investigates the relationship between maternal obesity and breastfeeding intention, initiation, intensity, duration and milk supply. A comprehensive search was performed through three major databases, including Medline, Cochrane Library and Cumulative Index For Nursing and Allied Health Literature, and by screening reference lists of the relevant publications. Selection criteria were: report of original research, studies on low-risk obese mothers and the comparison with normal weight mothers which met at least two of the following primary outcomes: breastfeeding intention; initiation; intensity; duration and/or milk supply. Furthermore, the included reports had to contain a clear definition of pre-pregnant obesity, use compensation mechanisms for potential confounding factors, have a prospective cohort design and had to have been published between 1997 and 2011 and in English, French or Dutch. Effects of obesity on breastfeeding intention, initiation, intensity, duration and milk supply were analysed, tabulated and summarised in this review. Studies have found that obese women are less likely to intend to breastfeed and that maternal obesity seems to be associated with a decreased initiation of breastfeeding, a shortened duration of breastfeeding, a less adequate milk supply and delayed onset of lactogenesis II, compared with their normal weight counterparts. This systematic review indicates therefore that maternal obesity is an adverse determinant for breastfeeding success. © 2012 JohnWiley & Sons Ltd.

  11. Preventing maternal and early childhood obesity: the fetal flaw in Australian perinatal care.

    Science.gov (United States)

    Miller, Margaret; Hearn, Lydia; van der Pligt, Paige; Wilcox, Jane; Campbell, Karen J

    2014-01-01

    Almost half of Australian women of child-bearing age are overweight or obese, with a rate of 30-50% reported in early pregnancy. Maternal adiposity is a costly challenge for Australian obstetric care, with associated serious maternal and neonatal complications. Excess gestational weight gain is an important predictor of offspring adiposity into adulthood and higher maternal weight later in life. Current public health and perinatal care approaches in Australia do not adequately address excess perinatal maternal weight or gestational weight gain. This paper argues that the failure of primary health-care providers to offer systematic advice and support regarding women's weight and related lifestyle behaviours in child-bearing years is an outstanding 'missed opportunity' for prevention of inter-generational overweight and obesity. Barriers to action could be addressed through greater attention to: clinical guidelines for maternal weight management for the perinatal period, training and support of maternal health-care providers to develop skills and confidence in raising weight issues with women, a variety of weight management programs provided by state maternal health services, and clear referral pathways to them. Attention is also required to service systems that clearly define roles in maternal weight management and ensure consistency and continuity of support across the perinatal period.

  12. Maternal obesity and high-fat diet program offspring metabolic syndrome.

    Science.gov (United States)

    Desai, Mina; Jellyman, Juanita K; Han, Guang; Beall, Marie; Lane, Robert H; Ross, Michael G

    2014-09-01

    We determined the potential programming effects of maternal obesity and high-fat (HF) diet during pregnancy and/or lactation on offspring metabolic syndrome. A rat model of maternal obesity was created using an HF diet prior to and throughout pregnancy and lactation. At birth, pups were cross-fostered, thereby generating 4 paradigms of maternal diets during pregnancy/lactation: (1) control (Con) diet during pregnancy and lactation (Con/Con), (2) HF during pregnancy and lactation (HF/HF), (3) HF during pregnancy alone (HF/Con), and (4) HF during lactation alone (Con/HF). Maternal phenotype during pregnancy and the end of lactation evidenced markedly elevated body fat and plasma corticosterone levels in HF dams. In the offspring, the maternal HF diet during pregnancy alone programmed increased offspring adiposity, although with normal body weight, whereas the maternal HF diet during lactation increased both body weight and adiposity. Metabolic disturbances, particularly that of hyperglycemia, were apparent in all groups exposed to the maternal HF diet (during pregnancy and/or lactation), although differences were apparent in the manifestation of insulin resistant vs insulin-deficient phenotypes. Elevated systolic blood pressure was manifest in all groups, implying that exposure to an obese/HF environment is disadvantageous for offspring health, regardless of pregnancy or lactation periods. Nonetheless, the underlying mechanism may differ because offspring that experienced in utero HF exposure had increased corticosterone levels. Maternal obesity/HF diet has a marked impact on offspring body composition and the risk of metabolic syndrome was dependent on the period of exposure during pregnancy and/or lactation. Copyright © 2014 Mosby, Inc. All rights reserved.

  13. Examining Maternal Psychopathology, Family Functioning and Coping Skills in Childhood Obesity: A Case-Control Study.

    Science.gov (United States)

    Blanco, Miriam; Sepulveda, Ana R; Lacruz, Tatiana; Parks, Melissa; Real, Beatriz; Martin-Peinador, Yolanda; Román, Francisco J

    2017-09-01

    The shared family environment is an important risk factor in the development of childhood obesity. This study aims to examine differences in maternal psychopathology, family functioning, expressed emotion and coping skills between families of a child with obesity and those with a normal-weight child. This case-control study consisted of 50 mothers with a child (age 8-12 years) with obesity (p ≥ 97) and a control group of 50 mothers of a child with normal weight (p obesity showed significant differences in levels of trait anxiety, criticism and over-protectiveness, and maladaptive coping skills. Structural equation modelling revealed that the mothers' psychopathology predicted children's body mass index (BMI) z-scores through expressed emotion and maladaptive coping scores. There were significant direct and indirect relations among maternal BMI, psychopathology, expressed emotion and coping, which all together explained 26.5% of variance of children's BMI z-scores. Considering this relation between maternal variables and child weight status, childhood obesity intervention programs may benefit from targeting maternal BMI, psychopathology, expressed emotion and coping skills. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.

  14. Maternal pre-pregnancy obesity and neuropsychological development in pre-school children: a prospective cohort study.

    Science.gov (United States)

    Casas, Maribel; Forns, Joan; Martínez, David; Guxens, Mònica; Fernandez-Somoano, Ana; Ibarluzea, Jesus; Lertxundi, Nerea; Murcia, Mario; Rebagliato, Marisa; Tardon, Adonina; Sunyer, Jordi; Vrijheid, Martine

    2017-10-01

    BackgroundMaternal pre-pregnancy obesity may impair infant neuropsychological development, but it is unclear whether intrauterine or confounding factors drive this association.MethodsWe assessed whether maternal pre-pregnancy obesity was associated with neuropsychological development in 1,827 Spanish children. At 5 years, cognitive and psychomotor development was assessed using McCarthy Scales of Children's Abilities, attention deficit hyperactivity disorder (ADHD) symptoms using the Criteria of Diagnostic and Statistical Manual of Mental Disorders, and autism spectrum disorder symptoms using the Childhood Asperger Syndrome Test. Models were adjusted for sociodemographic factors and maternal intelligence quotient. We used paternal obesity as negative control exposure as it involves the same source of confounding than maternal obesity.ResultsThe percentage of obese mothers and fathers was 8% and 12%, respectively. In unadjusted models, children of obese mothers had lower scores than children of normal weight mothers in all McCarthy subscales. After adjustment, only the verbal subscale remained statistically significantly reduced (β: -2.8; 95% confidence interval: -5.3, -0.2). No associations were observed among obese fathers. Maternal and paternal obesity were associated with an increase in ADHD-related symptoms. Parental obesity was not associated with autism symptoms.ConclusionMaternal pre-pregnancy obesity was associated with a reduction in offspring verbal scores at pre-school age.

  15. Maternal Obesity, 25-Hydroxy Vitamin D Concentration, and Bone Density in Breastfeeding Dyads.

    Science.gov (United States)

    Sen, Sarbattama; Penfield-Cyr, Annie; Hollis, Bruce W; Wagner, Carol L

    2017-08-01

    To examine the association between maternal body mass index (BMI) and serum 25-hydroxy vitamin D [25(OH)D] concentration and bone density in mother-infant pairs. The study was a secondary analysis of 234 exclusively breastfeeding dyads who were recruited in the first postpartum month for a randomized controlled trial of maternal vs infant vitamin D supplementation. Mean 25(OH)D concentrations and bone mineral density (BMD) were compared by BMI group. The adjusted association between maternal BMI and 25(OH)D and bone density was examined at 1, 4, and 7 months postpartum. Obese breastfeeding women had lower 25(OH)D concentrations and higher BMD than lean women at all 3 time points (P  maternal BMI was associated with lower maternal serum levels of 25(OH)D at 1, 4, and 7 months postpartum (adjusted β = -0.45 ng/ml per kg/m 2 , 95% CI -.076, -0.14, at 1 month) and higher BMD at the same time points (β = 0.006 BMD z score; 95% CI 0.003, 0.01 at 1 month). Seventy-six percent of infants were vitamin D deficient at 1 month of age. Infants born to overweight and obese mothers had lower 25(OH)D concentrations than infants of lean mothers (P maternal supplementation group, higher maternal BMI was associated with lower 25(OH)D concentrations at 4 months (β = -0.68; 95% CI -1.17, -0.20) and lower bone density at 7 months (β = -0.001; 95% CI -0.002, -0.0001). In exclusively breastfeeding dyads, maternal obesity is associated with lower maternal and infant serum 25(OH)D concentrations, which may impact infant bone density. ClinicalTrials.gov: NCT00412074. Copyright © 2017 Elsevier Inc. All rights reserved.

  16. Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4{sup +}CD25{sup +} regulatory T cells

    Energy Technology Data Exchange (ETDEWEB)

    Jin, Yulan; Purohit, Sharad [Center for Biotechnology and Genomic Medicine, Georgia Health Sciences University, GA (United States); Department of Pathology, Medical College of Georgia, Georgia Health Sciences University, GA (United States); Chen, Xueqin; Yi, Bing [Center for Biotechnology and Genomic Medicine, Georgia Health Sciences University, GA (United States); She, Jin-Xiong, E-mail: jshe@georgiahealth.edu [Center for Biotechnology and Genomic Medicine, Georgia Health Sciences University, GA (United States); Department of Pathology, Medical College of Georgia, Georgia Health Sciences University, GA (United States)

    2012-08-10

    Highlights: Black-Right-Pointing-Pointer This is the first study to provide direct evidence of the role of Stat5b in NOD mice. Black-Right-Pointing-Pointer Over-expression of wild type Stat5b transgene protects NOD mice against diabetes. Black-Right-Pointing-Pointer This protection may be mediated by the up-regulation of CD4{sup +}CD25{sup +} Tregs. -- Abstract: The signal transducers and activators of transcription (STAT) family of proteins play a critical role in cytokine signaling required for fine tuning of immune regulation. Previous reports showed that a mutation (L327M) in the Stat5b protein leads to aberrant cytokine signaling in the NOD mice. To further elaborate the role of Stat5b in diabetes, we established a NOD transgenic mouse that over-expresses the wild type Stat5b gene. The incidences of spontaneous diabetes as well as cyclophosphamide-induced diabetes were significantly reduced and delayed in the Stat5b transgenic NOD mice compared to their littermate controls. The total cell numbers of CD4{sup +} T cells and especially CD8{sup +} T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice. Consistent with these findings, CD4{sup +} and CD8{sup +} T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-{gamma}, TNF-{alpha} and IL-10 as well as anti-apoptotic gene Bcl-xl. Furthermore, the number and proportion of CD4{sup +}CD25{sup +} regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene. Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4{sup +}CD25{sup +} regulatory T cells.

  17. Preconceptional and maternal obesity: epidemiology and health consequences.

    Science.gov (United States)

    Poston, Lucilla; Caleyachetty, Rishi; Cnattingius, Sven; Corvalán, Camila; Uauy, Ricardo; Herring, Sharron; Gillman, Matthew W

    2016-12-01

    Obesity in women of reproductive age is increasing in prevelance worldwide. Obesity reduces fertility and increases time taken to conceive, and obesity-related comorbidities (such as type 2 diabetes and chronic hypertension) heighten the risk of adverse outcomes for mother and child if the woman becomes pregnant. Pregnant women who are obese are more likely to have early pregnancy loss, and have increased risk of congenital fetal malformations, delivery of large for gestational age infants, shoulder dystocia, spontaneous and medically indicated premature birth, and stillbirth. Late pregnancy complications include gestational diabetes and pre-eclampsia, both of which are associated with long-term morbidities post partum. Women with obesity can also experience difficulties during labour and delivery, and are more at risk of post-partum haemorrhage. Long-term health risks are associated with weight retention after delivery, and inherent complications for the next pregnancy. The wellbeing of the next generation is also compromised. All these health issues could be avoided by prevention of obesity among women of reproductive age, which should be viewed as a global public health priority. For women who are already obese, renewed efforts should be made towards improved management during pregnancy, especially of blood glucose, and increased attention to post-partum weight management. Effective interventions, tailored to ethnicity and culture, are needed at each of these stages to improve the health of women and their children in the context of the global obesity epidemic. Copyright © 2016 Elsevier Ltd. All rights reserved.

  18. Impact of maternal obesity and diabetes on fetal pancreatic development

    DEFF Research Database (Denmark)

    Nielsen, Jens Høiriis; Jaksch, Caroline Anna Mikaela; Lessi, Isabela

    2017-01-01

    The global epidemics of obesity and type 2 diabetes (T2D) are serious threats to human health and health-care expenses. Although genetics is an important factor, it does not explain this dramatic increase that involves environmental factors such as nutrients, gut microbiota, and lifestyles. Twenty...... under- and overnutrition before and during pregnancy may cause metabolic diseases like obesity and T2D. Studies in humans have shown that offspring of mothers with obesity, type 1 diabetes (T1D), T2D, or gestational diabetes mellitus (GDM) are prone to develop metabolic disorders such as obesity, T2D...... (Fisher et al. 2013). The clinical consequences of obesity and diabetes in pregnancy for the offspring will be dealt with in Chapters 13 and 14 of this book....

  19. Maternal obesity and perinatal oxidative stress: the strength of the association.

    Science.gov (United States)

    Negro, S; Boutsikou, T; Briana, D D; Tataranno, M L; Longini, M; Proietti, F; Bazzini, F; Dani, C; Malamitsi-Puchner, A; Buonocore, G; Perrone, S

    2017-01-01

    Maternal obesity is a chronic inflammatory state, which has been shown to induce increased levels of free fatty acids, reactive oxygen species and inflammatory cells. Recent evidence reveals increased levels of lipid peroxidation products in the plasma of obese women during pregnancy. The aim of this study was to test the hypothesis that maternal overweight or obesity is associated with increased oxidative stress (OS) in offspring. Two hundred and forty-five pregnant women and their newborns were prospectively enrolled. Mothers were divided in two groups: lean control - LC (n=175, Group I); overweight or obese (n=70, Group II) according to BMI ≥ 25 before pregnancy. Cord blood F2-isoprostanes (F2-IsoPs), as reliable markers of OS, were measured in all newborns. Lower 1 minute APGAR score and higher weight at discharge were found in Group II neonates, compared to those of Group I (p less than 0.05). Small for gestational age (SGA) newborns of both groups showed increased levels of F2-IsoPs than appropriate (AGA) or large (LGA) for gestational age (GA) (p less than 0.01). SGA newborns of Group II had higher F2-IsoPs levels compared to SGA of Group I (p less than 0.01), which were significantly correlated to maternal BMI at the end of pregnancy (r=0.451, p less than 0.01). Multivariate regression analysis corrected for confounding factors, showed that maternal overweight or obesity was significantly associated with high F2-IsoPs levels in SGA offspring (p less than 0.01). Maternal overweight or obesity is associated with increased OS in their SGA newborns. Data suggest the need of antioxidant protection for both mothers during pregnancy and infants soon after birth.

  20. Gestational diabetes predicts the risk of childhood overweight and abdominal circumference independent of maternal obesity.

    Science.gov (United States)

    Nehring, I; Chmitorz, A; Reulen, H; von Kries, R; Ensenauer, R

    2013-12-01

    Gestational diabetes mellitus is believed to be a risk factor for childhood overweight/obesity. We aimed to assess whether this association is either a reflection or independent of confounding by maternal BMI. Data from 7355 mother-child dyads of the German Perinatal Prevention of Obesity cohort with full anthropometric information on mothers and children, gestational diabetes and confounding factors were obtained at school entry health examination. We calculated crude and adjusted logistic regression models for the association of gestational diabetes and childhood overweight/obesity and abdominal adiposity defined by age- and sex-specific percentiles for BMI and waist circumference. Among all children (mean age 5.8 years), 8.1% were overweight, 2.6% were obese and 15.5% had abdominal adiposity. The prevalence of overweight (obesity) was 21% (8.2%) in children of mothers with gestational diabetes and 10.4% (2.4%) in children of healthy mothers. Analyses with adjustment for maternal BMI and other potential confounders yielded an odds ratio of 1.81 (95% CI 1.23-2.65) and 2.80 (95% CI 1.58-4.99) for the impact of gestational diabetes on childhood overweight and obesity, respectively. Similar results were obtained for the risk of childhood abdominal adiposity (odds ratio 1.64, 95% CI 1.16-2.33) by maternal gestational diabetes. The postulated increased risk of overweight and abdominal adiposity in offspring of mothers with gestational diabetes cannot be explained by maternal BMI alone and may be stronger for childhood obesity than for overweight. © 2013 The Authors. Diabetic Medicine © 2013 Diabetes UK.

  1. A review of national health policies and professional guidelines on maternal obesity and weight gain in pregnancy.

    Science.gov (United States)

    Schumann, N L; Brinsden, H; Lobstein, T

    2014-08-01

    Maternal obesity creates an additional demand for health-care services, as the routine obstetric care pathway requires alterations to ensure the most optimal care for obese women of childbearing age. This review examines the extent to which relevant national health documents reflect and respond to the health implications of maternal obesity and excessive gestational weight gain. A targeted search of peer-reviewed publications and grey literature was conducted for each country to identify national health documents, which were subsequently content analyzed according to an adapted framework. A total of 37 documents were identified, including one policy, 10 strategies and 26 guidelines, published within the last 10 years. Out of the 31 countries investigated, only 13 countries address maternal obesity while none address excessive gestational weight gain. We found inconsistencies and gaps in the recommendations to health-care service providers for the management of maternal obesity and weight gain in pregnancy. The findings show that only limited guidance on maternal obesity and gestational weight gain exists. The authors recommend that international, evidence-based guidelines on the management of maternal obesity and excessive gestational weight gain should be developed to reduce the associated health-care and economic costs. © 2014 The Authors. Clinical Obesity © 2014 World Obesity.

  2. Obesity and pregnancy: a transversal study from a low-risk maternity.

    Science.gov (United States)

    Calderon, Ana Carolina S; Quintana, Silvana M; Marcolin, Alessandra C; Berezowski, Aderson T; Brito, Luiz Gustavo O; Duarte, Geraldo; Cavalli, Ricardo C

    2014-07-28

    Obesity is a public health problem and is increasing in all populations, including pregnant women. It influences maternal and neonatal outcomes; however, data are scarce in developing countries. We aimed to compare perinatal results between obese and non-obese pregnant women in a low-risk maternity. Transversal study of 1,779 40-week-pregnancies from 2005 to 2009 that completed a standard questionnaire with sociodemographic, obstetrical and neonatal variables and performed an ultrasound with amniotic fluid index (AFI) measurement and foetal vitality (FBP, non-stress test). They were analysed about their association with obesity on pregnancy. When compared with non-obese women, the group of obese patients had higher systolic (118.1 vs 109.2 mmHg; p < 0.01) and diastolic (76.6 vs 70.4 mmHg; p < 0.01) pressure levels, AFI (12.52 vs. 9.61 cm; p = 0.02), presence of meconium on labour (20.52 vs. 14.67%; p = 0.02), birthweight (3602 vs. 3437 g; p < 0.01) and caesarean section (39.74 vs. 29.98%, p < 0.01). Labour induction before 40 weeks in the antenatal period associated with foetal weight estimation should be considered as a recommendation for decreasing high percentages of caesarean delivery found in obese women.

  3. Maternal obesity during gestation impairs fatty acid oxidation and mitochondrial SIRT3 expression in rat offspring at weaning

    Science.gov (United States)

    In utero exposure to maternal obesity increases the offspring’s risk of obesity in later life. We have also previously reported that offspring of obese rat dams develop hepatic steatosis, mild hyperinsulinemia, and a lipogenic gene signature in the liver at postnatal day (PND) 21. In the current s...

  4. Maternal Obesity and Pre-Pregnancy Folic Acid Supplementation

    Directory of Open Access Journals (Sweden)

    Nadine Farah

    2013-04-01

    Full Text Available Objective: The purpose of this nested cohort study was to compare the rate of pre-pregnancy supplementation in obese women with that of women with a normal BMI. Methods: Pregnant women were enrolled at their convenience in a large university hospital. Weight and height were measured in the first trimester and BMI categorised. Results: Of the 288 women, 35.1% were in the normal, 29.5% in the overweight and 35.4% in the obese BMI categories. Only 45.1% (n = 46 of the obese women took pre-pregnancy folic acid compared with 60.4% (n = 61 of women with a normal BMI (p Conclusions: Obese women should take folate supplements whether they are planning to conceive or not.

  5. Maternal obesity reduces oxidative capacity in fetal skeletal muscle of Japanese macaques

    Science.gov (United States)

    McCurdy, Carrie E.; Hetrick, Byron; Houck, Julie; Drew, Brian G.; Kaye, Spencer; Lashbrook, Melanie; Bergman, Bryan C.; Takahashi, Diana L.; Dean, Tyler A.; Gertsman, Ilya; Hansen, Kirk C.; Philp, Andrew; Hevener, Andrea L.; Chicco, Adam J.; Aagaard, Kjersti M.; Grove, Kevin L.; Friedman, Jacob E.

    2016-01-01

    Maternal obesity is proposed to alter the programming of metabolic systems in the offspring, increasing the risk for developing metabolic diseases; however, the cellular mechanisms remain poorly understood. Here, we used a nonhuman primate model to examine the impact of a maternal Western-style diet (WSD) alone, or in combination with obesity (Ob/WSD), on fetal skeletal muscle metabolism studied in the early third trimester. We find that fetal muscle responds to Ob/WSD by upregulating fatty acid metabolism, mitochondrial complex activity, and metabolic switches (CPT-1, PDK4) that promote lipid utilization over glucose oxidation. Ob/WSD fetuses also had reduced mitochondrial content, diminished oxidative capacity, and lower mitochondrial efficiency in muscle. The decrease in oxidative capacity and glucose metabolism was persistent in primary myotubes from Ob/WSD fetuses despite no additional lipid-induced stress. Switching obese mothers to a healthy diet prior to pregnancy did not improve fetal muscle mitochondrial function. Lastly, while maternal WSD alone led only to intermediary changes in fetal muscle metabolism, it was sufficient to increase oxidative damage and cellular stress. Our findings suggest that maternal obesity or WSD, alone or in combination, leads to programmed decreases in oxidative metabolism in offspring muscle. These alterations may have important implications for future health. PMID:27734025

  6. Impact of Low Maternal Education on Early Childhood Overweight and Obesity in Europe

    NARCIS (Netherlands)

    Ruiz, Milagros; Goldblatt, Peter; Morrison, Joana; Porta, Daniela; Forastiere, Francesco; Hryhorczuk, Daniel; Antipkin, Youriy; Saurel-Cubizolles, Marie-Josèphe; Lioret, Sandrine; Vrijheid, Martine; Torrent, Maties; Iñiguez, Carmen; Larrañaga, Isabel; Bakoula, Chryssa; Veltsista, Alexandra; van Eijsden, Manon; Vrijkotte, Tanja G. M.; Andrýsková, Lenka; Dušek, Ladislav; Barros, Henrique; Correia, Sofia; Järvelin, Marjo-Riitta; Taanila, Anja; Ludvigsson, Johnny; Faresjö, Tomas; Marmot, Michael; Pikhart, Hynek

    2016-01-01

    Comparable evidence on adiposity inequalities in early life is lacking across a range of European countries. This study investigates whether low maternal education is associated with overweight and obesity risk in children from distinct European settings during early childhood. Prospective data of

  7. Maternal Obesity and Occurrence of Fetal Macrosomia: A Systematic Review and Meta-Analysis

    Science.gov (United States)

    Gaudet, Laura; Ferraro, Zachary M.; Walker, Mark

    2014-01-01

    Objective. To determine a precise estimate for the contribution of maternal obesity to macrosomia. Data Sources. The search strategy included database searches in 2011 of PubMed, Medline (In-Process & Other Non-Indexed Citations and Ovid Medline, 1950–2011), and EMBASE Classic + EMBASE. Appropriate search terms were used for each database. Reference lists of retrieved articles and review articles were cross-referenced. Methods of Study Selection. All studies that examined the relationship between maternal obesity (BMI ≥30 kg/m2) (pregravid or at 1st prenatal visit) and fetal macrosomia (birth weight ≥4000 g, ≥4500 g, or ≥90th percentile) were considered for inclusion. Tabulation, Integration, and Results. Data regarding the outcomes of interest and study quality were independently extracted by two reviewers. Results from the meta-analysis showed that maternal obesity is associated with fetal overgrowth, defined as birth weight ≥ 4000 g (OR 2.17, 95% CI 1.92, 2.45), birth weight ≥4500 g (OR 2.77,95% CI 2.22, 3.45), and birth weight ≥90% ile for gestational age (OR 2.42, 95% CI 2.16, 2.72). Conclusion. Maternal obesity appears to play a significant role in the development of fetal overgrowth. There is a critical need for effective personal and public health initiatives designed to decrease prepregnancy weight and optimize gestational weight gain. PMID:25544943

  8. Maternal Obesity and Occurrence of Fetal Macrosomia: A Systematic Review and Meta-Analysis

    Directory of Open Access Journals (Sweden)

    Laura Gaudet

    2014-01-01

    Full Text Available Objective. To determine a precise estimate for the contribution of maternal obesity to macrosomia. Data Sources. The search strategy included database searches in 2011 of PubMed, Medline (In-Process & Other Non-Indexed Citations and Ovid Medline, 1950–2011, and EMBASE Classic + EMBASE. Appropriate search terms were used for each database. Reference lists of retrieved articles and review articles were cross-referenced. Methods of Study Selection. All studies that examined the relationship between maternal obesity (BMI ≥30 kg/m2 (pregravid or at 1st prenatal visit and fetal macrosomia (birth weight ≥4000 g, ≥4500 g, or ≥90th percentile were considered for inclusion. Tabulation, Integration, and Results. Data regarding the outcomes of interest and study quality were independently extracted by two reviewers. Results from the meta-analysis showed that maternal obesity is associated with fetal overgrowth, defined as birth weight ≥ 4000 g (OR 2.17, 95% CI 1.92, 2.45, birth weight ≥4500 g (OR 2.77,95% CI 2.22, 3.45, and birth weight ≥90% ile for gestational age (OR 2.42, 95% CI 2.16, 2.72. Conclusion. Maternal obesity appears to play a significant role in the development of fetal overgrowth. There is a critical need for effective personal and public health initiatives designed to decrease prepregnancy weight and optimize gestational weight gain.

  9. Maternal History of Child Abuse and Obesity Risk in Offspring: Mediation by Weight in Pregnancy.

    Science.gov (United States)

    Leonard, Stephanie A; Petito, Lucia C; Rehkopf, David H; Ritchie, Lorrene D; Abrams, Barbara

    2017-08-01

    Women's experience of childhood adversity may contribute to their children's risk of obesity. Possible causal pathways include higher maternal weight and gestational weight gain, which have been associated with both maternal childhood adversity and obesity in offspring. This study included 6718 mother-child pairs from the National Longitudinal Survey of Youth 1979 in the United States (1979-2012). We applied multiple log-binomial regression models to estimate associations between three markers of childhood adversity (physical abuse, household alcoholism, and household mental illness) and offspring obesity in childhood. We estimated natural direct effects to evaluate mediation by prepregnancy BMI and gestational weight gain. Among every 100 mothers who reported physical abuse in childhood, there were 3.7 (95% confidence interval: -0.1 to 7.5) excess cases of obesity in 2- to 5-year olds compared with mothers who did not report physical abuse. Differences in prepregnancy BMI, but not gestational weight gain, accounted for 25.7% of these excess cases. There was no evidence of a similar relationship for household alcoholism or mental illness or for obesity in older children. In this national, prospective cohort study, prepregnancy BMI partially explained an association between maternal physical abuse in childhood and obesity in preschool-age children. These findings underscore the importance of life-course exposures in the etiology of child obesity and the potential multi-generational consequences of child abuse. Research is needed to determine whether screening for childhood abuse and treatment of its sequelae could strengthen efforts to prevent obesity in mothers and their children.

  10. Persistent influence of maternal obesity on offspring health: Mechanisms from animal models and clinical studies.

    Science.gov (United States)

    Wankhade, Umesh D; Thakali, Keshari M; Shankar, Kartik

    2016-11-05

    The consequences of excessive maternal weight and adiposity at conception for the offspring are now well recognized. Maternal obesity increases the risk of overweight and obesity even in children born with appropriate-for-gestational age (AGA) birth weights. Studies in animal models have employed both caloric excess and manipulation of macronutrients (especially high-fat) to mimic hypercaloric intake present in obesity. Findings from these studies show transmission of susceptibility to obesity, metabolic dysfunction, alterations in glucose homeostasis, hepatic steatosis, skeletal muscle metabolism and neuroendocrine changes in the offspring. This review summarizes the essential literature in this area in both experimental and clinical domains and focuses on the translatable aspects of these experimental studies. Moreover this review highlights emerging mechanisms broadly explaining maternal obesity-associated developmental programming. The roles of early developmental alterations and placental adaptations are also reviewed. Increasing evidence also points to changes in the epigenome and other emerging mechanisms such as alterations in the microbiome that may contribute to persistent changes in the offspring. Finally, we examine potential interventions that have been employed in clinical cohorts. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  11. Is maternal obesity related to semen quality in the male offspring? A pilot study

    DEFF Research Database (Denmark)

    Ramlau-Hansen, Cecilia Høst; Nøhr, Ellen Aagaard; Thulstrup, A M

    2007-01-01

    BACKGROUND: Obesity is a strong predictor of fecundity and maternal obesity may well program semen quality during pregnancy, but to our knowledge, no published studies have evaluated this hypothesis. METHODS: From a Danish pregnancy cohort established in 1984-87, 347 out of 5109 sons were selected...... for a follow-up study conducted from February 2005 to January 2006. Semen and blood samples were analyzed for conventional semen characteristics and reproductive hormones and related to information on maternal pre-pregnant body mass index (BMI) that was available for 328 men. Of these, 34 were sons...... of underweight, and 25 sons of overweight, mothers. RESULTS: Inhibin B decreased with increasing maternal BMI (P = 0.04) and the point estimates for sperm concentration, semen volume, percent motile sperm, testosterone and FSH suggested an impaired reproductive status among sons of overweight mothers, but none...

  12. Interventions to prevent adverse fetal programming due to maternal obesity during pregnancy.

    Science.gov (United States)

    Nathanielsz, Peter W; Ford, Stephen P; Long, Nathan M; Vega, Claudia C; Reyes-Castro, Luis A; Zambrano, Elena

    2013-10-01

    Maternal obesity is a global epidemic affecting both developed and developing countries. Human and animal studies indicate that maternal obesity adversely programs the development of offspring, predisposing them to chronic diseases later in life. Several mechanisms act together to produce these adverse health effects. There is a consequent need for effective interventions that can be used in the management of human pregnancy to prevent these outcomes. The present review analyzes the dietary and exercise intervention studies performed to date in both altricial and precocial animals, rats and sheep, with the aim of preventing adverse offspring outcomes. The results of these interventions present exciting opportunities to prevent, at least in part, adverse metabolic and other outcomes in obese mothers and their offspring. © 2013 International Life Sciences Institute.

  13. Infant Gut Microbiota Development Is Driven by Transition to Family Foods Independent of Maternal Obesity

    DEFF Research Database (Denmark)

    Laursen, Martin Frederik; Andersen, Louise B. B.; Michaelsen, Kim F.

    composition and alpha diversity were thus strongly affected by introduction of family foods with high protein and fiber contents. Specifically, intake of meats, cheeses and Danish rye bread, rich in protein and fiber, were associated with increased alpha diversity. Our results reveal that the transition from......The first years of life are paramount in establishing our endogenous gut microbiota, which is strongly affected by diet and has repeatedly been linked with obesity. However, very few studies have addressed the influence of maternal obesity on infant gut microbiota, which may occur either through...... either of a random sample of healthy mothers (n = 114), or of obese mothers (n = 113), were profiled by 16S rRNA amplicon sequencing. Gut microbiota data were compared to breastfeeding patterns and detailed individual dietary recordings to assess effects of the complementary diet. We found that maternal...

  14. Infant Gut Microbiota Development Is Driven by Transition to Family Foods Independent of Maternal Obesity

    DEFF Research Database (Denmark)

    Laursen, Martin Frederik; Andersen, Louise B. B.; Michaelsen, Kim F.

    2016-01-01

    composition and alpha diversity were thus strongly affected by introduction of family foods with high protein and fiber contents. Specifically, intake of meats, cheeses, and Danish rye bread, rich in protein and fiber, were associated with increased alpha diversity. Our results reveal that the transition from......The first years of life are paramount in establishing our endogenous gut microbiota, which is strongly affected by diet and has repeatedly been linked with obesity. However, very few studies have addressed the influence of maternal obesity on infant gut microbiota, which may occur either through...... either of a random sample of healthy mothers (n = 114), or of obese mothers (n = 113), were profiled by 16S rRNA amplicon sequencing. Gut microbiota data were compared to breastfeeding patterns and detailed individual dietary recordings to assess effects of the complementary diet. We found that maternal...

  15. Maternal Obesity Induces Sustained Inflammation in Both Fetal and Offspring Large Intestine of Sheep

    Science.gov (United States)

    Yan, Xu; Huang, Yan; Wang, Hui; Du, Min; Hess, Bret W.; Ford, Stephen P.; Nathanielsz, Peter W.; Zhu, Mei-Jun

    2010-01-01

    Background Both maternal obesity and inflammatory bowel diseases (IBDs) are increasing. It was hypothesized that maternal obesity induces an inflammatory response in the fetal large intestine, predisposing offspring to IBDs. Methods Nonpregnant ewes were assigned to a control (Con, 100% of National Research Council [NRC] recommendations) or obesogenic (OB, 150% of NRC) diet from 60 days before conception. The large intestine was sampled from fetuses at 135 days (term 150 days) after conception and from offspring lambs at 22.5 ± 0.5 months of age. Results Maternal obesity enhanced mRNA expression tumor necrosis factor (TNF)α, interleukin (IL)1α, IL1β, IL6, IL8, and monocyte/macrophage chemotactic protein-1 (MCP1), as well as macrophage markers, CD11b, CD14, and CD68 in fetal gut. mRNA expression of Toll-like receptor (TLR) 2 and TLR4 was increased in OB versus Con fetuses; correspondingly, inflammatory NF-κB and JNK signaling pathways were also upregulated. Both mRNA expression and protein content of transforming growth factor (TGF) β was increased. The IL-17A mRNA expression and protein content was higher in OB compared to Con samples, which was associated with fibrosis in the large intestine of OB fetuses. Similar inflammatory responses and enhanced fibrosis were detected in OB compared to Con offspring. Conclusions Maternal obesity induced inflammation and enhanced expression of proinflammatory cytokines in fetal and offspring large intestine, which correlated with increased TGFβ and IL17 expression. These data show that maternal obesity may predispose offspring gut to IBDs. PMID:21674707

  16. Maternal-fetal hepatic and placental metabolome profiles are associated with reduced fetal growth in a rat model of maternal obesity

    DEFF Research Database (Denmark)

    Mumme, Karen; Gray, Clint; Reynolds, Clare M.

    2016-01-01

    : Metabolomic profiling was used to reveal altered maternal and fetal metabolic pathways in a model of diet induced obesity during pregnancy, leading to reduced fetal growth. Methods: We examined the metabolome of maternal and fetal livers, and placenta following a high fat and salt intake. Sprague–Dawley rats...

  17. Improved maternal nutrition decreases children’s long-term risk of non-communicable diseases (NCDs) and obesity

    DEFF Research Database (Denmark)

    Robertson, Aileen

    Improved maternal nutrition to decrease children’s long-term risk of non-communicable diseases (NCDs) and obesity The nutritional well-being of pregnant women affects not only their health and their fetuses' development but also children's long-term risk of developing NCDs or obesity, according...... to a new report from WHO/Europe. "Good maternal nutrition. The best start in life" was launched under the auspices of the Minister of Health of Latvia during a consultation on maternal nutrition, in Riga on 27–28 June 2016. While the importance of good nutrition in the early development of children has...... – affects not only her child's health as an infant but also the child's risk of obesity and related chronic diseases as an adult. In short, maternal nutrition can truly have an intergenerational impact. Fighting NCDs and obesity through measures to improve maternal nutrition: NCDs are the leading cause...

  18. Maternal depressive symptoms and child obesity in low-income urban families.

    Science.gov (United States)

    Gross, Rachel S; Velazco, Nerissa K; Briggs, Rahil D; Racine, Andrew D

    2013-01-01

    To characterize the relationship between maternal depressive symptoms and child weight status, obesity-promoting feeding practices, and activity-related behaviors in low-income urban families. We conducted a cross-sectional survey of mothers with 5-year-old children receiving pediatric care at a federally qualified community health center. We used regression analyses to examine the relationship between maternal depressive symptoms (trichotomized: none, mild, moderate to severe) and 1) child weight status; 2) obesity-promoting feeding practices, including mealtime practices and feeding styles; and 3) activity-related behaviors, including sleep time, screen time, and outdoor playtime. The sample included 401 mother-child pairs (78.3% response rate), with 23.4% of mothers reporting depressive symptoms (15.7% mild, 7.7% moderate to severe). Mothers with moderate to severe depressive symptoms were more likely to have overweight and obese children than mothers without depressive symptoms (adjusted odds ratio 2.62; 95% confidence interval 1.02-6.70). Children of mildly depressed mothers were more likely to consume sweetened drinks and to eat out at restaurants and were less likely to eat breakfast than children of nondepressed mothers. Mothers with depressive symptoms were less likely to set limits, to use food as a reward, to restrict their child's intake, and to model healthy eating than nondepressed mothers. Children with depressed mothers had less sleep and outdoor playtime per day than children of nondepressed mothers. Maternal depressive symptoms are associated with child overweight and obese status and with several obesity-promoting practices. These results support the need for maternal depression screening in pediatric obesity prevention programs. Further research should explore how to incorporate needed mental health support. Copyright © 2013 Academic Pediatric Association. Published by Elsevier Inc. All rights reserved.

  19. Maternal obesity disrupts circadian rhythms of clock and metabolic genes in the offspring heart and liver.

    Science.gov (United States)

    Wang, Danfeng; Chen, Siyu; Liu, Mei; Liu, Chang

    2015-06-01

    Early life nutritional adversity is tightly associated with the development of long-term metabolic disorders. Particularly, maternal obesity and high-fat diets cause high risk of obesity in the offspring. Those offspring are also prone to develop hyperinsulinemia, hepatic steatosis and cardiovascular diseases. However, the precise underlying mechanisms leading to these metabolic dysregulation in the offspring remain unclear. On the other hand, disruptions of diurnal circadian rhythms are known to impair metabolic homeostasis in various tissues including the heart and liver. Therefore, we investigated that whether maternal obesity perturbs the circadian expression rhythms of clock, metabolic and inflammatory genes in offspring heart and liver by using RT-qPCR and Western blotting analysis. Offspring from lean and obese dams were examined on postnatal day 17 and 35, when pups were nursed by their mothers or took food independently. On P17, genes examined in the heart either showed anti-phase oscillations (Cpt1b, Pparα, Per2) or had greater oscillation amplitudes (Bmal1, Tnf-α, Il-6). Such phase abnormalities of these genes were improved on P35, while defects in amplitudes still existed. In the liver of 17-day-old pups exposed to maternal obesity, the oscillation amplitudes of most rhythmic genes examined (except Bmal1) were strongly suppressed. On P35, the oscillations of circadian and inflammatory genes became more robust in the liver, while metabolic genes were still kept non-rhythmic. Maternal obesity also had a profound influence in the protein expression levels of examined genes in offspring heart and liver. Our observations indicate that the circadian clock undergoes nutritional programing, which may contribute to the alternations in energy metabolism associated with the development of metabolic disorders in early life and adulthood.

  20. Higher Birthweight and Maternal Pre-pregnancy BMI Persist with Obesity Association at Age 9 in High Risk Latino Children.

    Science.gov (United States)

    Kjaer, Thora Wesenberg; Faurholt-Jepsen, Daniel; Medrano, Rosalinda; Elwan, Deena; Mehta, Kala; Christensen, Vibeke Brix; Wojcicki, Janet M

    2018-02-03

    Childhood obesity is increasing especially in Latinos and early intervention is essential to prevent later obesity complications. Latino children (n = 201) recruited at two San Francisco hospitals were assessed at birth including infant anthropometrics and feeding practices and followed to age 9 with annual anthropometric assessments. We evaluated the relationship between perinatal risk factors and obesity at age 9 and chronic obesity (obesity at both 5 and 9 years). Higher birthweight [odds ratio (OR) 2.48, 95% confidence interval (CI) 1.06-5.81] and maternal pre-pregnancy body mass index (BMI) (OR 1.09, 95% CI 1.00-1.18) were associated with increased risk for obesity at 9 years. Higher maternal pre-pregnancy BMI (OR 1.10, 95% CI 1.01-1.20) was associated with chronic obesity. Additionally, prenatal depression symptoms were protective (OR 0.33, 95% CI 0.11-0.94) against chronic obesity. We found no association between maternal age and education, exclusive breastfeeding at 4-6 weeks, rapid infant weight gain, and obesity or chronic obesity. Perinatal risk factors for obesity including higher birthweight and maternal pre-pregnancy BMI persisted until age 9, whereas, other variables significant at age 5 in our cohort and other populations including exclusive breastfeeding and rapid infant weight gain were no longer associated with increased risk.

  1. Ceramide-induced TCR up-regulation

    DEFF Research Database (Denmark)

    Menné, C; Lauritsen, Jens Peter Holst; Dietrich, J

    2000-01-01

    to increase T cell responsiveness. The purpose of this study was to identify and characterize potential pathways for TCR up-regulation. We found that ceramide affected TCR recycling dynamics and induced TCR up-regulation in a concentration- and time-dependent manner. Experiments applying phosphatase......The TCR is a constitutively recycling receptor meaning that a constant fraction of TCR from the plasma membrane is transported inside the cell at the same time as a constant fraction of TCR from the intracellular pool is transported to the plasma membrane. TCR recycling is affected by protein...... kinase C activity. Thus, an increase in protein kinase C activity affects TCR recycling kinetics leading to a new TCR equilibrium with a reduced level of TCR expressed at the T cell surface. Down-regulation of TCR expression compromises T cell activation. Conversely, TCR up-regulation is expected...

  2. Developmental Programming of Obesity and Liver Metabolism by Maternal Perinatal Nutrition Involves the Melanocortin System

    Directory of Open Access Journals (Sweden)

    Paul Cordero

    2017-09-01

    Full Text Available Maternal obesity predisposes offspring to metabolic dysfunction and Non-Alcoholic Fatty Liver Disease (NAFLD. Melanocortin-4 receptor (Mc4r-deficient mouse models exhibit obesity during adulthood. Here, we aim to determine the influence of the Mc4r gene on the liver of mice subjected to perinatal diet-induced obesity. Female mice heterozygous for Mc4r fed an obesogenic or a control diet for 5 weeks were mated with heterozygous males, with the same diet continued throughout pregnancy and lactation, generating four offspring groups: control wild type (C_wt, control knockout (C_KO, obese wild type (Ob_wt, and obese knockout (Ob_KO. At 21 days, offspring were genotyped, weaned onto a control diet, and sacrificed at 6 months old. Offspring phenotypic characteristics, plasma biochemical profile, liver histology, and hepatic gene expression were analyzed. Mc4r_ko offspring showed higher body, liver and adipose tissue weights respect to the wild type animals. Histological examination showed mild hepatic steatosis in offspring group C_KO. The expression of hepatic genes involved in regulating inflammation, fibrosis, and immune cell infiltration were upregulated by the absence of the Mc4r gene. These results demonstrate that maternal obesogenic feeding during the perinatal period programs offspring obesity development with involvement of the Mc4r system.

  3. Maternal obesity programs mitochondrial and lipid metabolism gene expression in infant umbilical vein endothelial cells.

    Science.gov (United States)

    Costa, S M R; Isganaitis, E; Matthews, T J; Hughes, K; Daher, G; Dreyfuss, J M; da Silva, G A P; Patti, M-E

    2016-11-01

    Maternal obesity increases risk for childhood obesity, but molecular mechanisms are not well understood. We hypothesized that primary umbilical vein endothelial cells (HUVEC) from infants of overweight and obese mothers would harbor transcriptional patterns reflecting offspring obesity risk. In this observational cohort study, we recruited 13 lean (pre-pregnancy body mass index (BMI) obese ('ov-ob', BMI⩾25.0 kg m -2 ) women. We isolated primary HUVEC, and analyzed both gene expression (Primeview, Affymetrix) and cord blood levels of hormones and adipokines. A total of 142 transcripts were differentially expressed in HUVEC from infants of overweight-obese mothers (false discovery rate, FDRmaternal BMI (FDRmaternal obesity, we analyzed the cord blood lipidome and noted significant increases in the levels of total free fatty acids (lean: 95.5±37.1 μg ml -1 , ov-ob: 124.1±46.0 μg ml -1 , P=0.049), palmitate (lean: 34.5±12.7 μg ml -1 , ov-ob: 46.3±18.4 μg ml -1 , P=0.03) and stearate (lean: 20.8±8.2 μg ml -1 , ov-ob: 29.7±17.2 μg ml -1 , P=0.04), in infants of overweight-obese mothers. Prenatal exposure to maternal obesity alters HUVEC expression of genes involved in mitochondrial and lipid metabolism, potentially reflecting developmentally programmed differences in oxidative and lipid metabolism.

  4. Independent and joint effects of prenatal maternal smoking and maternal exposure to second-hand smoke on the development of adolescent obesity: a longitudinal study.

    Science.gov (United States)

    Wang, Liang; Mamudu, Hadii M; Alamian, Arsham; Anderson, James L; Brooks, Billy

    2014-11-01

    To examine associations of prenatal maternal smoking and second-hand smoke (SHS) exposure with the development of adolescent obesity. Longitudinal data (1991-2007) from National Institute of Child Health and Human Development Study of Early Child Care and Youth Development involving mothers that smoked and or exposed to SHS during the year before birth were analysed. Adolescent obesity in ages 12.0-15.9 years was defined as a BMI ≥ 95th percentile. Generalised estimating equations (GEE) were used for the analyses. Obesity was more prevalent among adolescents whose mothers smoked or had SHS exposure than those that did not smoke or exposed to SHS. After adjusting for maternal and child factors, GEE models showed that odds of adolescent obesity increased with prenatal maternal smoking (OR = 1.57, 95% CI = 1.03-2.39) and SHS exposure (OR = 1.53, 95% CI = 1.04-2.27). The odds for obesity increased more than two times among adolescents exposed to both maternal smoking and SHS (OR = 2.10, 95% CI = 1.24, 3.56) compared with those without exposure. Additionally, not breastfeeding, maternal obesity, and longer screen viewing hours per day were associated with increased odds of obesity. There is possibly a long-term joint effect of prenatal maternal smoke (smoking and SHS) exposure on obesity among adolescent offspring, and the effect is independent of birthweight. These findings suggest that adolescent obesity could possibly be curtailed with the development and promotion of smoking cessation programmes for families during the year before birth. © 2014 The Authors. Journal of Paediatrics and Child Health © 2014 Paediatrics and Child Health Division (Royal Australasian College of Physicians).

  5. Qing brick tea (QBT) aqueous extract protects monosodium glutamate-induced obese mice against metabolic syndrome and involves up-regulation Transcription Factor Nuclear Factor-Erythroid 2-Related Factor 2 (Nrf2) antioxidant pathway.

    Science.gov (United States)

    Gao, Wenqi; Xiao, Changyi; Hu, Jun; Chen, Biaoxin; Wang, Chunyan; Cui, Bangping; Deng, Pengyi; Yang, Jian; Deng, Zhifang

    2018-04-18

    Qing brick tea (QBT), traditional and popular beverage for Chinese people, is an important post-fermentation dark tea. Our present study was performed to investigate the ameliorative effects of QBT aqueous extract on metabolic syndrome (Mets) in monosodium glutamate-induced obese mice and the potential mechanisms. Monosodium glutamate-induced obese mice were used to evaluate the anti-Mets effects of QBT. Content levels of malonaldehyde (MDA), reactive oxygen species (ROS) and protein carbonylation, antioxidant enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione reductase (GR) in the skeletal muscle were assessed by commercial kits, respectively. Western blot and Q-PCR were used to detect the expressions of Transcription Factor Nuclear Factor-Erythroid 2-Related Factor 2 (Nrf2) signaling pathway and downstream antioxidant factors. In addition, activity of AKT signaling and expression of glucose transporter type 4 (GLUT4) in the skeletal muscle were investigated by western blot. QBT treatment limited gain of body weight, waistline and LEE index, improved insulin resistance and glucose intolerance, reduced lipid level in MSG mice. Content levels of MDA, ROS and protein carbonylation in skeletal muscle of QBT group were significantly improved compared to those of MSG mice. The antioxidant enzyme activities of SOD, GPx, CAT, and GR were increased in skeletal muscle of MSG mice intervened with QBT. After 20-week QBT treatment, Nrf2 signaling pathway and downstream antioxidant factors were both increased in the skeletal muscle. In addition, QBT treatment improved insulin signaling by preferentially augmenting AKT signaling, as well as increased the protein expression of GLUT4 in the skeletal muscle. Our results showed that QBT intake was effective in protecting monosodium glutamate-induced obese mice against metabolic syndrome and involved in the Nrf2 signaling pathway in the skeletal muscle. Copyright © 2018

  6. Obesity and overweight: Impact on maternal and milk microbiome and their role for infant health and nutrition

    OpenAIRE

    Garcia-Mantrana, Izaskun; Collado, Maria Carmen

    2016-01-01

    Obesity, particularly in infants, is becoming a significant public health problem that has reached “epidemic” status worldwide. Obese children have an increased risk of developing obesity-related diseases, such as metabolic syndromes and diabetes, as well as increased risk of mortality and adverse health outcomes later in life. Experimental data show that maternal obesity has negative effects on the offspring's health in the short and long term. Increasing evidence suggests a key role for mic...

  7. A nationally representative study of maternal obesity in England, UK : trends in incidence and demographic inequalities in 619323 births, 1989-2007.

    OpenAIRE

    Heslehurst, N.; Rankin, J.; Wilkinson, J.R.; Summerbell, C.D.

    2010-01-01

    Background: There is an absence of national statistics for maternal obesity in the UK. This study is the first to describe a nationally representative maternal obesity research data set in England. Design: Retrospective epidemiological study of first trimester obesity. Methods: Data from 34 maternity units were analysed, including 619 323 births between 1989 and 2007. Data analysis included trends in first trimester maternal body bass index status over time, and geographical distribut...

  8. Pre-pregnancy maternal overweight and obesity increase the risk for affective disorders in offspring.

    Science.gov (United States)

    Robinson, M; Zubrick, S R; Pennell, C E; Van Lieshout, R J; Jacoby, P; Beilin, L J; Mori, T A; Stanley, F J; Newnham, J P; Oddy, W H

    2013-02-01

    Maternal pre-pregnancy obesity has been linked with an increased risk for negative emotionality and inattentiveness in offspring in early childhood. The aim of this study was to examine the association between maternal pre-pregnancy body mass index (BMI) and the development of affective problems (dysthymic disorder, major depressive disorder) throughout childhood and adolescence. In the Western Australian Pregnancy Cohort (Raine) Study, 2900 women provided data on their pre-pregnancy weight, and height measurements were taken at 18 weeks of gestation. BMI was calculated and categorized using standardized methods. Live-born children (n = 2868) were followed up at ages 5, 8, 10, 14 and 17 years using the Diagnostic and Statistical Manual of Mental Disorders-oriented scales of the Child Behavior Checklist (CBCL/4-18). Longitudinal models were applied to assess the relationships between maternal pre-pregnancy BMI and affective problems from age 5 through 17. There was a higher risk of affective problems between the ages of 5 and 17 years among children of women who were overweight and obese compared with the offspring of women in the healthy pre-pregnancy weight range (BMI 18.5-24.99) after adjustment for confounders, including paternal BMI. Maternal pre-pregnancy overweight and obesity may be implicated in the development of affective problems, including depression, in their offspring later in life.

  9. The effect of androgen excess on maternal metabolism, placental function and fetal growth in obese dams.

    Science.gov (United States)

    Fornes, Romina; Maliqueo, Manuel; Hu, Min; Hadi, Laila; Jimenez-Andrade, Juan M; Ebefors, Kerstin; Nyström, Jenny; Labrie, Fernand; Jansson, Thomas; Benrick, Anna; Stener-Victorin, Elisabet

    2017-08-14

    Pregnant women with polycystic ovary syndrome (PCOS) are often overweight or obese. To study the effects of maternal androgen excess in obese dams on metabolism, placental function and fetal growth, female C57Bl6J mice were fed a control (CD) or a high fat/high sucrose (HF/HS) diet for 4-10 weeks, and then mated. On gestational day (GD) 15.5-17.5, dams were injected with dihydrotestosterone (CD-DHT, HF/HS-DHT) or a vehicle (CD-Veh, HF/HS-Veh). HF/HS dams had higher fat content, both before mating and on GD18.5, with no difference in glucose homeostasis, whereas the insulin sensitivity was higher in DHT-exposed dams. Compared to the CD groups, the livers from HF/HS dams weighed more on GD18.5, the triglyceride content was higher, and there was a dysregulation of liver enzymes related to lipogenesis and higher mRNA expression of Fitm1. Fetuses from HF/HS-Veh dams had lower liver triglyceride content and mRNA expression of Srebf1c. Maternal DHT exposure, regardless of diet, decreased fetal liver Pparg mRNA expression and increased placental androgen receptor protein expression. Maternal diet-induced obesity, together with androgen excess, affects maternal and fetal liver function as demonstrated by increased triglyceride content and dysfunctional expression of enzymes and transcription factors involved in de novo lipogenesis and fat storage.

  10. Maternal weight misperceptions and smoking are associated with overweight and obesity in low SES preschoolers.

    Science.gov (United States)

    Kaufman-Shriqui, V; Fraser, D; Novack, Y; Bilenko, N; Vardi, H; Abu-Saad, K; Elhadad, N; Feine, Z; Mor, K; Shahar, D R

    2012-02-01

    To identify modifiable risk factors for obesity among low socioeconomic status (LSES) children. Cross-sectional data were obtained from 238 4-7-year-old children and 224 mothers from LSES preschools. Anthropometric measurements were obtained; mothers were interviewed about sociodemographic characteristics, health behaviors, perceptions and beliefs. The combined prevalence of overweight and obesity (OWOB) among children was 29.8% based on the new World Health Organization (WHO) growth standard. Prevalence of OWOB (body mass index ≥25) among mothers was 51.8%. Mean age, sleeping hours, gender distribution and poverty level were similar between normal and OWOB children. Over 82% of mothers underestimated their child's weight status. Of the 62 OWOB children, 74.2% were perceived by their mothers as having 'normal weight' (NW) and 8% were perceived as 'thin'. Mothers perceived 67 out of 158 NW children (42.4%) as 'thin' (Pmaternal underestimation on child's OWOB may be mediated through child's daily sedentary hours (P=0.06). In a multivariable logistic-regression analysis controlling for maternal obesity, knowledge regarding breakfast's importance and child's daily sedentary hours, maternal underestimation of the child's weight status (odds ratio=7.33; 95% confidence interval (CI):2.41-22.37; PMaternal perception of child's weight status and parental smoking are associated with childhood OWOB among LSES children. These parameters can help identify children at risk for obesity. Maternal perception may be amenable to intervention.

  11. Maternal prepregnancy obesity and achievement of infant motor developmental milestones in the upstate KIDS study.

    Science.gov (United States)

    Wylie, Amanda; Sundaram, Rajeshwari; Kus, Christopher; Ghassabian, Akhgar; Yeung, Edwina H

    2015-04-01

    Maternal prepregnancy obesity is associated with several poor infant health outcomes; however, studies that investigated motor development have been inconsistent. Thus, maternal prepregnancy weight status and infants' gross motor development were examined. Participants consisted of 4,901 mother-infant pairs from the Upstate KIDS study, a longitudinal cohort in New York. Mothers indicated dates when infants achieved each of six gross motor milestones when infants were 4, 8, 12, 18, and 24 months old. Failure time modeling under a Weibull distribution was utilized to compare time to achievement across three levels of maternal prepregnancy BMI. Hazard ratios (HR) below one indicate a lower "risk" of achieving the milestone and translate to later achievement. Compared to infants born to thin and normal-weight mothers (BMI obesity (BMI > 30) were slower to sit without support (HR = 0.91, P = 0.03) and crawl on hands and knees (HR = 0.86, P obesity was associated with a slightly longer time for infant to sit and crawl, potentially due to a compromised intrauterine environment or reduced physically active play. © 2015 The Obesity Society.

  12. Toddlers' bias to look at average versus obese figures relates to maternal anti-fat prejudice.

    Science.gov (United States)

    Ruffman, Ted; O'Brien, Kerry S; Taumoepeau, Mele; Latner, Janet D; Hunter, John A

    2016-02-01

    Anti-fat prejudice (weight bias, obesity stigma) is strong, prevalent, and increasing in adults and is associated with negative outcomes for those with obesity. However, it is unknown how early in life this prejudice forms and the reasons for its development. We examined whether infants and toddlers might display an anti-fat bias and, if so, whether it was influenced by maternal anti-fat attitudes through a process of social learning. Mother-child dyads (N=70) split into four age groups participated in a preferential looking paradigm whereby children were presented with 10 pairs of average and obese human figures in random order, and their viewing times (preferential looking) for the figures were measured. Mothers' anti-fat prejudice and education were measured along with mothers' and fathers' body mass index (BMI) and children's television viewing time. We found that older infants (M=11months) had a bias for looking at the obese figures, whereas older toddlers (M=32months) instead preferred looking at the average-sized figures. Furthermore, older toddlers' preferential looking was correlated significantly with maternal anti-fat attitudes. Parental BMI, education, and children's television viewing time were unrelated to preferential looking. Looking times might signal a precursor to explicit fat prejudice socialized via maternal anti-fat attitudes. Copyright © 2015 Elsevier Inc. All rights reserved.

  13. Adiponectin supplementation in pregnant mice prevents the adverse effects of maternal obesity on placental function and fetal growth.

    Science.gov (United States)

    Aye, Irving L M H; Rosario, Fredrick J; Powell, Theresa L; Jansson, Thomas

    2015-10-13

    Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth. Compared with dams on a control diet, female C57BL/6J mice fed an obesogenic diet before mating and throughout gestation had increased fasting serum leptin, insulin, and C-peptide, and reduced high-molecular-weight ADN at embryonic day (E) 18.5. Placental insulin and mTORC1 signaling was activated, peroxisome proliferator-activated receptor-α (PPARα) phosphorylation was reduced, placental transport of glucose and amino acids in vivo was increased, and fetal weights were 29% higher in obese dams. Maternal ADN infusion in obese dams from E14.5 to E18.5 normalized maternal insulin sensitivity, placental insulin/mTORC1 and PPARα signaling, nutrient transport, and fetal growth without affecting maternal fat mass. Using a mouse model with striking similarities to obese pregnant women, we demonstrate that ADN functions as an endocrine link between maternal adipose tissue and fetal growth by regulating placental function. Importantly, maternal ADN supplementation reversed the adverse effects of maternal obesity on placental function and fetal growth. Improving maternal ADN levels may serve as an effective intervention strategy to prevent fetal overgrowth caused by maternal obesity.

  14. Impact of Low Maternal Education on Early Childhood Overweight and Obesity in Europe.

    Science.gov (United States)

    Ruiz, Milagros; Goldblatt, Peter; Morrison, Joana; Porta, Daniela; Forastiere, Francesco; Hryhorczuk, Daniel; Antipkin, Youriy; Saurel-Cubizolles, Marie-Josèphe; Lioret, Sandrine; Vrijheid, Martine; Torrent, Maties; Iñiguez, Carmen; Larrañaga, Isabel; Bakoula, Chryssa; Veltsista, Alexandra; van Eijsden, Manon; Vrijkotte, Tanja G M; Andrýsková, Lenka; Dušek, Ladislav; Barros, Henrique; Correia, Sofia; Järvelin, Marjo-Riitta; Taanila, Anja; Ludvigsson, Johnny; Faresjö, Tomas; Marmot, Michael; Pikhart, Hynek

    2016-05-01

    Comparable evidence on adiposity inequalities in early life is lacking across a range of European countries. This study investigates whether low maternal education is associated with overweight and obesity risk in children from distinct European settings during early childhood. Prospective data of 45 413 children from 11 European cohorts were used. Children's height and weight obtained at ages 4-7 years were used to assess prevalent overweight and obesity according to the International Obesity Task Force definition. The Relative/Slope Indices of Inequality (RII/SII) were estimated within each cohort and by gender to investigate adiposity risk among children born to mothers with low education as compared to counterparts born to mothers with high education. Individual-data meta-analyses were conducted to obtain aggregate estimates and to assess heterogeneity between cohorts. Low maternal education yielded a substantial risk of early childhood adiposity across 11 European countries. Low maternal education yielded a mean risk ratio of 1.58 (95% confidence interval (CI) 1.34, 1.85) and a mean risk difference of 7.78% (5.34, 10.22) in early childhood overweight, respectively, measured by the RII and SII. Early childhood obesity risk by low maternal education was as substantial for all cohorts combined (RII = 2.61 (2.10, 3.23)) and (SII = 4.01% (3.14, 4.88)). Inequalities in early childhood adiposity were consistent among boys, but varied among girls in a few cohorts. Considerable inequalities in overweight and obesity are evident among European children in early life. Tackling early childhood adiposity is necessary to promote children's immediate health and well-being and throughout the life course. © 2016 John Wiley & Sons Ltd.

  15. Hypothalamic neuroendocrine circuitry is programmed by maternal obesity: interaction with postnatal nutritional environment.

    Directory of Open Access Journals (Sweden)

    Hui Chen

    Full Text Available OBJECTIVE: Early life nutrition is critical for the development of hypothalamic neurons involved in energy homeostasis. We previously showed that intrauterine and early postnatal overnutrition programmed hypothalamic neurons expressing the appetite stimulator neuropeptide Y (NPY and suppressor proopiomelanocortin (POMC in offspring at weaning. However, the long-term effects of such programming and its interactions with post-weaning high-fat-diet (HFD consumption are unclear. RESEARCH DESIGN AND METHODS: Female Sprague Dawley rats were exposed to chow or HFD for 5 weeks before mating, throughout gestation and lactation. On postnatal day 1, litters were adjusted to 3/litter to induce postnatal overnutrition (vs. 12 in control. At postnatal day 20, half of the rats from each maternal group were weaned onto chow or HFD for 15 weeks. Hypothalamic appetite regulators, and fuel (glucose and lipid metabolic markers were measured. RESULTS: Offspring from obese dams gained more weight than those from lean dams independent of post-weaning diet. Maternal obesity interacted with post-weaning HFD consumption to cause greater levels of hyperphagia, adiposity, hyperlipidemia, and glucose intolerance in offspring. This was linked to increased hypothalamic NPY signaling and leptin resistance in adult offspring. Litter size reduction had a detrimental impact on insulin and adiponectin, while hypothalamic NPY and POMC mRNA expression were suppressed in the face of normal energy intake and weight gain. CONCLUSIONS: Maternal obesity, postnatal litter size reduction and post-weaning HFD consumption caused obesity via different neuroendocrine mechanism. There were strong additive effects of maternal obesity and post-weaning HFD consumption to increase the metabolic disorders in offspring.

  16. Swedish and American studies show that initiatives to decrease maternal obesity could play a key role in reducing preterm birth.

    Science.gov (United States)

    Gould, Jeffrey B; Mayo, Jonathan; Shaw, Gary M; Stevenson, David K

    2014-06-01

    Maternal obesity is a major source of preventable perinatal morbidity, but studies of the relationship between obesity and preterm birth have been inconsistent. This review looks at two major studies covering just under 3.5 million births, from California, USA, and Sweden. Inconsistent findings in previous studies appear to stem from the complex relationship between obesity and preterm birth. Initiatives to decrease maternal obesity represent an important strategy in reducing preterm birth. ©2014 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

  17. Maternal High-Fat Diet and Obesity Impact Palatable Food Intake and Dopamine Signaling in Nonhuman Primate Offspring

    Science.gov (United States)

    Rivera, Heidi M.; Kievit, Paul; Kirigiti, Melissa A.; Bauman, Leigh Ann; Baquero, Karalee; Blundell, Peter; Dean, Tyler A.; Valleau, Jeanette C.; Takahashi, Diana L.; Frazee, Tim; Douville, Luke; Majer, Jordan; Smith, M. Susan; Grove, Kevin L.; Sullivan, Elinor L.

    2015-01-01

    Objective To utilize a nonhuman primate model to examine the impact of maternal high-fat diet (HFD) consumption and pre-pregnancy obesity on offspring intake of palatable food. We will also examine whether maternal HFD consumption impaired development of the dopamine system, critical for the regulation of hedonic feeding. Methods The impact of exposure to maternal HFD and obesity on offspring consumption of diets of varying composition was assessed after weaning. We also examined the influence of maternal HFD consumption on the development of the prefrontal cortex-dopamine system at 13 months of age. Results During a preference test, offspring exposed to maternal obesity and HFD consumption displayed increased intake of food high in fat and sugar content relative to offspring from lean control mothers. Maternal HFD consumption suppressed offspring dopamine signaling (as assessed by immunohistochemistry) relative to control offspring. Specifically, there was decreased abundance of dopamine fibers and of dopamine receptor 1 and 2 protein. Conclusion Our findings reveal that offspring exposed to both maternal HFD consumption and maternal obesity during early development are at increased risk for obesity due to overconsumption of palatable energy-dense food, a behavior that may be related to reduced central dopamine signaling. PMID:26530932

  18. Paternal and maternal obesity but not gestational weight gain is associated with type 1 diabetes

    DEFF Research Database (Denmark)

    Magnus, Maria C; Olsen, Sjurdur F; Granstrom, Charlotta

    2018-01-01

    100 000 person-years in MoBa and 28.5 per 100 000 person-years in DNBC. Both maternal pre-pregnancy obesity, adjusted hazard ratio (HR) 1.41 [95% confidence interval (CI): 1.06, 1.89] and paternal obesity, adjusted HR 1.51 (95% CI: 1.11, 2.04), were associated with childhood-onset type 1 diabetes......Background: Our objective was to examine the associations of parental body mass index (BMI) and maternal gestational weight gain with childhood-onset type 1 diabetes. Comparing the associations of maternal and paternal BMI with type 1 diabetes in the offspring will provide further insight...... included parental BMI and maternal gestational weight gain obtained by maternal report. We used Cox-proportional hazards regression to examine the risk of type 1 diabetes (n=499 cases), which was ascertained by national childhood diabetes registers. Results: The incidence of type 1 diabetes was 32.7 per...

  19. Maternal Diet-Induced Obesity Programmes Cardiac Dysfunction in Male Mice Independently of Post-Weaning Diet.

    Science.gov (United States)

    Loche, Elena; Blackmore, Heather L; Carpenter, Asha A M; Beeson, Jessica H; Pinnock, Adele; Ashmore, Thomas J; Aiken, Catherine E; de Almeida-Faria, Juliana; Schoonejans, Josca; Giussani, Dino A; Fernandez-Twinn, Denise S; Ozanne, Susan E

    2018-04-04

    Obesity during pregnancy increases risk of cardiovascular disease (CVD) in the offspring and individuals exposed to over-nutrition during fetal life are likely to be exposed to a calorie-rich environment postnatally. Here, we established the consequences of combined exposure to a maternal and post-weaning obesogenic diet on offspring cardiac structure and function using an established mouse model of maternal diet-induced obesity. The impact of the maternal and postnatal environment on the offspring metabolic profile, arterial blood pressure, cardiac structure and function was assessed in 8-week old C57BL/6 male mice. Measurement of cardiomyocyte cell area, the transcriptional re-activation of cardiac fetal genes as well as genes involved in the regulation of contractile function and matrix remodelling in the adult heart were determined as potential mediators of effects on cardiac function. In the adult offspring: a post-weaning obesogenic diet coupled with exposure to maternal obesity increased serum insulin (P<0.0001) and leptin levels (P<0.0001); maternal obesity (P=0.001) and a post-weaning obesogenic diet (P=0.002) increased absolute heart weight; maternal obesity (P=0.01) and offspring obesity (P=0.01) caused cardiac dysfunction but effects were not additive; cardiac dysfunction resulting from maternal obesity was associated with re-expression of cardiac fetal genes (Myh7:Myh6 ratio; P=0.0004), however these genes were not affected by offspring diet; maternal obesity (P=0.02) and offspring obesity (P=0.05) caused hypertension and effects were additive. Maternal diet-induced obesity and offspring obesity independently promote cardiac dysfunction and hypertension in adult male progeny. Exposure to maternal obesity alone programmed cardiac dysfunction, associated with hallmarks of pathological left ventricular hypertrophy, including increased cardiomyocyte area, upregulation of fetal genes and remodelling of cardiac structure. These data highlight that the

  20. Dietary alleviation of maternal obesity and diabetes: increased resistance to diet-induced obesity transcriptional and epigenetic signatures.

    Science.gov (United States)

    Attig, Linda; Vigé, Alexandre; Gabory, Anne; Karimi, Moshen; Beauger, Aurore; Gross, Marie-Sylvie; Athias, Anne; Gallou-Kabani, Catherine; Gambert, Philippe; Ekstrom, Tomas J; Jais, Jean-Philippe; Junien, Claudine

    2013-01-01

    According to the developmental origins of health and diseases (DOHaD), and in line with the findings of many studies, obesity during pregnancy is clearly a threat to the health and well-being of the offspring, later in adulthood. We previously showed that 20% of male and female inbred mice can cope with the obesogenic effects of a high-fat diet (HFD) for 20 weeks after weaning, remaining lean. However the feeding of a control diet (CD) to DIO mice during the periconceptional/gestation/lactation period led to a pronounced sex-specific shift (17% to 43%) from susceptibility to resistance to HFD, in the female offspring only. Our aim in this study was to determine how, in the context of maternal obesity and T2D, a CD could increase resistance on female fetuses. Transcriptional analyses were carried out with a custom-built mouse liver microarray and by quantitative RT-PCR for muscle and adipose tissue. Both global DNA methylation and levels of pertinent histone marks were assessed by LUMA and western blotting, and the expression of 15 relevant genes encoding chromatin-modifying enzymes was analyzed in tissues presenting global epigenetic changes. Resistance was associated with an enhancement of hepatic pathways protecting against steatosis, the unexpected upregulation of neurotransmission-related genes and the modulation of a vast imprinted gene network. Adipose tissue displayed a pronounced dysregulation of gene expression, with an upregulation of genes involved in lipid storage and adipocyte hypertrophy or hyperplasia in obese mice born to lean and obese mothers, respectively. Global DNA methylation, several histone marks and key epigenetic regulators were also altered. Whether they were themselves lean (resistant) or obese (sensitive), the offspring of lean and obese mice clearly differed in terms of several metabolic features and epigenetic marks suggesting that the effects of a HFD depend on the leanness or obesity of the mother.

  1. Programming of Fetal Insulin Resistance in Pregnancies with Maternal Obesity by ER Stress and Inflammation

    Directory of Open Access Journals (Sweden)

    Francisco Westermeier

    2014-01-01

    Full Text Available The global epidemics of obesity during pregnancy and excessive gestational weight gain (GWG are major public health problems worldwide. Obesity and excessive GWG are related to several maternal and fetal complications, including diabetes (pregestational and gestational diabetes and intrauterine programming of insulin resistance (IR. Maternal obesity (MO and neonatal IR are associated with long-term development of obesity, diabetes mellitus, and increased global cardiovascular risk in the offspring. Multiple mechanisms of insulin signaling pathway impairment have been described in obese individuals, involving complex interactions of chronically elevated inflammatory mediators, adipokines, and the critical role of the endoplasmic reticulum (ER stress-dependent unfolded protein response (UPR. However, the underlying cellular processes linking MO and IR in the offspring have not been fully elucidated. Here, we summarize the state-of-the-art evidence supporting the possibility that adverse metabolic postnatal outcomes such as IR in the offspring of pregnancies with MO and/or excessive GWG may be related to intrauterine activation of ER stress response.

  2. Maternal obesity and congenital heart defects: a population-based study123

    Science.gov (United States)

    Mills, James L; Troendle, James; Conley, Mary R; Carter, Tonia; Druschel, Charlotte M

    2010-01-01

    Background: Obesity affects almost one-third of pregnant women and causes many complications, including neural tube defects. It is not clear whether the risk of congenital heart defects, the most common malformations, is also increased. Objective: This study was conducted to determine whether obesity is associated with an increased risk of congenital heart defects. Design: A population-based, nested, case-control study was conducted in infants born with congenital heart defects and unaffected controls from the cohort of all births (n = 1,536,828) between 1993 and 2003 in New York State, excluding New York City. The type of congenital heart defect, maternal body mass index (BMI; in kg/m2), and other risk factors were obtained from the Congenital Malformations Registry and vital records. Mothers of 7392 congenital heart defect cases and 56,304 unaffected controls were studied. Results: All obese women (BMI ≥ 30) were significantly more likely than normal-weight women (BMI: 19–24.9) to have children with a congenital heart defect [odds ratio (OR): 1.15; 95% CI: 1.07, 1.23; P heart defects with increasing maternal obesity (P heart syndrome, aortic stenosis, pulmonic stenosis, and tetralogy of Fallot. Conclusions: Obese, but not overweight, women are at significantly increased risk of bearing children with a range of congenital heart defects, and the risk increases with increasing BMI. Weight reduction as a way to reduce risk should be investigated. PMID:20375192

  3. Programming of Fetal Insulin Resistance in Pregnancies with Maternal Obesity by ER Stress and Inflammation

    Science.gov (United States)

    Sáez, Pablo J.; Villalobos-Labra, Roberto; Farías-Jofré, Marcelo

    2014-01-01

    The global epidemics of obesity during pregnancy and excessive gestational weight gain (GWG) are major public health problems worldwide. Obesity and excessive GWG are related to several maternal and fetal complications, including diabetes (pregestational and gestational diabetes) and intrauterine programming of insulin resistance (IR). Maternal obesity (MO) and neonatal IR are associated with long-term development of obesity, diabetes mellitus, and increased global cardiovascular risk in the offspring. Multiple mechanisms of insulin signaling pathway impairment have been described in obese individuals, involving complex interactions of chronically elevated inflammatory mediators, adipokines, and the critical role of the endoplasmic reticulum (ER) stress-dependent unfolded protein response (UPR). However, the underlying cellular processes linking MO and IR in the offspring have not been fully elucidated. Here, we summarize the state-of-the-art evidence supporting the possibility that adverse metabolic postnatal outcomes such as IR in the offspring of pregnancies with MO and/or excessive GWG may be related to intrauterine activation of ER stress response. PMID:25093191

  4. Maternal obesity in pregnancy, gestational weight gain, and risk of childhood asthma.

    Science.gov (United States)

    Forno, Erick; Young, Omar M; Kumar, Rajesh; Simhan, Hyagriv; Celedón, Juan C

    2014-08-01

    Environmental or lifestyle exposures in utero may influence the development of childhood asthma. In this meta-analysis, we aimed to assess whether maternal obesity in pregnancy (MOP) or increased maternal gestational weight gain (GWG) increased the risk of asthma in offspring. We included all observational studies published until October 2013 in PubMed, Embase, CINAHL, Scopus, The Cochrane Database, and Ovid. Random effects models with inverse variance weights were used to calculate pooled risk estimates. Fourteen studies were included (N = 108 321 mother-child pairs). Twelve studies reported maternal obesity, and 5 reported GWG. Age of children was 14 months to 16 years. MOP was associated with higher odds of asthma or wheeze ever (OR = 1.31; 95% confidence interval [CI], 1.16-1.49) or current (OR = 1.21; 95% CI, 1.07-1.37); each 1-kg/m(2) increase in maternal BMI was associated with a 2% to 3% increase in the odds of childhood asthma. High GWG was associated with higher odds of asthma or wheeze ever (OR = 1.16; 95% CI, 1.001-1.34). Maternal underweight and low GWG were not associated with childhood asthma or wheeze. Meta-regression showed a negative association of borderline significance for maternal asthma history (P = .07). The significant heterogeneity among existing studies indicates a need for standardized approaches to future studies on the topic. MOP and high GWG are associated with an elevated risk of childhood asthma; this finding may be particularly significant for mothers without asthma history. Prospective randomized trials of maternal weight management are needed. Copyright © 2014 by the American Academy of Pediatrics.

  5. Maternal ratings of child health and child obesity, variations by mother's race/ethnicity and nativity.

    Science.gov (United States)

    Baker, Elizabeth H; Altman, Claire E

    2015-05-01

    We examined whether indicators of child health, focusing on obesity, are associated with maternal ratings of child health (MRCH) and its variation by mother's ethnicity/nativity, focusing on Hispanics. The early childhood longitudinal study, kindergarten cohort kindergarten-eighth grade waves (n = 48,814) and nested general linear mixed modeling are used to examine excellent MRCH. The only indicator of child health that varies by mother's ethnicity/nativity for MRCH is child obesity. Child obesity did not influence MRCH for foreign-born Hispanic mothers, especially among less acculturated mothers, though significant differences among immigrants by acculturation were not found. However, among native-born white, black, and Hispanic mothers child obesity was associated with a lower likelihood of excellent MRCH even after controls for socioeconomic characteristics, family characteristics, and other indicators of child health are included. MRCH reflect not only child's actual health, but also the mother's perception of what contributes to poor child health. Our findings suggest that less acculturated foreign-born Hispanic mothers are less likely to associate child obesity with poor child health. Cultural orientations that prefer heavier children or are unlikely to associate child obesity with poor child health may contribute to the higher levels of obesity found among their children.

  6. Maternal BMI and migration status as predictors of childhood obesity in Mexico.

    Science.gov (United States)

    Jiménez-Cruz, A; Wojcicki, J M; Bacardí-Gascón, M; Castellón-Zaragoza, A; García-Gallardo, J L; Schwartz, N; Heyman, M B

    2011-01-01

    To assess the association of maternal migration to Baja California, body mass index (BMI) status, children's perceived food insecurity, and childhood lifestyle behaviors with overweight (BMI > 85% ile), obesity (BMI > 95% ile) and abdominal obesity (Waist Circumference > 90% ile). Convenience sampling methods were used to recruit a cross-sectional sample of 4th, 5th and 6th grade children and their parents at Tijuana and Tecate Public Schools. Children's and parents' weights and heights were measured. Children were considered to have migrant parents if parents were not born in Baja California. One hundred and twenty-two children and their parents were recruited. The mean age of the children was 10.1 ± 1.0 years. Forty nine per cent of children were overweight or obese. Children with obese parents (BMI > 30) had greater odds of being obese, Odds Ratio (OR) 4.9 (95% Confidence Interval (CI), 1.2-19, p = 0.03). Children with migrant parents had greater odds of being obese, OR= 3.7 (95% CI, 1.6-8.3), p = 0.01) and of having abdominal obesity, OR = 3.2 (95% CI, 1.4-7.1, p = 0.01). Children from migrant parents have greater risk of higher consumption of potato chips, OR = 8.0 (95% CI, 2.1-29.1, p = 0.01). Children from non-migrant parents had greater odds of being at risk of hunger. Parental obesity and migration are associated with increased risk of obesity among Mexican children. Children whose parents were born in Baja California have greater odds of being at risk of hunger. Further studies should evaluate the role of migration on risk for childhood obesity.

  7. From fatalism to mitigation: a conceptual framework for mitigating fetal programming of chronic disease by maternal obesity

    OpenAIRE

    Boone-Heinonen, Janne; Messer, Lynne C.; Fortmann, Stephen P.; Wallack, Lawrence; Thornburg, Kent L.

    2015-01-01

    Prenatal development is recognized as a critical period in the etiology of obesity and cardiometabolic disease. Potential strategies to reduce maternal obesity-induced risk later in life have been largely overlooked. In this paper, we first propose a conceptual framework for the role of public health and preventive medicine in mitigating the effects of fetal programming. Second, we review a small but growing body of research (through August 2015) that examines interactive effects of maternal ...

  8. [Effect of breastfeeding on obesity of schoolchildren: influence of maternal education].

    Science.gov (United States)

    Pudla, Katia Jakovljevic; Gonzaléz-Chica, David Alejandro; de Vasconcelos, Francisco de Assis Guedes

    2015-01-01

    To evaluate the association between duration of breastfeeding (BF) and obesity in schoolchildren of Florianópolis (SC), and the role of possible effect modifiers. Cross-sectional study with a random sample of 2,826 schoolchildren (7-14 years). Weight and height were measured according to standardized procedures. Data concerning BF and sociodemographic variables were obtained from a questionnaire sent to parents/guardians. Children's nutritional status was evaluated by BMI-for-age z-score for gender (WHO reference curves). Adjusted analyses were performed through logistic regression, considering a possible interaction among variables. Prevalence of obesity was 8.6% (95% CI: 7.6-9.7%) and 55.7% (95% CI: 53.8-57.6%) received breastmilk for ≥6 months. BF was not associated with obesity, even in the adjusted analysis. Stratified analysis according to maternal schooling showed that, in children aged 7-10 years and children whose mothers had 0-8 years of schooling, the chance of obesity was lower among those breastfeed for >1 month, especially among those who received breastmilk for 1-5 months (OR=0.22; 95% CI 0.08-0.62). Among children of women with higher educational level (>8 years), the chance of obesity was 44% lower in those who were breastfed for >12 months (p-value for interaction children (11-14 years). Among children of women with lower schooling, BF for any period longer than 1 month is protective against obesity; however, for a higher maternal schooling, BF for less than 12 months increases the odds of obesity. Copyright © 2015 Sociedade de Pediatria de São Paulo. Publicado por Elsevier Editora Ltda. All rights reserved.

  9. Maternal obesity increases inflammation and exacerbates damage following neonatal hypoxic-ischaemic brain injury in rats.

    Science.gov (United States)

    Teo, Jonathan D; Morris, Margaret J; Jones, Nicole M

    2017-07-01

    In humans, maternal obesity is associated with an increase in the incidence of birth related difficulties. However, the impact of maternal obesity on the severity of brain injury in offspring is not known. Recent studies have found evidence of increased glial response and inflammatory mediators in the brains as a result of obesity in humans and rodents. We hypothesised that hypoxic-ischaemic (HI) brain injury is greater in neonatal offspring from obese rat mothers compared to lean controls. Female Sprague Dawley rats were randomly allocated to high fat (HFD, n=8) or chow (n=4) diet and mated with lean male rats. On postnatal day 7 (P7), male and female pups were randomly assigned to HI injury or control (C) groups. HI injury was induced by occlusion of the right carotid artery followed by 3h exposure to 8% oxygen, at 37°C. Control pups were removed from the mother for the same duration under ambient conditions. Righting behaviour was measured on day 1 and 7 following HI. The extent of brain injury was quantified in brain sections from P14 pups using cresyl violet staining and the difference in volume between brain hemispheres was measured. Before mating, HFD mothers were 11% heavier than Chow mothers (pmaternal weight. Similar observations were made with neuronal staining showing a greater loss of neurons in the brain of offspring from HFD-mothers following HI compared to Chow. Astrocytes appeared to more hypertrophic and a greater number of microglia were present in the injured hemisphere in offspring from mothers on HFD. HI caused an increase in the proportion of amoeboid microglia and exposure to maternal HFD exacerbated this response. In the contralateral hemisphere, offspring exposed to maternal HFD displayed a reduced proportion of ramified microglia. Our data clearly demonstrate that maternal obesity can exacerbate the severity of brain damage caused by HI in neonatal offspring. Given that previous studies have shown enhanced inflammatory responses in

  10. Maternal obesity alters feto-placental Cytochrome P4501A1 activity

    Science.gov (United States)

    DuBois, Barent N.; O’Tierney, Perrie; Pearson, Jacob; Friedman, Jacob E.; Thornburg, Kent; Cherala, Ganesh

    2012-01-01

    Cytochrome P4501A1 (CYP1A1), an important drug metabolizing enzyme, is expressed in human placenta throughout gestation as well as in fetal liver. Obesity, a chronic inflammatory condition, is known to alter CYP enzyme expression in non-placental tissues. In the present study, we test the hypothesis that maternal obesity alters the distribution of CYP1A1 activity in feto-placental unit. Placentas were collected from non-obese (BMI30) women at term. Livers were collected from gestation day 130 fetuses of non-human primates fed either control diet or high-fat diet (HFD). Cytosol and microsomes were collected using differential centrifugation, and incubated with 7-Ethoxyresorufin. The CYP1A1 specific activity (pmoles of resorufin formed/min/mg of protein) was measured at excitation/emission wavelength of 530/590nm. Placentas of obese women had significantly reduced microsomal CYP1A1 activity compared to non-obese women (0.046 vs. 0.082; p<0.05); however no such effect was observed on cytosolic activity. Similarly, fetal liver from HFD fed mothers had significantly reduced microsomal CYP1A1 activity (0.44±0.04 vs. 0.20±0.10; p<0.05), with no significant difference in cytosolic CYP1A1 activity (control, 1.23±0.20; HFD, 0.80±0.40). Interestingly, multiple linear regression analyses of placental efficiency indicates cytosolic CYP1A1 activity is a main effect (5.67±2.32 (β±SEM); p=0.022) along with BMI (−0.57±0.26; p=0.037), fetal gender (1.07±0.26; p<0.001), and maternal age (0.07±0.03; p=0.011). In summary, while maternal obesity affects microsomal CYP1A1 activity alone, cytosolic activity along with maternal BMI is an important determinant of placental efficiency. Together, these data suggest that maternal lifestyle could have a significant impact on CYP1A1 activity, and hints at a possible role for CYP1A1 in feto-placental growth and thereby well-being of fetus. PMID:23046808

  11. Developmental ORIgins of Healthy and Unhealthy AgeiNg: The Role of Maternal Obesity - Introduction to DORIAN

    Directory of Open Access Journals (Sweden)

    Patricia Iozzo

    2014-04-01

    Full Text Available Europe has the highest proportion of elderly people in the world. Cardiovascular disease, type 2 diabetes, sarcopenia and cognitive decline frequently coexist in the same aged individual, sharing common early risk factors and being mutually reinforcing. Among conditions which may contribute to establish early risk factors, this review focuses on maternal obesity, since the epidemic of obesity involves an ever growing number of women of reproductive age and children, calling for appropriate studies to understand the consequences of maternal obesity on the offspring's health and for developing effective measures and policies to improve people's health before their conception and birth. Though the current knowledge suggests that the long-term impact of maternal obesity on the offspring's health may be substantial, the outcomes of maternal obesity over the lifespan have not been quantified, and the molecular changes induced by maternal obesity remain poorly characterized. We hypothesize that maternal insulin resistance and reduced placental glucocorticoid catabolism, leading to oxidative stress, may damage the DNA, either in its structure (telomere shortening or in its function (via epigenetic changes, resulting in altered gene expression/repair, disease during life, and pathological ageing. This review illustrates the background to the EU-FP7-HEALTH-DORIAN project.

  12. Influence of Maternal Obesity and Gestational Weight Gain on Maternal and Foetal Lipid Profile.

    Science.gov (United States)

    Cinelli, Giulia; Fabrizi, Marta; Ravà, Lucilla; Ciofi Degli Atti, Marta; Vernocchi, Pamela; Vallone, Cristina; Pietrantoni, Emanuela; Lanciotti, Rosalba; Signore, Fabrizio; Manco, Melania

    2016-06-15

    Fatty acids (FAs) are fundamental for a foetus's growth, serving as an energy source, structural constituents of cellular membranes and precursors of bioactive molecules, as well as being essential for cell signalling. Long-chain polyunsaturated FAs (LC-PUFAs) are pivotal in brain and visual development. It is of interest to investigate whether and how specific pregnancy conditions, which alter fatty acid metabolism (excessive pre-pregnancy body mass index (BMI) or gestational weight gain (GWG)), affect lipid supply to the foetus. For this purpose, we evaluated the erythrocyte FAs of mothers and offspring (cord-blood) at birth, in relation to pre-pregnancy BMI and GWG. A total of 435 mothers and their offspring (237 males, 51%) were included in the study. Distribution of linoleic acid (LA) and α-linolenic acid (ALA), and their metabolites, arachidonic acid, dihomogamma linoleic (DGLA) and ecosapentanoic acid, was significantly different in maternal and foetal erythrocytes. Pre-pregnancy BMI was significantly associated with maternal percentage of MUFAs (Coeff: -0.112; p = 0.021), LA (Coeff: -0.033; p = 0.044) and DHA (Coeff. = 0.055; p = 0.0016); inadequate GWG with DPA (Coeff: 0.637; p = 0.001); excessive GWG with docosaexahenoic acid (DHA) (Coeff. = -0.714; p = 0.004). Moreover, pre-pregnancy BMI was associated with foetus percentage of PUFAs (Coeff: -0.172; p = 0.009), omega 6 (Coeff: -0.098; p = 0.015) and DHA (Coeff: -0.0285; p = 0.036), even after adjusting for maternal lipids. Our findings show that maternal GWG affects maternal but not foetal lipid profile, differently from pre-pregnancy BMI, which influences both.

  13. Infant Gut Microbiota Development Is Driven by Transition to Family Foods Independent of Maternal Obesity.

    Science.gov (United States)

    Laursen, Martin Frederik; Andersen, Louise B B; Michaelsen, Kim F; Mølgaard, Christian; Trolle, Ellen; Bahl, Martin Iain; Licht, Tine Rask

    2016-01-01

    The first years of life are paramount in establishing our endogenous gut microbiota, which is strongly affected by diet and has repeatedly been linked with obesity. However, very few studies have addressed the influence of maternal obesity on infant gut microbiota, which may occur either through vertically transmitted microbes or through the dietary habits of the family. Additionally, very little is known about the effect of diet during the complementary feeding period, which is potentially important for gut microbiota development. Here, the gut microbiotas of two different cohorts of infants, born either of a random sample of healthy mothers (n = 114), or of obese mothers (n = 113), were profiled by 16S rRNA amplicon sequencing. Gut microbiota data were compared to breastfeeding patterns and detailed individual dietary recordings to assess effects of the complementary diet. We found that maternal obesity did not influence microbial diversity or specific taxon abundances during the complementary feeding period. Across cohorts, breastfeeding duration and composition of the complementary diet were found to be the major determinants of gut microbiota development. In both cohorts, gut microbial composition and alpha diversity were thus strongly affected by introduction of family foods with high protein and fiber contents. Specifically, intake of meats, cheeses, and Danish rye bread, rich in protein and fiber, were associated with increased alpha diversity. Our results reveal that the transition from early infant feeding to family foods is a major determinant for gut microbiota development. IMPORTANCE The potential influence of maternal obesity on infant gut microbiota may occur either through vertically transmitted microbes or through the dietary habits of the family. Recent studies have suggested that the heritability of obesity may partly be caused by the transmission of "obesogenic" gut microbes. However, the findings presented here suggest that maternal obesity per

  14. Maternal obesity support services: a qualitative study of the perspectives of women and midwives

    Directory of Open Access Journals (Sweden)

    Dearden Andy M

    2011-10-01

    Full Text Available Abstract Background Twenty percent of pregnant women in the UK are obese (BMI ≥ 30 kg/m2, reflecting the growing public health challenge of obesity in the 21st century. Obesity increases the risk of adverse outcomes during pregnancy and birth and has significant cost implications for maternity services. Gestational weight management strategies are a high priority; however the evidence for effective, feasible and acceptable weight control interventions is limited and inconclusive. This qualitative study explored the experiences and perceptions of pregnant women and midwives regarding existing support for weight management in pregnancy and their ideas for service development. Methods A purposive sample of 6 women and 7 midwives from Doncaster, UK, participated in two separate focus groups. Transcripts were analysed thematically. Results Two overarching themes were identified, 'Explanations for obesity and weight management' and 'Best care for pregnant women'. 'Explanations' included a lack of knowledge about weight, diet and exercise during pregnancy; self-talk messages which excused overeating; difficulties maintaining motivation for a healthy lifestyle; the importance of social support; stigmatisation; and sensitivity surrounding communication about obesity between midwives and their clients. 'Best care' suggested that weight management required care which was consistent and continuous, supportive and non-judgemental, and which created opportunities for interaction and mutual support between obese pregnant women. Conclusions Women need unambiguous advice regarding healthy lifestyles, diet and exercise in pregnancy to address a lack of knowledge and a tendency towards unhelpful self-talk messages. Midwives expressed difficulties in communicating with their clients about their weight, given awareness that obesity is a sensitive and potentially stigmatising issue. This indicates more could be done to educate and support them in their work with

  15. Maternal obesity, gestational weight gain and childhood cardiac outcomes: role of childhood body mass index.

    Science.gov (United States)

    Toemen, L; Gishti, O; van Osch-Gevers, L; Steegers, E A P; Helbing, W A; Felix, J F; Reiss, I K M; Duijts, L; Gaillard, R; Jaddoe, V W V

    2016-07-01

    Maternal obesity may affect cardiovascular outcomes in the offspring. We examined the associations of maternal prepregnancy body mass index and gestational weight gain with childhood cardiac outcomes and explored whether these associations were explained by parental characteristics, infant characteristics or childhood body mass index. In a population-based prospective cohort study among 4852 parents and their children, we obtained maternal weight before pregnancy and in early, mid- and late pregnancy. At age 6 years, we measured aortic root diameter (cm) and left ventricular dimensions. We calculated left ventricular mass (g), left ventricular mass index (g m(-2.7)), relative wall thickness ((2 × left ventricular posterior wall thickness)/left ventricular diameter), fractional shorting (%), eccentric left ventricular hypertrophy and concentric remodeling. A one standard deviation score (SDS) higher maternal prepregnancy body mass index was associated with higher left ventricular mass (0.10 SDS (95% confidence interval (CI) 0.08, 0.13)), left ventricular mass index (0.06 SDS (95% CI 0.03, 0.09)) and aortic root diameter (0.09 SDS (95% CI 0.06, 0.12)), but not with relative wall thickness or fractional shortening. A one SDS higher maternal prepregnancy body mass index was associated with an increased risk of eccentric left ventricular hypertrophy (odds ratio 1.21 (95% CI 1.03, 1.41)), but not of concentric remodeling. When analyzing the effects of maternal weight in different periods simultaneously, only maternal prepregnancy weight and early pregnancy weight were associated with left ventricular mass, left ventricular mass index and aortic root diameter (P-valuesMaternal prepregnancy body mass index and weight gain in early pregnancy are both associated with offspring cardiac structure in childhood, but these associations seem to be fully explained by childhood body mass index.

  16. Maternal pre-pregnancy overweight and obesity, and child neuropsychological development: two Southern European birth cohort studies.

    Science.gov (United States)

    Casas, Maribel; Chatzi, Leda; Carsin, Anne-Elie; Amiano, Pilar; Guxens, Mònica; Kogevinas, Manolis; Koutra, Katerina; Lertxundi, Nerea; Murcia, Mario; Rebagliato, Marisa; Riaño, Isolina; Rodríguez-Bernal, Clara L; Roumeliotaki, Theano; Sunyer, Jordi; Mendez, Michelle; Vrijheid, Martine

    2013-04-01

    Maternal pre-pregnancy obesity may be associated with impaired infant neuropsychological development; however, there are few studies and it is unclear if reported associations are due to intrauterine mechanisms. We assessed whether maternal pre-pregnancy overweight and obesity were associated with cognitive and psychomotor development scores (mean 100 ± 15) of children aged 11-22 months in two birth cohorts: Environment and Childhood (INMA, Spain; n = 1967) and Mother-Child (RHEA, Greece: n = 412). Paternal body mass index (BMI) was used as a negative control exposure. The percentage of overweight and obese mothers was 18% and 8%, respectively, in INMA and 20% and 11% in RHEA, respectively. Maternal pre-pregnancy obesity was associated with reduced infant cognitive development scores in both INMA (score reduction: -2.72; 95% CI: -5.35, -0.10) and RHEA (score reduction: -3.71; 95% CI: -8.45, 1.02), after adjusting for socioeconomic variables and paternal BMI. There was evidence in both cohorts of a dose-response relationship with continuous maternal BMI. Paternal overweight/obesity was not associated with infant cognitive development. Associations with psychomotor scores were not consistent between cohorts, and were stronger for paternal than maternal BMI in RHEA. This study in two birth cohorts with moderately high obesity prevalence suggests that maternal pre-pregnancy obesity is associated with reduced child cognitive development at early ages. This association appears more likely to be due to maternal than shared family and social mechanisms, but further research is needed to disentangle a direct intrauterine effect from other maternal confounding factors.

  17. Management of reproduction and pregnancy complications in maternal obesity: which role for dietary polyphenols?

    Science.gov (United States)

    Santangelo, Carmela; Varì, Rosaria; Scazzocchio, Beatrice; Filesi, Carmelina; Masella, Roberta

    2014-01-01

    Obesity is a global and dramatic public health problem; maternal obesity represents one of the main risk factors of infertility and pregnancy complications as it is associated with adverse maternal and offspring outcomes. In the last few years, adipose tissue dysfunction associated with altered adipocytokine secretion has been suggested to play a critical role in all the phases of reproductive process. Obesity is a nutrition-related disorder. In this regard, dietary intervention strategies, such as high intake of fruit and vegetables, have shown significant effects in both preserving health and counteracting obesity-associated diseases. Evidence has been provided that polyphenols, important constituents of plant-derived food, can influence developmental program of oocyte and embryo, as well as pregnancy progression by modulating several cellular pathways. This review will examine the controversial results so far obtained on adipocytokine involvement in fertility impairment and pregnancy complications. Furthermore, the different effects exerted by polyphenols on oocyte, embryo, and pregnancy development will be also taken in account. © 2013 International Union of Biochemistry and Molecular Biology.

  18. Effect of Maternal Obesity on Fetal Growth and Expression of Placental Fatty Acid Transporters.

    Science.gov (United States)

    Ye, Kui; Li, Li; Zhang, Dan; Li, Yi; Wang, Hai Qing; Lai, Han Lin; Hu, Chuan Lai

    2017-12-15

    To explore the effects of maternal high-fat (HF) diet-induced obesity on fetal growth and the expression of placental nutrient transporters. Maternal obesity was established in rats by 8 weeks of pre-pregnancy fed HF diet, while rats in the control group were fed normal (CON) diet. Diet-induced obesity (DIO) rats and diet-induced obesity-resistant (DIR) rats were selected according to body weight gain over this period. After copulation, the CON rats were divided into two groups: switched to HF diet (CON-HF group) or maintained on the CON diet (CON-CON group). The DIO rats and DIR rats were maintained on the HF diet throughout pregnancy. Pregnant rats were euthanized at day 21 gestation, fetal and placental weights were recorded, and placental tissue was collected. Reverse transcription-polymerase chain reaction was used to determine mRNA expression of placental nutrient transporters. Protein expression was determined by Western blot. Average fetal weight of DIO dams was reduced by 6.9%, and the placentas of CON-HF and DIO dams were significantly heavier than the placentas of CON-CON and DIR dams at day 21 of gestation (pobesity induced by a HF diet led to intrauterine growth retardation and down-regulated the expression of placental fatty acid transporters.

  19. Behavioral counseling to prevent childhood obesity – study protocol of a pragmatic trial in maternity and child health care

    OpenAIRE

    Mustila, Taina; Keskinen, Päivi; Luoto, Riitta

    2012-01-01

    Abstract Background Prevention is considered effective in combating the obesity epidemic. Prenatal environment may increase offspring's risk for obesity. A child starts to adopt food preferences and other behavioral habits affecting weight gain during preschool years. We report the study protocol of a pragmatic lifestyle intervention aiming at primary prevention of childhood obesity. Methods/Design A non-randomized controlled pragmatic trial in maternity and child health care clinics. The con...

  20. The Impact of maternal obesity and race/ethnicity on perinatal outcomes: Independent and joint effects.

    Science.gov (United States)

    Snowden, Jonathan M; Mission, John F; Marshall, Nicole E; Quigley, Brian; Main, Elliott; Gilbert, William M; Chung, Judith H; Caughey, Aaron B

    2016-07-01

    Independent and joint impacts of maternal race/ethnicity and obesity on adverse birth outcomes, including pre-eclampsia, low birth weight, and macrosomia, were characterized. Retrospective cohort study of all 2007 California births was conducted using vital records and claims data. Maternal race/ethnicity and maternal body mass index (BMI) were the key exposures; their independent and joint impact on outcomes using regression models was analyzed. Racial/ethnic minority women of normal weight generally had higher risk as compared with white women of normal weight (e.g., African-American women, pre-eclampsia adjusted odds ratio [aOR] 1.60, 95% confidence interval [CI]: 1.48-1.74 vs. white women). However, elevated BMI did not usually confer additional risk (e.g., pre-eclampsia aOR comparing African-American women with excess weight with white women with excess weight, 1.17, 95% CI: 0.89-1.54). Obesity was a risk factor for low birth weight only among white women (excess weight aOR, 1.24, 95% CI: 1.04-1.49 vs. white women of normal weight) and not among racial/ethnic minority women (e.g., African-American women, 0.95, 95% CI: 0.83-1.08). These findings add nuance to our understanding of the interplay between maternal race/ethnicity, BMI, and perinatal outcomes. While the BMI/adverse outcome gradient appears weaker in racial/ethnic minority women, this reflects the overall risk increase in racial/ethnic minority women of all body sizes. © 2016 The Obesity Society.

  1. Programming of mouse obesity by maternal exposure to concentrated ambient fine particles.

    Science.gov (United States)

    Chen, Minjie; Wang, Xiaoke; Hu, Ziying; Zhou, Huifen; Xu, Yanyi; Qiu, Lianglin; Qin, Xiaobo; Zhang, Yuhao; Ying, Zhekang

    2017-06-23

    Many diseases including obesity may originate through alterations in the early-life environment that interrupts fetal development. Increasing evidence has shown that exposure to ambient fine particles (PM 2.5 ) is associated with abnormal fetal development. However, its long-term metabolic effects on offspring have not been systematically investigated. To determine if maternal exposure to PM 2.5 programs offspring obesity, female C57Bl/6j mice were exposed to filtered air (FA) or concentrated ambient PM 2.5 (CAP) during pre-conception, pregnancy, and lactation, and the developmental and metabolic responses of offspring were assessed. The growth trajectory of offspring revealed that maternal exposure to CAP significantly decreased offspring birth weight but increased body weight of adult male but not female offspring, and the latter was expressed as increased adiposity. These adult male offspring had increased food intake, but were sensitive to exogenous leptin. Their hypothalamic expression of Socs3 and Pomc, two target genes of leptin, was not changed, and the hypothalamic expression of NPY, an orexigenic peptide that is inhibited by leptin, was significantly increased. These decreases in central anorexigenic signaling were accompanied by reduced plasma leptin and its expression in adipose tissues, the primary source of circulating leptin. In contrast, maternal exposure did not significantly change any of these indexes in adult female offspring. Pyrosequencing demonstrated that the leptin promoter methylation of adipocytes was significantly increased in CAP-exposed male but not female offspring. Our data indicate that maternal exposure to ambient PM 2.5 programs obesity in male offspring probably through alterations in the methylation of the promoter region of the leptin gene.

  2. Maternal recalled gestational weight gain, pre-pregnancy body mass index, and obesity in the daughter

    Science.gov (United States)

    Stuebe, Alison M.; Forman, Michele R.; Michels, Karin B.

    2009-01-01

    Objective Emerging evidence suggests that exposures during fetal life affect adult metabolism. We assessed the relation between recalled maternal pre-pregnancy body mass, gestational weight gain (GWG), and adiposity in the daughter. Design Retrospective cohort study among mother-nurse daughter dyads in the Nurses’ Health Study II and the Nurses’ Mothers’ Cohort. Mothers of participants completed questionnaires regarding their nurse-daughter in 2001. Participants 26,506 mother-nurse daughter dyads born between 1946 and 1964. Main outcome measures Body mass index of the nurse-daughter at age 18 and in 2001. Results At age 18, 561 (2.1%) daughters were obese (BMI greater than 30), and in 2001, 5,442 (22.0%) were obese. Adjusting for covariates, women whose mothers had a recalled pre-pregnancy BMI of 29 had a 6.1-fold increased risk of obesity at age 18 and a 3.4-fold risk of obesity in 2001, compared with women whose mothers had a pre-pregnancy BMI of 21. We found a U-shaped association between recalled GWG and offspring obesity. Compared with a maternal weight gain of 15–19 lb, GWG obesity risk at age 18 (odds ratio[OR] 1.54, 95% confidence interval[CI] 1.02–2.34) and in 2001 (OR 1.27, 95%CI 1.05–1.53). High weight gain (40+ lbs) was also associated with obesity risk at age 18 (OR 1.81, 95%CI 1.22–2.69) and in 2001 (OR 1.74, 95%CI 1.48–2.04). These associations were stronger among mothers who were overweight prior to pregnancy (p for interaction = 0.03), and they persisted with adjustment for birth weight. Conclusion A high recalled pre-pregnancy BMI and extremes of recalled GWG are associated with an increased risk of adolescent and adult obesity in offspring, particularly when the mother is overweight. Pre-pregnancy weight and GWG may be modifiable fetal origins of overweight and obesity in women. PMID:19528964

  3. Exploring the contribution of maternal antibiotics and breastfeeding to development of the infant microbiome and pediatric obesity.

    Science.gov (United States)

    Lemas, Dominick J; Yee, Shanique; Cacho, Nicole; Miller, Darci; Cardel, Michelle; Gurka, Matthew; Janicke, David; Shenkman, Elizabeth

    2016-12-01

    Pediatric obesity, a significant public health concern, has been associated with adult premature mortality and the development of type 2 diabetes and cardiovascular disease. Evidence has suggested that the gut microbiota is associated with pediatric obesity. Establishment of the infant gut microbiome is dependent on a dynamic maternal-infant microbiota exchange during early life. The objective of this review is to describe maternal factors such as feeding practices and antibiotic use that may influence the infant gut microbiome and risk for obesity. The complex components in human milk have many nutritional benefits to the infant; however, the microbiome in human milk may be an important factor to help regulate the infant's weight. We discuss maternal antibiotics and the effects on breast milk as critical exposures that alter the infant's gut microbiome and influence the risk of pediatric obesity. Copyright © 2016 Elsevier Ltd. All rights reserved.

  4. Maternal prepregnancy obesity is an independent risk factor for frequent wheezing in infants by age 14 months.

    Science.gov (United States)

    Guerra, Stefano; Sartini, Claudio; Mendez, Michelle; Morales, Eva; Guxens, Mònica; Basterrechea, Mikel; Arranz, Leonor; Sunyer, Jordi

    2013-01-01

    Maternal prepregnancy obesity has been linked to the offspring's risk for subsequent asthma. We determined whether maternal obesity is associated with increased risk of wheezing phenotypes early in life. We used data on 1107 mother-child pairs from two birth cohorts from the INMA-INfancia y Medio Ambiente project. Maternal height was measured and prepregnancy weight self-reported at enrolment (on average at 13.7 ± 2 weeks of gestation). Maternal prepregnancy body mass index was categorised as underweight, normal, overweight and obese according to WHO recommendations. Information on child's wheezing was obtained through questionnaires up to the age of 14 (± 1) months. Wheezing was classified as infrequent (<4 reported wheezing episodes) or frequent (≥ 4 episodes). Weight and length of infants were measured by trained study staff at 14.6 (± 1) months of age and weight-for-length z-scores computed. Although maternal obesity did not increase the risk of the child to have any or infrequent wheezing, children of obese mothers were more likely to have frequent wheezing than children of normal-weight mothers (11.8% vs. 3.8%; P = 0.002). In fully adjusted multinomial logistic regression models, including infants' weight-for-length z-scores and other covariates, maternal prepregnancy obesity was associated with increased risk of frequent [adjusted relative risk (RR) 4.18, 95% confidence interval (CI) 1.55, 11.3] but not infrequent (RR 1.05 [95% CI 0.55, 2.01]) wheezing in their children. Maternal prepregnancy obesity is independently associated with an increased risk of frequent wheezing in the infant by the age of 14 months. These findings add evidence on the potential effects of in utero exposures on asthma-related phenotypes. © 2012 Blackwell Publishing Ltd.

  5. Maternal smoking and risk of obesity in school children: Investigating early life theory from the GRECO study

    Directory of Open Access Journals (Sweden)

    Emmanuella Magriplis

    2017-12-01

    Full Text Available Based on the Early Life Theory, maternal smoking may be a factor affecting child weight status, adiposity level and blood pressure later in life. The purpose of this study was primarily to examine the risk of maternal smoking during pregnancy with overweight and obesity, central and total adiposity in school children. Secondarily, to assess the effect of maternal smoking, with children's blood pressure (BP.Data from the Greek Childhood Obesity cross sectional study (GRECO, conducted from October 2008 to May 2009, were used. A total of 2400 questionnaires gathered from children and their parents were analysed. Maternal and gestational data were gathered by a self-administered questionnaire. Women were categorized as non-smokers or smokers if they smoked ≥1 cigarettes/day during pregnancy. Children's body weight, height, waist circumference and BP were measured. Multiple logistic and linear regression analysis was conducted, adjusting for covariates. Four models were used in the process.The study found that children of maternal-smokers were more likely to be overweight or obese (OR: 1.6 to 1.82 and to have a larger waist circumference (OR: 1.73 to 1.85, compared to children of non-smokers in all models used. Total fat percentage was not significantly associated with maternal smoking when adjusted. Systolic and diastolic BP was not associated with maternal smoking. Results of this study strengthen the need for smoking cessation during pregnancy in order to possibly reduce the childhood obesity epidemic. Creating public health awareness of the potential risk of maternal-smoking on children's weight status later in life is warranted. Keywords: Maternal smoking, Central adiposity, Childhood obesity, Blood pressure, Public health

  6. Offspring predisposition to obesity due to maternal-diet-induced obesity in rats is preventable by dietary normalization before mating.

    Science.gov (United States)

    Castro, Heriberto; Pomar, Catalina Amadora; Palou, Andreu; Picó, Catalina; Sánchez, Juana

    2017-03-01

    We studied in rats whether the expected detrimental effects in offspring associated to maternal dietary obesity may be reverted by obesogenic diet removal 1 month before mating. Female rats were fed a cafeteria diet (CD) from days 10 to 100 and then a standard diet (SD) (postcafeteria rats). One month after CD removal, postcafeteria rats and a group of SD-fed female rats (controls) were mated with males. At weaning, offspring were fed SD and followed until 4 months old. CD was effective at inducing obesity in dams. Its removal led to a reduction in body weight, although, after 30 days, rats retained excess body weight and fat than controls. During lactation, postcafeteria dams showed greater body fat, and higher leptin and adiponectin levels in milk than controls. From 2 months of life, offspring of postcafeteria dams displayed lower body weight than controls, with no differences in the percentage of fat, homeostatic model assessment for insulin resistance, or circulating parameters. Removal of CD in obese rats before gestation, although without complete reversion of body weight excess, may prevent the expected detrimental effects in offspring associated to an excess fat accumulation in adulthood and the related metabolic disturbances. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  7. Genetic Evidence for Causal Relationships Between Maternal Obesity-Related Traits and Birth Weight.

    Science.gov (United States)

    Tyrrell, Jessica; Richmond, Rebecca C; Palmer, Tom M; Feenstra, Bjarke; Rangarajan, Janani; Metrustry, Sarah; Cavadino, Alana; Paternoster, Lavinia; Armstrong, Loren L; De Silva, N Maneka G; Wood, Andrew R; Horikoshi, Momoko; Geller, Frank; Myhre, Ronny; Bradfield, Jonathan P; Kreiner-Møller, Eskil; Huikari, Ville; Painter, Jodie N; Hottenga, Jouke-Jan; Allard, Catherine; Berry, Diane J; Bouchard, Luigi; Das, Shikta; Evans, David M; Hakonarson, Hakon; Hayes, M Geoffrey; Heikkinen, Jani; Hofman, Albert; Knight, Bridget; Lind, Penelope A; McCarthy, Mark I; McMahon, George; Medland, Sarah E; Melbye, Mads; Morris, Andrew P; Nodzenski, Michael; Reichetzeder, Christoph; Ring, Susan M; Sebert, Sylvain; Sengpiel, Verena; Sørensen, Thorkild I A; Willemsen, Gonneke; de Geus, Eco J C; Martin, Nicholas G; Spector, Tim D; Power, Christine; Järvelin, Marjo-Riitta; Bisgaard, Hans; Grant, Struan F A; Nohr, Ellen A; Jaddoe, Vincent W; Jacobsson, Bo; Murray, Jeffrey C; Hocher, Berthold; Hattersley, Andrew T; Scholtens, Denise M; Davey Smith, George; Hivert, Marie-France; Felix, Janine F; Hyppönen, Elina; Lowe, William L; Frayling, Timothy M; Lawlor, Debbie A; Freathy, Rachel M

    2016-03-15

    Neonates born to overweight or obese women are larger and at higher risk of birth complications. Many maternal obesity-related traits are observationally associated with birth weight, but the causal nature of these associations is uncertain. To test for genetic evidence of causal associations of maternal body mass index (BMI) and related traits with birth weight. Mendelian randomization to test whether maternal BMI and obesity-related traits are potentially causally related to offspring birth weight. Data from 30,487 women in 18 studies were analyzed. Participants were of European ancestry from population- or community-based studies in Europe, North America, or Australia and were part of the Early Growth Genetics Consortium. Live, term, singleton offspring born between 1929 and 2013 were included. Genetic scores for BMI, fasting glucose level, type 2 diabetes, systolic blood pressure (SBP), triglyceride level, high-density lipoprotein cholesterol (HDL-C) level, vitamin D status, and adiponectin level. Offspring birth weight from 18 studies. Among the 30,487 newborns the mean birth weight in the various cohorts ranged from 3325 g to 3679 g. The maternal genetic score for BMI was associated with a 2-g (95% CI, 0 to 3 g) higher offspring birth weight per maternal BMI-raising allele (P = .008). The maternal genetic scores for fasting glucose and SBP were also associated with birth weight with effect sizes of 8 g (95% CI, 6 to 10 g) per glucose-raising allele (P = 7 × 10(-14)) and -4 g (95% CI, -6 to -2 g) per SBP-raising allele (P = 1×10(-5)), respectively. A 1-SD ( ≈ 4 points) genetically higher maternal BMI was associated with a 55-g higher offspring birth weight (95% CI, 17 to 93 g). A 1-SD ( ≈ 7.2 mg/dL) genetically higher maternal fasting glucose concentration was associated with 114-g higher offspring birth weight (95% CI, 80 to 147 g). However, a 1-SD ( ≈ 10 mm Hg) genetically higher maternal SBP was associated with a 208-g

  8. Maternal obesity and malnourishment exacerbate perinatal oxidative stress resulting in diabetogenic programming in F1 offspring.

    Science.gov (United States)

    Saad, M I; Abdelkhalek, T M; Haiba, M M; Saleh, M M; Hanafi, M Y; Tawfik, S H; Kamel, M A

    2016-06-01

    The effect of in-utero environment on fetal health and survival is long-lasting, and this is known as the fetal origin hypothesis. The oxidative stress state during gestation could play a pivotal role in fetal programming and development of diseases such as diabetes. In this study, we investigated the effect of intra-uterine obesity and malnutrition on oxidative stress markers in pancreatic and peripheral tissues of F1 offspring both prenatally and postnatally. Furthermore, the effect of postnatal diet on oxidative stress profile was evaluated. The results indicated that intra-uterine obesity and malnourishment significantly increased oxidative stress in F1 offspring. Moreover, the programming effect of obesity was more pronounced and protracted than malnutrition. The obesity-induced programming of offspring tissues was independent of high-caloric environment that the offspring endured; however, high-caloric diet potentiated its effect. In addition, pancreas and liver were the most affected tissues by fetal reprogramming both prenatally and postnatally. In conclusion, maternal obesity and malnutrition-induced oxidative stress could predispose offspring to insulin resistance and diabetes.

  9. [Coexistence of maternal overweight or obesity and stunted children in south-western Benin households].

    Science.gov (United States)

    Dembélé, Bernard; Sossa Jérôme, Charles; Saizonou, Jacques; Makoutodé, Patrick Charles; Mongbo Adé, Virginie; Guedègbé Capo-Chichi, Justine; Dona Ouendo, Marius-Edgard

    To determine the prevalence and determinants of coexistence of maternal overweight or obesity and stunted children (DBM / SCOM) in south-western Benin households. This cross-sectional study was carried out in June 2015 on 357 mother-child pairs randomly selected by a two-stage sampling technique in the city of Comè and its surroundings. Data on socio-economic factors, family, health care, dietary quality were collected by questionnaires, observation and documentary review. Anthropometric measurements were performed in mothers and children. A logistic regression analysis model was used to search for determinants of the coexistence of the two aspects of malnutrition. 19.3% of mothers were overweight and 5.7% were obese. 46% of children were stunted. The prevalence of DBM / SCOM was 11.5%. The main factors associated with DBM/SCOM were the child's age, the mother's occupation, ethnicity, social status and educational level, and the size, economic level, transportation means and food insecurity of the household. A high frequency of the coexistence of maternal overweight or obesity and stunting was observed in Comè households. Interventions based on the identified determinants are needed to act simultaneously on the double burden of malnutrition in Comè.

  10. High fat diet and in utero exposure to maternal obesity disrupts circadian rhythm and leads to metabolic programming of liver in rat offspring

    Science.gov (United States)

    The risk of obesity in adulthood is subject to programming beginning at conception. In animal models, exposure to maternal obesity and high fat diets influences the risk of obesity in the offspring. Among other long-term changes, offspring from obese rats develop hyperinsulinemia, hepatic steatosi...

  11. Growth and obesity through the first 7 y of life in association with levels of maternal glycemia during pregnancy

    DEFF Research Database (Denmark)

    Zhu, Yeyi; Olsen, Sjurdur F; Mendola, Pauline

    2016-01-01

    Background: Given the long-term adverse sequelae of childhood obesity, identification of early life factors related to fetal growth and childhood obesity is warranted. Investigation on growth and obesity in early life in association with intrauterine exposure to maternal hyperglycemia, a common...... metabolic pregnancy complication, is of public health significance and clinical implications. Objective: We investigated the association of fasting plasma glucose (FPG) concentrations during pregnancy with offspring growth and risk of overweight/obesity through age 7 y, after adjustment for confounders......, including maternal prepregnancy obesity status. Design: FPG concentrations at 28 gestational weeks (IQR: 22-32 wk) were extracted from medical records for 661 pregnancies complicated by gestational diabetes mellitus in the Danish National Birth Cohort (1996-2002). Offspring's ponderal index was derived from...

  12. Association between maternal obesity and offspring Apgar score or cord pH: a systematic review and meta-analysis.

    Science.gov (United States)

    Zhu, Tingting; Tang, Jun; Zhao, Fengyan; Qu, Yi; Mu, Dezhi

    2015-12-22

    Previous results are inconsistent regarding the association between maternal obesity and Apgar score or cord pH in humans. The aim of this study was to investigate the association between maternal pre-pregnancy and pregnancy body mass index (BMI) and infant Apgar score or cord pH. We conducted a systematic review of studies published in English before 20 August 2015 using PubMed, EMBASE, and Cochrane Library. Eleven cohort studies with a total of 2,586,265 participants finally met our inclusion criteria. Pooled results revealed the following factors associated with Apgar score obese (OR 1.40; 95% CI, 1.27-1.54), and very obese (OR 1.71; 95% CI, 1.55-1.89). The pooled analysis also revealed that maternal overweight or obesity increased the risk for Apgar score maternal BMI and neonatal cord pH. Thus, this study suggests that maternal overweight and obesity affect baby's condition immediately after birth in general. More studies are needed to confirm these results and detect the influence of variables across studies.

  13. Maternal Western diet increases adiposity even in male offspring of obesity-resistant rat dams: early endocrine risk markers.

    Science.gov (United States)

    Frihauf, Jennifer B; Fekete, Éva M; Nagy, Tim R; Levin, Barry E; Zorrilla, Eric P

    2016-12-01

    Maternal overnutrition or associated complications putatively mediate the obesogenic effects of perinatal high-fat diet on developing offspring. Here, we tested the hypothesis that a Western diet developmental environment increases adiposity not only in male offspring from obesity-prone (DIO) mothers, but also in those from obesity-resistant (DR) dams, implicating a deleterious role for the Western diet per se. Selectively bred DIO and DR female rats were fed chow (17% kcal fat) or Western diet (32%) for 54 days before mating and, thereafter, through weaning. As intended, despite chow-like caloric intake, Western diet increased prepregnancy weight gain and circulating leptin levels in DIO, but not DR, dams. Yet, in both genotypes, maternal Western diet increased the weight and adiposity of preweanlings, as early as in DR offspring, and increased plasma leptin, insulin, and adiponectin of weanlings. Although body weight normalized with chow feeding during adolescence, young adult Western diet offspring subsequently showed decreased energy expenditure and, in DR offspring, decreased lipid utilization as a fuel substrate. By mid-adulthood, maternal Western diet DR offspring ate more chow, weighed more, and were fatter than controls. Thus, maternal Western diet covertly programmed increased adiposity in childhood and adulthood, disrupted relations of energy regulatory hormones with body fat, and decreased energy expenditure in offspring of lean, genetically obesity-resistant mothers. Maternal Western diet exposure alone, without maternal obesity or overnutrition, can promote offspring weight gain. Copyright © 2016 Frihauf et al.

  14. Chronic maternal inflammation or high-fat-feeding programs offspring obesity in a sex-dependent manner

    DEFF Research Database (Denmark)

    Dudele, A; Hougaard, K S; Kjølby, M

    2017-01-01

    Background/Objectives: The current world-wide obesity epidemic partially results from a vicious circle whereby maternal obesity during pregnancy predisposes the offspring for accelerated weight gain and development of metabolic syndrome. Here we investigate whether low-grade inflammation......, characteristic of the obese state, provides a causal role for this disastrous fetal programming in mice. Methods: We exposed pregnant and lactating C57BL/6JBom female mice to either high-fat diet (HFD), or continuous infusion of lipopolysaccharide (LPS), a potent trigger of innate immunity, and studied offspring...... inflammatory response to HFD at adulthood. Conclusions: This supports our hypothesis and highlights the programming potential of inflammation in obese pregnancies....

  15. Maternal obesity, gestational weight gain, and risk of asthma and atopic disease in offspring

    DEFF Research Database (Denmark)

    Harpsøe, Maria C; Basit, Saima; Bager, Peter

    2013-01-01

    -onset wheezing (adjusted OR, 1.87; 95% CI, 1.28-2.73). Maternal BMI and GWG were not associated with AE or hay fever. CONCLUSIONS: Maternal obesity during pregnancy was associated with increased risk of asthma and wheezing in offspring but not with AE and hay fever, suggesting that pathways may be nonallergic....... calculated by logistic regression with adjustment for potential confounders. RESULTS: During the first 7 years of life, 10.4% of children developed doctor-diagnosed asthma, 25.8% AE, and 4.6% hay fever. Maternal BMI and to a lesser extent GWG were associated with doctor-diagnosed asthma ever. In particular......, BMI ≥ 35 (adjusted OR, 1.87; 95% CI, 0.95-3.68) and GWG ≥ 25 kg (adjusted OR, 1.97; 95% CI, 1.38-2.83) were associated with current severe asthma at age 7 years. Maternal BMI was also associated with wheezing in offspring, with the strongest association observed between BMI ≥ 35 and late...

  16. Maternal obesity, gestational weight gain, and risk of asthma and atopic disease in offspring

    DEFF Research Database (Denmark)

    Harpsøe, Maria C; Basit, Saima; Bager, Peter

    2012-01-01

    -onset wheezing (adjusted OR, 1.87; 95% CI, 1.28-2.73). Maternal BMI and GWG were not associated with AE or hay fever. CONCLUSIONS: Maternal obesity during pregnancy was associated with increased risk of asthma and wheezing in offspring but not with AE and hay fever, suggesting that pathways may be nonallergic....... calculated by logistic regression with adjustment for potential confounders. RESULTS: During the first 7 years of life, 10.4% of children developed doctor-diagnosed asthma, 25.8% AE, and 4.6% hay fever. Maternal BMI and to a lesser extent GWG were associated with doctor-diagnosed asthma ever. In particular......, BMI ≥ 35 (adjusted OR, 1.87; 95% CI, 0.95-3.68) and GWG ≥ 25 kg (adjusted OR, 1.97; 95% CI, 1.38-2.83) were associated with current severe asthma at age 7 years. Maternal BMI was also associated with wheezing in offspring, with the strongest association observed between BMI ≥ 35 and late...

  17. Obesity in pregnancy: why we must be concerned about maternal nutrition again

    Directory of Open Access Journals (Sweden)

    Marcelo Farías Jofré

    2012-08-01

    Full Text Available The causes of the nutritional transition in our country can be accounted for by the reduction in the number of malnourished people, on the one hand, and the explosive increase in the proportion of overweight and obesity in all age groups, on the other. It comes as no surprise then that more than half of Chilean pregnant women are overweight and obese at their first prenatal visit and thus have an almost inevitable tendency to gain excess gestational weight. The purpose of this article is to review the adverse effects of maternal overweight on women and their offspring, and the potential benefits of nutritional interventions in this area. Multiple population and experimental studies have demonstrated a two to three times greater likelihood of developing maternal and perinatal complications in pregnant women with overweight and obesity compared to women with normal nutritional status. Since the gestational period is critical for the development of an individual, metabolic changes in nutrients, hormones and inflammatory mediators could explain many of the adverse outcomes described in the medium and long term in children of mothers with excess weight during pregnancy. No significant effects on birth weight have been seen after employing various interventional strategies. However, both dietary interventions and those involving controlled physical activity during pregnancy have been found to limit total gestational weight gain. In consequence, it appears to be feasible to further evaluate potentially clinically significant differences, both at the maternal-fetal metabolic injury level during pregnancy, as well as later on in life in mothers and their offspring.

  18. Maternal obesity alters brain derived neurotrophic factor (BDNF) signaling in the placenta in a sexually dimorphic manner.

    Science.gov (United States)

    Prince, Calais S; Maloyan, Alina; Myatt, Leslie

    2017-01-01

    Obesity is a major clinical problem in obstetrics being associated with adverse pregnancy outcomes and fetal programming. Brain derived neurotrophic factor (BDNF), a validated miR-210 target, is necessary for placental development, fetal growth, glucose metabolism, and energy homeostasis. Plasma BDNF levels are reduced in obese individuals; however, placental BDNF has yet to be studied in the context of maternal obesity. In this study, we investigated the effect of maternal obesity and sexual dimorphism on placental BDNF signaling. BDNF signaling was measured in placentas from lean (pre-pregnancy BMI 30) women at term without medical complications that delivered via cesarean section without labor. MiRNA-210, BDNF mRNA, proBDNF, and mature BDNF were measured by RT - PCR, ELISA, and Western blot. Downstream signaling via TRKB (BDNF receptor) was measured using Western blot. Maternal obesity was associated with increased miRNA-210 and decreased BDNF mRNA in placentas from female fetuses, and decreased proBDNF in placentas from male fetuses. We also identified decreased mature BDNF in placentas from male fetuses when compared to female fetuses. Mir-210 expression was negatively correlated with mature BDNF protein. TRKB phosphorylated at tyrosine 817, not tyrosine 515, was increased in placentas from obese women. Maternal obesity was associated with increased phosphorylation of MAPK p38 in placentas from male fetuses, but not phosphorylation of ERK p42/44. BDNF regulation is complex and highly regulated. Pre-pregnancy/early maternal obesity adversely affects BDNF/TRKB signaling in the placenta in a sexually dimorphic manner. These data collectively suggest that induction of placental TRKB signaling could ameliorate the placental OB phenotype, thus improving perinatal outcome. Copyright © 2016 Elsevier Ltd. All rights reserved.

  19. Maternal Blood Pressure Rise During Pregnancy and Offspring Obesity Risk at 4 to 7 Years Old: The Jiaxing Birth Cohort.

    Science.gov (United States)

    Zheng, Ju-Sheng; Liu, Huijuan; Ong, Ken K; Huang, Tao; Guan, Yuhong; Huang, Yuan; Yang, Bo; Wang, Fenglei; Li, Duo

    2017-11-01

    Maternal hypertensive disorders during pregnancy are suggested to affect obesity risk in offspring. However, little is known about the prospective association of rise in maternal blood pressure within normal range during pregnancy with this risk for obesity. To clarify the associations of diastolic and systolic blood pressure during pregnancy among normotensive women with the risk for obesity in offspring. Prospective cohort study. Southeast China. Up to 2013, a total of 88,406 mother-child pairs with anthropometric measurements of offspring age 4 to 7 years were included in the present analysis. Overweight/obesity risk in offspring. Among normotensive women, second- and third-trimester diastolic and systolic blood pressures were positively associated with risk for overweight/obesity in offspring: odds ratios per 10-mm Hg higher second- and third-trimester diastolic blood pressure were 1.05 [95% confidence interval (CI), 1.01 to 1.09] and 1.05 (95% CI, 1.02 to 1.10), respectively, and for systolic blood pressure were 1.08 (95% CI, 1.05 to 1.11) and 1.06 (95% CI, 1.03 to 1.09). Each 10-mm Hg greater rise in blood pressure between first and third trimesters was associated with a higher risk for offspring overweight/obesity: diastolic, 1.06 (95% CI, 1.01 to 1.10); systolic, 1.05 (95% CI, 1.02 to 1.07). Among all women (combining normotensive and hypertensive women), maternal hypertension in the second and third trimesters was associated with 49% and 14% higher risks for overweight/obesity in offspring, respectively. These results suggest that rise in maternal blood pressure during pregnancy and hypertension during pregnancy, independent of maternal body size before pregnancy, are risk factors for offspring childhood obesity.

  20. Maternal Obesity and Excessive Gestational Weight Gain Are Associated with Components of Child Cognition.

    Science.gov (United States)

    Pugh, Sarah J; Richardson, Gale A; Hutcheon, Jennifer A; Himes, Katherine P; Brooks, Maria M; Day, Nancy L; Bodnar, Lisa M

    2015-11-01

    Maternal overweight and obesity affect two-thirds of women of childbearing age and may increase the risk of impaired child cognition. Our objective was to test the hypothesis that high/low gestational weight gain (GWG) and high/low prepregnancy BMI were associated with offspring intelligence quotient (IQ) and executive function at age 10. Mother-infant dyads (n = 763) enrolled in a birth cohort study were followed from early pregnancy to 10 y postpartum. IQ was assessed by trained examiners with the use of the Stanford Binet Intelligence Scale-4th edition. Executive function was assessed by the number of perseverative errors on the Wisconsin Card Sorting Test and time to complete Part B on the Trail Making Test. Self-reported total GWG was converted to gestational-age-standardized GWG z score. Multivariable linear regression and negative binomial regression were used to estimate independent and joint effects of GWG and BMI on outcomes while adjusting for covariates. At enrollment, the majority of women in the Maternal Health Practices and Child Development cohort were unmarried and unemployed, and more than one-half reported their race as black. The mean ± SD GWG z score was -0.5 ± 1.8, and 27% of women had a pregravid BMI ≥ 25. The median (IQR) number of perseverative errors was 23 (17, 29), the mean ± SD time on Part B was 103 ± 42.6 s, and 44% of children had a low average IQ (≤ 89). Maternal obesity was associated with 3.2 lower IQ points (95% CI: -5.6, -0.8) and a slower time to complete the executive function scale Part B (adjusted β: 12.7 s; 95% CI: 2.8, 23 s) compared with offspring of normal-weight mothers. Offspring of mothers whose GWG was >+1 SD, compared with -1 to +1 SD, performed 15 s slower on the executive function task (95% CI: 1.8, 28 s). There was no association between GWG z score and offspring composite IQ score (adjusted β: -0.32; 95% CI: -0.72, 0.10). Prepregnancy BMI did not modify these associations. Although GWG may be important

  1. Maternal obesity increases the risk of metabolic disease and impacts renal health in offspring

    Science.gov (United States)

    Glastras, Sarah J.; Chen, Hui; Pollock, Carol A.; Saad, Sonia

    2018-01-01

    Obesity, together with insulin resistance, promotes multiple metabolic abnormalities and is strongly associated with an increased risk of chronic disease including type 2 diabetes (T2D), hypertension, cardiovascular disease, non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). The incidence of obesity continues to rise in astronomical proportions throughout the world and affects all the different stages of the lifespan. Importantly, the proportion of women of reproductive age who are overweight or obese is increasing at an alarming rate and has potential ramifications for offspring health and disease risk. Evidence suggests a strong link between the intrauterine environment and disease programming. The current review will describe the importance of the intrauterine environment in the development of metabolic disease, including kidney disease. It will detail the known mechanisms of fetal programming, including the role of epigenetic modulation. The evidence for the role of maternal obesity in the developmental programming of CKD is derived mostly from our rodent models which will be described. The clinical implication of such findings will also be discussed. PMID:29483369

  2. Pre-pregnancy obesity and maternal nutritional biomarker status during pregnancy: a factor analysis.

    Science.gov (United States)

    Tomedi, Laura E; Chang, Chung-Chou H; Newby, P K; Evans, Rhobert W; Luther, James F; Wisner, Katherine L; Bodnar, Lisa M

    2013-08-01

    Pre-pregnancy obesity has been associated with adverse birth outcomes. Poor essential fatty acid (EFA) and micronutrient status during pregnancy may contribute to these associations. We assessed the associations between pre-pregnancy BMI and nutritional patterns of maternal micronutrient and EFA status during mid-pregnancy. A cross-sectional analysis from a prospective cohort study. Women provided non-fasting blood samples at ≥ 20 weeks’ gestation that were assayed for red cell EFA; plasma folate, homocysteine and ascorbic acid; and serum retinol, 25-hydroxyvitamin D, a-tocopherol, soluble transferrin receptors and carotenoids. These nutritional biomarkers were employed in a factor analysis and three patterns were derived: EFA, Micronutrients and Carotenoids. The Antidepressant Use During Pregnancy Study, Pittsburgh, PA, USA. Pregnant women (n 129). After adjustment for parity, race/ethnicity and age, obese pregnant women were 3.0 (95% CI 1.1, 7.7) times more likely to be in the lowest tertile of the EFA pattern and 4.5 (95% CI 1.7, 12.3) times more likely to be in the lowest tertile of the Carotenoid pattern compared with their lean counterparts. We found no association between pre-pregnancy obesity and the Micronutrient pattern after confounder adjustment. Our results suggest that obese pregnant women have diminished EFA and carotenoid concentrations.

  3. Maternal thyroid function, prepregnancy obesity and gestational weight gain-The Generation R Study: A prospective cohort study.

    Science.gov (United States)

    Collares, Fernanda M; Korevaar, Tim I M; Hofman, Albert; Steegers, Eric A P; Peeters, Robin P; Jaddoe, Vincent W V; Gaillard, Romy

    2017-12-01

    Maternal prepregnancy obesity and excessive gestational weight gain are associated with pregnancy complications. Thyroid function is related to differences in body mass index (BMI) in adult populations. We examined the associations of maternal thyroid function in early pregnancy with maternal BMI and weight gain during pregnancy. In a population-based prospective cohort study among 5726 mothers, we measured maternal TSH and FT4 levels at 13.5 weeks of gestation (95% range: 9.7-17.6 weeks). Maternal weight was assessed before pregnancy and in each trimester. Higher maternal TSH levels were associated with higher prepregnancy BMI (difference: 0.18 kg/m 2 [95% CI: 0.01, 0.36] per SD increase in maternal TSH level) and higher total gestational weight gain (difference: 0.02 kg/wk [95% CI: 0.01, 0.03] per SD increase in maternal TSH level). Higher maternal FT4 levels were associated with lower prepregnancy BMI (difference: -0.44 kg/m 2 [95% CI: -0.63, -0.26] per SD increase in maternal FT4 level) and lower total gestational weight gain (difference: -0.01 kg/wk [95% CI: -0.02, -0.01] per SD increase in maternal FT4 level). The associations of maternal thyroid function with weight gain in early pregnancy were stronger than those with weight gain in mid and late-pregnancy. Maternal hypothyroidism was associated with higher prepregnancy BMI and early pregnancy weight gain, whereas opposite effects were observed for maternal hyperthyroidism (Pgain. Further studies are needed to explore maternal and foetal consequences. © 2017 John Wiley & Sons Ltd.

  4. Obesity and overweight: Impact on maternal and milk microbiome and their role for infant health and nutrition.

    Science.gov (United States)

    Garcia-Mantrana, Izaskun; Collado, Maria Carmen

    2016-08-01

    Obesity, particularly in infants, is becoming a significant public health problem that has reached "epidemic" status worldwide. Obese children have an increased risk of developing obesity-related diseases, such as metabolic syndromes and diabetes, as well as increased risk of mortality and adverse health outcomes later in life. Experimental data show that maternal obesity has negative effects on the offspring's health in the short and long term. Increasing evidence suggests a key role for microbiota in host metabolism and energy harvest, providing novel tools for obesity prevention and management. The maternal environment, including nutrition and microbes, influences the likelihood of developing childhood diseases, which may persist and be exacerbated in adulthood. Maternal obesity and weight gain also influence microbiota composition and activity during pregnancy and lactation. They affect microbial diversity in the gut and breast milk. Such microbial changes may be transferred to the offspring during delivery and also during lactation, affecting infant microbial colonisation and immune system maturation. Thus, an adequate nutritional and microbial environment during the peri-natal period may provide a window of opportunity to reduce the risk of obesity and overweight in our infants using targeted strategies aimed at modulating the microbiota during early life. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  5. Maternal pre-pregnancy obesity and child ADHD symptoms, executive function and cortical thickness

    Directory of Open Access Journals (Sweden)

    Claudia Buss

    2012-09-01

    Full Text Available Rationale/statement of the problem : Increasing evidence suggests exposure to adverse conditions in intrauterine life may increase the risk of developing attention-deficit/hyperactivity disorder (ADHD in childhood. High maternal pre-pregnancy body mass index (BMI has been shown to predict child ADHD symptoms; however, the neurocognitive processes underlying this relationship are not known. The aim of the present study was to test the hypothesis that this association is mediated by alterations in child executive function and cortical development. Methods : A population-based cohort of 174 children (mean age = 7.3±0.9 (SD years, 55% girls was evaluated for ADHD symptoms, using the Child Behavior Checklist, and for neurocognitive function, using the Go/No-go Task. This cohort had been followed prospectively from early gestation and birth through infancy and childhood with serial measures of maternal and child prenatal and postnatal factors. In 108 children, a structural MRI scan was acquired and the association between maternal obesity and child cortical thickness was investigated using Freesurfer software. Results : Maternal pre-pregnancy BMI was a significant predictor of child ADHD symptoms (F (1,158=4.80, p = 0.03 and of child performance on the Go/No-go Task (F (1,157=8.37, p=0.004 after controlling for key potential confounding variables. A test of the mediation model revealed that the association between higher maternal pre-pregnancy BMI and child ADHD symptoms was mediated by impaired executive function (inefficient/less attentive processing; Sobel test: t=2.39 (±0.002, SEM; p=0.02. Interestingly, after controlling for key potential confounding variables pre-pregnancy obesity was furthermore associated with region-specific thinner cortices, including regions previously reported to be thinner in children with ADHD, like the prefrontal cortex. Conclusion : To the best of our knowledge, this is the first study to report the

  6. Higher Maternal Protectiveness Is Associated with Higher Odds of Child Overweight and Obesity: A Longitudinal Australian Study

    Science.gov (United States)

    Hancock, Kirsten J.; Lawrence, David; Zubrick, Stephen R.

    2014-01-01

    In recent years there has been an increasing interest in overprotective parenting and the potential role it plays in child development. While some have argued that a trend towards increased parental fear and reduced opportunity for independent mobility may be linked to increasing rates of child overweight and obesity, there is limited empirical information available to support this claim. Using data from the Longitudinal Study of Australian Children, this study aimed to examine the longitudinal relationships between maternal protectiveness and child overweight and obesity. A cohort of 4–5 year old children was followed up at 6–7, 8–9 and 10–11 years of age (n  =  2596). Measures included a protective parenting scale administered when children were 6–7 and 8–9 years of age, child body mass index (BMI), family characteristics including household income, neighbourhood disadvantage, child's position amongst siblings, and maternal BMI, education, employment, mental health and age at first birth. International Obesity Taskforce age- and sex-specific BMI cut points were used to determine if children were in the normal, overweight or obese BMI range. There was no association between maternal protectiveness and the odds of children being overweight or obese at age 4–5, 6–7 or 8–9 years. However at age 10–11 years, a 1 standard deviation increase in maternal protectiveness was associated with a 13% increase in the odds of children being overweight or obese. The results provide evidence of a relationship between maternal protectiveness and child overweight and obesity, however further research is required to understand the mechanism(s) that links the two concepts. PMID:24955586

  7. Higher maternal protectiveness is associated with higher odds of child overweight and obesity: a longitudinal Australian study.

    Directory of Open Access Journals (Sweden)

    Kirsten J Hancock

    Full Text Available In recent years there has been an increasing interest in overprotective parenting and the potential role it plays in child development. While some have argued that a trend towards increased parental fear and reduced opportunity for independent mobility may be linked to increasing rates of child overweight and obesity, there is limited empirical information available to support this claim. Using data from the Longitudinal Study of Australian Children, this study aimed to examine the longitudinal relationships between maternal protectiveness and child overweight and obesity. A cohort of 4-5 year old children was followed up at 6-7, 8-9 and 10-11 years of age (n  =  2596. Measures included a protective parenting scale administered when children were 6-7 and 8-9 years of age, child body mass index (BMI, family characteristics including household income, neighbourhood disadvantage, child's position amongst siblings, and maternal BMI, education, employment, mental health and age at first birth. International Obesity Taskforce age- and sex-specific BMI cut points were used to determine if children were in the normal, overweight or obese BMI range. There was no association between maternal protectiveness and the odds of children being overweight or obese at age 4-5, 6-7 or 8-9 years. However at age 10-11 years, a 1 standard deviation increase in maternal protectiveness was associated with a 13% increase in the odds of children being overweight or obese. The results provide evidence of a relationship between maternal protectiveness and child overweight and obesity, however further research is required to understand the mechanism(s that links the two concepts.

  8. The impact of maternal obesity on iron status, placental transferrin receptor expression and hepcidin expression in human pregnancy.

    Science.gov (United States)

    Garcia-Valdes, L; Campoy, C; Hayes, H; Florido, J; Rusanova, I; Miranda, M T; McArdle, H J

    2015-04-01

    Obesity is associated with decreased iron status, possibly due to a rise in hepcidin, an inflammatory protein known to reduce iron absorption. In animals, we have shown that maternal iron deficiency is minimised in the foetus by increased expression of placental transferrin receptor (pTFR1), resulting in increased iron transfer at the expense of maternal iron stores. This study examines the effect of obesity during pregnancy on maternal and neonatal iron status in human cohorts and whether the placenta can compensate for decreased maternal iron stores by increasing pTFR1 expression. A total of 240 women were included in this study. One hundred and fifty-eight placentas (Normal: 90; Overweight: 37; Obese: 31) were collected at delivery. Maternal iron status was measured by determining serum transferrin receptor (sTFR) and ferritin levels at 24 and 34 weeks and at delivery. Hepcidin in maternal and cord blood was measured by ELISA and pTFR1 in placentas by western blotting and real-time RT-PCR. Low iron stores were more common in obese women. Hepcidin levels (ng ml(-1)) at the end of the pregnancy were higher in obese than normal women (26.03±12.95 vs 18.00±10.77, PMaternal hepcidin levels were correlated with maternal iron status (sTFR r=0.2 P=0.025), but not with neonatal values. mRNA and protein levels of pTFR1 were both inversely related to maternal iron status. For mRNA and all women, sTFR r=0.2 P=0.044. Ferritin mRNA levels correlated only in overweight women r=-0.5 P=0.039 with hepcidin (r=0.1 P=0.349), irrespective of maternal body mass index (BMI). The data support the hypothesis that obese pregnant women have a greater risk of iron deficiency and that hepcidin may be a regulatory factor. Further, we show that the placenta responds to decreased maternal iron status by increasing pTFR1 expression.

  9. Maternal Weight Gain in Pregnancy and Risk of Obesity among Offspring: A Systematic Review

    Directory of Open Access Journals (Sweden)

    Erica Y. Lau

    2014-01-01

    Full Text Available Objectives. To systematically review the evidence from prospective and retrospective cohort studies on the association between gestational weight gain (GWG and offspring’s body weight. Methods. Electronic databases PubMed, Web of Science, CINAHL, and Academic Search Premiere were searched from inception through March 18, 2013. Included studies (n=23 were English articles that examined the independent associations of GWG with body mass index (BMI and/or overweight status in the offspring aged 2 to 18.9 years. Two authors independently extracted the data and assessed methodological quality of the included studies. Results. Evidence from cohort studies supports that total GWG and exceeding the Institute of Medicine maternal weight gain recommendation were associated with higher BMI z-score and elevated risk of overweight or obesity in offspring. The evidence of high rate of GWG during early- and mid-pregnancy is suggestive. Additionally, the evidence on inadequate GWG and net GWG in relation to body weight outcomes in offspring is insufficient to draw conclusions. Conclusions. These findings suggest that GWG is a potential risk factor for childhood obesity. However, findings should be interpreted with caution due to measurement issues of GWG and potential confounding effects of shared familial characteristics (i.e., genetics and maternal and child’s lifestyle factors.

  10. Early Parturition: Is Young Maternal Age at First Birth Associated with Obesity?

    Science.gov (United States)

    Patchen, Loral; Leoutsakos, Jeannie-Marie; Astone, Nan M

    2017-10-01

    Examine the association of age at first birth with body mass index (BMI), and explore the role of young maternal age and subsequent obesity. This study analyzed data from the Panel Study of Income Dynamics, a nationally representative longitudinal study of US families. Analyses were conducted using a mixed effects longitudinal linear regression with a random intercept to examine the effect of aging, age at first birth, and minority status using nested data. Study criteria yielded a final sample of 146 women with 707 observations. BMI. Age at first birth exhibited a significant association with BMI. The association of age at first birth with BMI was greatest for women age 21 and younger. Overall, women who experienced their first birth at age 21 or younger had a BMI 5 units greater than women who delayed childbearing until at least age 30 (point estimate, 5.02; P = .02; 95% confidence interval, 0.65-9.40). Young maternal age at first birth might be associated with increased BMI. Minority women also experience their first birth at younger ages compared with white women, suggesting possible linkages between the timing of reproductive events and obesity disparities. Copyright © 2016 North American Society for Pediatric and Adolescent Gynecology. Published by Elsevier Inc. All rights reserved.

  11. Stronger influence of maternal than paternal obesity on infant and early childhood body mass index: the Fels Longitudinal Study.

    Science.gov (United States)

    Linabery, A M; Nahhas, R W; Johnson, W; Choh, A C; Towne, B; Odegaard, A O; Czerwinski, S A; Demerath, E W

    2013-06-01

    Excessive early childhood adiposity is a prevalent and increasing concern in many parts of the world. Parental obesity is one of the several factors previously associated with infant and early childhood weight, length and adiposity. Parental obesity represents a surrogate marker of the complex interplay among genetic, epigenetic and shared environmental factors, and is potentially modifiable. The relative contributions of maternal and paternal body mass index (BMI) to infant and early childhood growth, as well as the timing of such effects, have not been firmly established. Utilizing serial infant measurements and growth curve modelling, this is the largest study to fully characterize and formally compare associations between maternal and paternal BMI and offspring growth across the entire infancy and early childhood period. Maternal obesity is a stronger determinant of offspring BMI than paternal obesity at birth and from 2 to 3 years of age, suggesting that prevention efforts focused particularly on maternal lifestyle and BMI may be important in reducing excess infant BMI. The observation that maternal BMI effects are not constant, but rather present at birth, wane and re-emerge during late infancy, suggests that there is a window of opportunity in early infancy when targeted interventions on children of obese mothers may be most effective. Parental obesity influences infant body size. To fully characterize their relative effects on infant adiposity, associations between maternal and paternal body mass index (BMI) category (normal: ≤25 kg m(-2) , overweight: 25 - obese: ≥30 kg m(-2) ) and infant BMI were compared in Fels Longitudinal Study participants. A median of 9 serial weight and length measures from birth to 3.5 years were obtained from 912 European American children born in 1928-2008. Using multivariable mixed effects regression, contributions of maternal vs. paternal BMI status to infant BMI growth curves were evaluated. Cubic spline models

  12. The impact of maternal obesity on intra-partum events during pregnancy: a retrospective study at Puducherry

    OpenAIRE

    Ulagammal A.

    2016-01-01

    Background: Women with excessive weight at the time of conception are prone to a wide spectrum of adverse pregnancy outcomes including major postpartum haemorrhage, increased caesarean section rates, increased operational vaginal deliveries and higher risks of maternal hypertension, gestational diabetes and fetal death. Methods: This retrospective case-control study was conducted at a tertiary care hospital in Ariyur, Puducherry by comparing 100 obese women (cases) with 100 Non-obese, norm...

  13. Effect of maternal obesity on birthweight and neonatal fat mass: A prospective clinical trial.

    Directory of Open Access Journals (Sweden)

    Delphine Mitanchez

    Full Text Available To discriminate the effect of maternal obesity and gestational diabetes on birth weight and adipose tissue of the newborn.Normal BMI women (group N, n = 243; 18.5≤ BMI<25 kg/m2 and obese women (group Ob, n = 253; BMI≥30 kg/m2 were recruited in a prospective study between 15 and 18 weeks of gestation. All women were submitted to a 75g oral glucose tolerance test in the second and third trimester. First trimester fasting blood glucose was also obtained from Ob women. All women with one measurement above normal values were considered positive for gestational diabetes and first treated by dietary intervention. When dietary measures were not efficient, they were treated by insulin. Neonatal anthropometrics, sum of skinfolds and cord serum hormones were measured.222 N and 226 Ob mothers and their newborns were included in the analysis. Diabetes was diagnosed in 20% and 45.2% of N and Ob women, respectively. Birth weight was not statistically different between groups (boys: 3456g±433 and 3392g±463; girls: 3316g±402 and 3391g±408 for N and Ob, respectively. Multivariate analysis demonstrated that skinfold thickness and serum leptin concentrations were significantly increased in girls born to women with obesity (18.0mm±0.6 versus 19.7mm±0.5, p = 0.004 and 11.3ng/mL±1.0 versus 15.3ng/mL±1.0, p = 0.02, but not in boys (18.4mm±0.6 versus 18.5mm±0.5, p = 0.9 and 9.3ng/mL±1.0 versus 9.0ng/mL±1.0, p = 0.9. Based on data from 136 N and 124 Ob women, maternal insulin resistance at 37 weeks was also positively related to skinfold in girls, only, with a 1-point increase in HOMA-IR corresponding to a 0.33mm±0.08 increase in skinfold (p<0.0001.Regardless of gestational diabetes, maternal obesity and insulin resistance were associated with increased adiposity in girls only. Persistence of this sexual dimorphism remains to be explored during infancy.

  14. Childhood overweight and obesity among Kenyan pre-school children: association with maternal and early child nutritional factors.

    Science.gov (United States)

    Gewa, Constance A

    2010-04-01

    To report on the prevalence of overweight and obesity among pre-school children in Kenya and examine the associations between childhood overweight and selected maternal and child-related factors. Demographic Health Survey data, multistage stratified cluster sampling methodology. Rural and urban areas of Kenya. A total of 1495 children between the ages of 3 and 5 years in Kenya. Over 30 % of the children were stunted, approximately 16 % were underweight, 4 % were wasted, approximately 18 % were overweight and 4 % were obese; 8 % were both overweight/obese and stunted. Maternal overweight and obesity, higher levels of maternal education, being a large or very large child at birth, and being stunted were each associated with higher odds of overweight and obesity among Kenyan children. Older children and large household size were each associated with lower odds of overweight and obesity among Kenyan children. The analysis demonstrates the presence of under- and overnutrition among Kenyan pre-school children and the importance of focusing on expanding efforts to prevent and treat malnutrition within this population. It also identifies some of the modifiable factors that can be targeted in these efforts.

  15. The Childhood Obesity Epidemic As a Result of Non-Genetic Evolution: the Maternal Resources Hypothesis

    Science.gov (United States)

    Archer, Edward

    2014-01-01

    Over the past century, socio-environmental evolution (e.g., reduced pathogenic load, decreased physical activity [PA], improved nutrition) led to cumulative increments in maternal energy resources (i.e., body mass, adiposity) and decrements in energy expenditure and metabolic control. These decrements reduced the competition between maternal and fetal energy demands and increased the availability of energy substrates to the intrauterine milieu. This perturbation of mother-conceptus energy partitioning stimulated fetal pancreatic beta-cell and adipocyte hyperplasia, thereby inducing an enduring competitive advantage of adipocytes over other tissues in the acquisition and sequestering of nutrient-energy via intensified insulin secretion and hyperplastic adiposity. At menarche, the competitive dominance of adipocytes was further amplified via hormone-induced adipocyte hyperplasia and weight-induced decrements in PA. These metabolic and behavioral effects were propagated progressively when obese, inactive, metabolically compromised women produced progressively larger, more inactive and metabolically compromised children. Consequently, the evolution of human energy metabolism was significantly altered. This phenotypic evolution was exacerbated by increments in the use of Caesarian sections that allowed both the larger fetuses and the metabolically compromised mothers who produced them to survive and reproduce. Thus, natural selection was iatrogenically rendered artificial selection, and the frequency of obese, inactive, metabolically compromised phenotypes increased in the global population. By the late 20th century, a metabolic tipping point was reached in which the post-prandial insulin response was so intense, the relative number of adipocytes so magnified, and inactivity so pervasive that the competitive dominance of adipocytes in the sequestering of nutrient-energy was inevitable, and obesity was unavoidable. PMID:25440888

  16. Adiposidade em adolescentes e obesidade materna Relationship between maternal obesity and adiposity in adolescents

    Directory of Open Access Journals (Sweden)

    Maria Fernanda Petroli Frutoso

    2011-02-01

    Full Text Available OBJETIVO: Descrever a relação entre adiposidade na adolescência e obesidade materna. MÉTODOS: Foi realizado estudo transversal com 660 indivíduos de 8 a 18 anos, de ambos os sexos, matriculados em uma escola pública e outra privada do município de São Paulo. A coleta de dados foi realizada por meio de entrevista, medidas antropométricas e inquérito alimentar. A adiposidade na adolescência foi mensurada a partir do índice de massa corporal e, por meio de análise de regressão, verificou-se sua relação com a obesidade materna, ajustada por sexo, idade, estágio de maturação sexual, valor energético total da dieta, atividade física, sedentarismo, peso ao nascer e escolaridade materna. RESULTADOS: Dos adolescentes estudados, 64,7% eram do sexo feminino. A média (desvio-padrão de idade foi de 12,4 (1,80, variando de 8 a 17 anos. Verificou-se maior prevalência de excesso de peso e obesidade entre os indivíduos do sexo masculino, não sendo observada associação significativa entre estado nutricional e sexo. Após ajuste pelas covariáveis, detectou-se que filhos de mães obesas têm risco quatro vezes maior de ser obesos, quando comparados aos adolescentes filhos de mães não obesas. CONCLUSÃO: Conclui-se que a obesidade materna representa fator de risco importante para o desenvolvimento da obesidade na adolescência.OBJECTIVE: This study aimed to describe the relationship between teenager's adiposity and maternal obesity. METHODS: A cross-sectional study was done with 660 teenagers aged 8 to 18 years, of both genders, students of private and public schools of São Paulo. The data were collected by interviews, anthropometric measurements and food intake records. Teenagers' adiposity was determined by body mass index and regression analyses was used to verify its relationship with maternal obesity adjusted for gender, age, stage of sexual development, energy intake, physical activity, sedentary lifestyle, birth weight and

  17. Maternal obesity caused by overnutrition exposure leads to reversal learning deficits and striatal disturbance in rats.

    Directory of Open Access Journals (Sweden)

    Ting Wu

    Full Text Available Maternal obesity caused by overnutrition during pregnancy increases susceptibility to metabolic risks in adulthood, such as obesity, insulin resistance, and type 2 diabetes; however, whether and how it affects the cognitive system associated with the brain remains elusive. Here, we report that pregnant obesity induced by exposure to excessive high fatty or highly palatable food specifically impaired reversal learning, a kind of adaptive behavior, while leaving serum metabolic metrics intact in the offspring of rats, suggesting a much earlier functional and structural defects possibly occurred in the central nervous system than in the metabolic system in the offspring born in unfavorable intrauterine nutritional environment. Mechanically, we found that above mentioned cognitive inflexibility might be associated with significant striatal disturbance including impaired dopamine homeostasis and disrupted leptin signaling in the adult offspring. These collective data add a novel perspective of understanding the adverse postnatal sequelae in central nervous system induced by developmental programming and the related molecular mechanism through which priming of risk for developmental disorders may occur during early life.

  18. A Qualitative Study of the Maternity Care Experiences of Women with Obesity: "More than Just a Number on the Scale".

    Science.gov (United States)

    DeJoy, Sharon Bernecki; Bittner, Krystle; Mandel, Deborah

    2016-01-01

    The prevalence of obesity among pregnant women in the United States is high. Obesity can have long-term health consequences for both women and their offspring, so high-quality perinatal care for women with obesity is essential. However, stigmatizing encounters with health care professionals can decrease quality and promote avoidance of care. The purpose of this study was to explore the experiences of women with obesity in the maternity care system in the United States. In-depth telephone interviews were conducted with 16 women with a body mass index of 30 or greater. The authors used an inductive analytical process to translate women's experiences into themes. Women with obesity reported diverse maternity care experiences, with some reporting appropriate and satisfactory care, while most reported at least one negative encounter over the course of perinatal care. Three major themes emerged from the analysis: personalized care, depersonalized care, and setting the tone. Interactions with providers during pregnancy had psychological and emotional effects on women with obesity and influenced the content and perceived quality of their care. Further research is required to explore this phenomenon and its implications for care of women during pregnancy and birth outcomes. In the meantime, providers may wish to consider greater sensitivity to the needs of women with obesity during the perinatal period. © 2016 by the American College of Nurse-Midwives.

  19. Maternal high-fat diet associated with altered gene expression, DNA methylation, and obesity risk in mouse offspring.

    Science.gov (United States)

    Keleher, Madeline Rose; Zaidi, Rabab; Shah, Shyam; Oakley, M Elsa; Pavlatos, Cassondra; El Idrissi, Samir; Xing, Xiaoyun; Li, Daofeng; Wang, Ting; Cheverud, James M

    2018-01-01

    We investigated maternal obesity in inbred SM/J mice by assigning females to a high-fat diet or a low-fat diet at weaning, mating them to low-fat-fed males, cross-fostering the offspring to low-fat-fed SM/J nurses at birth, and weaning the offspring onto a high-fat or low-fat diet. A maternal high-fat diet exacerbated obesity in the high-fat-fed daughters, causing them to weigh more, have more fat, and have higher serum levels of leptin as adults, accompanied by dozens of gene expression changes and thousands of DNA methylation changes in their livers and hearts. Maternal diet particularly affected genes involved in RNA processing, immune response, and mitochondria. Between one-quarter and one-third of differentially expressed genes contained a differentially methylated region associated with maternal diet. An offspring high-fat diet reduced overall variation in DNA methylation, increased body weight and organ weights, increased long bone lengths and weights, decreased insulin sensitivity, and changed the expression of 3,908 genes in the liver. Although the offspring were more affected by their own diet, their maternal diet had epigenetic effects lasting through adulthood, and in the daughters these effects were accompanied by phenotypic changes relevant to obesity and diabetes.

  20. Maternal high-fat diet associated with altered gene expression, DNA methylation, and obesity risk in mouse offspring

    Science.gov (United States)

    Zaidi, Rabab; Shah, Shyam; Oakley, M. Elsa; Pavlatos, Cassondra; El Idrissi, Samir; Xing, Xiaoyun; Li, Daofeng; Wang, Ting; Cheverud, James M.

    2018-01-01

    We investigated maternal obesity in inbred SM/J mice by assigning females to a high-fat diet or a low-fat diet at weaning, mating them to low-fat-fed males, cross-fostering the offspring to low-fat-fed SM/J nurses at birth, and weaning the offspring onto a high-fat or low-fat diet. A maternal high-fat diet exacerbated obesity in the high-fat-fed daughters, causing them to weigh more, have more fat, and have higher serum levels of leptin as adults, accompanied by dozens of gene expression changes and thousands of DNA methylation changes in their livers and hearts. Maternal diet particularly affected genes involved in RNA processing, immune response, and mitochondria. Between one-quarter and one-third of differentially expressed genes contained a differentially methylated region associated with maternal diet. An offspring high-fat diet reduced overall variation in DNA methylation, increased body weight and organ weights, increased long bone lengths and weights, decreased insulin sensitivity, and changed the expression of 3,908 genes in the liver. Although the offspring were more affected by their own diet, their maternal diet had epigenetic effects lasting through adulthood, and in the daughters these effects were accompanied by phenotypic changes relevant to obesity and diabetes. PMID:29447215

  1. Prenatal exposure to maternal very severe obesity is associated with impaired neurodevelopment and executive functioning in children.

    Science.gov (United States)

    Mina, Theresia H; Lahti, Marius; Drake, Amanda J; Denison, Fiona C; Räikkönen, Katri; Norman, Jane E; Reynolds, Rebecca M

    2017-07-01

    BackgroundPrenatal maternal obesity has been associated with an increased risk of neurocognitive problems in childhood, but there are fewer studies on executive functioning.MethodsTests and questionnaires to assess neurodevelopment, executive functioning, and the ability to delay gratification were conducted in 113 children (mean (SD)=4.24 (0.63) years of age) born to mothers with very severe obesity (SO, body mass index (BMI)⩾40 kg/m 2 , n=51) or to lean mothers (BMI⩽25 kg/m 2 , n=62).ResultsPrenatal maternal SO predicted poorer neurodevelopment (unstandardized regression coefficient (B)=-0.42, 95% confidence interval (CI) (-0.82; -0.02)), worse problem-solving (odd ratio (OR)=0.60, 95% CI (1.13; 0.07)), and fine motor skills (OR=4.91, 95% CI (1.27; 19.04)), poorer executive functioning in areas of attention, inhibitory control, and working memory (standardized B=3.75, 95% CI (1.01; 13.93)) but not in self-gratification delay. The effects were independent of maternal concurrent psychological well-being and child's BMI, but not independent of maternal education.ConclusionFuture studies should investigate whether perinatal management of maternal obesity could prevent adverse outcomes in child neurodevelopment.

  2. Maternal obesity and physical activity and exercise levels as pregnancy advances: an observational study.

    Science.gov (United States)

    Daly, N; Mitchell, C; Farren, M; Kennelly, M M; Hussey, J; Turner, M J

    2016-05-01

    Increases in clinical complications associated with maternal obesity have generated interest in increasing physical activity (PA) and exercise levels as an intervention to improve pregnancy outcomes. The objective of this study was to examine the relationship between BMI categorisation and PA and exercise levels as pregnancy advances. This was an observational study in a large university maternity hospital. Women were recruited at their convenience before they left hospital after delivering a baby weighing 500 g or more. They completed a detailed customised physical activity and exercise questionnaire. BMI categorisation was based on the measurement of weight and height in early pregnancy. Of the 155 women recruited, 42.5 % (n = 66) were primigravidas and 10.3 % (n = 16) were smokers. Mean Body Mass Index (BMI) was 24.6 kg/m(2) and 14.2 % (n = 22) were obese, based on a BMI >29.9 kg/m(2). Overall, women decreased their exercise from an average 194 min (range 0-650 min) per week pre-pregnancy to 98 min antenatally (range 0-420 min) (p Obese women exercised least pre-pregnancy and antenatally at 187.5 and 75 min per week, respectively, compared with 193.2 and 95.5 min per week in the normal BMI group and 239.3 and 106.7 min per week in the overweight group. The mean gestation at which all women reduced their activity levels was 29 weeks. We found that women decreased their PA  and exercise levels significantly in the third trimester and, thus, in the absence of a medical contra-indication there is considerable scope for an exercise intervention to improve activity  and exercise levels as pregnancy advances. However, an increase in PA levels in obese women needs further studies to determine whether it will improve the clinical outcomes for the woman and her offspring.

  3. Impact of Restricted Maternal Weight Gain on Fetal Growth and Perinatal Morbidity in Obese Women With Type 2 Diabetes

    DEFF Research Database (Denmark)

    Asbjörnsdóttir, Björg; Rasmussen, S.S.; Kelstrup, Louise

    2013-01-01

    OBJECTIVESince January 2008, obese women with type 2 diabetes were advised to gain 0-5 kg during pregnancy. The aim with this study was to evaluate fetal growth and perinatal morbidity in relation to gestational weight gain in these women.RESEARCH DESIGN AND METHODSA retrospective cohort comprised...... the records of 58 singleton pregnancies in obese women (BMI ≥30 kg/m(2)) with type 2 diabetes giving birth between 2008 and 2011. Birth weight was evaluated by SD z score to adjust for gestational age and sex.RESULTSSeventeen women (29%) gained ≤5 kg, and the remaining 41 gained >5 kg. The median (range...... with pregnancies with maternal weight gain >5 kg.CONCLUSIONIn this pilot study in obese women with type 2 diabetes, maternal gestational weight gain ≤5 kg was associated with a more proportionate birth weight and less perinatal morbidity....

  4. Differential hypothalamic leptin sensitivity in obese rat offspring exposed to maternal and postnatal intake of chocolate and soft drink

    DEFF Research Database (Denmark)

    Gerstenberg, Marina Kjærgaard; Nilsson, C; Secher, A

    2017-01-01

    Background/objective: Intake of high-energy foods and maternal nutrient overload increases the risk of metabolic diseases in the progeny such as obesity and diabetes. We hypothesized that maternal and postnatal intake of chocolate and soft drink will affect leptin sensitivity and hypothalamic...... for the metabolic phenotype in the offspring if they continued on the S diet in postnatal life. These offspring displayed obesity despite lowered energy intake associated with alterations in hypothalamic leptin signalling....... assigned to either S or C diet, giving four groups until the end of the experiment at 26 weeks of age. Results: As expected, adult offspring fed the S diet post weaning became obese (body weight: P

  5. Maternal obesity and tobacco use modify the impact of genetic variants on the occurrence of conotruncal heart defects.

    Science.gov (United States)

    Tang, Xinyu; Nick, Todd G; Cleves, Mario A; Erickson, Stephen W; Li, Ming; Li, Jingyun; MacLeod, Stewart L; Hobbs, Charlotte A

    2014-01-01

    Conotruncal heart defects (CTDs) are among the most severe birth defects worldwide. Studies of CTDs indicate both lifestyle behaviors and genetic variation contribute to the risk of CTDs. Based on a hybrid design using data from 616 case-parental and 1645 control-parental triads recruited for the National Birth Defects Prevention Study between 1997 and 2008, we investigated whether the occurrence of CTDs is associated with interactions between 921 maternal and/or fetal single nucleotide polymorphisms (SNPs) and maternal obesity and tobacco use. The maternal genotypes of the variants in the glutamate-cysteine ligase, catalytic subunit (GCLC) gene and the fetal genotypes of the variants in the glutathione S-transferase alpha 3 (GSTA3) gene were associated with an elevated risk of CTDs among obese mothers. The risk of delivering infants with CTDs among obese mothers carrying AC genotype for a variant in the GCLC gene (rs6458939) was 2.00 times the risk among those carrying CC genotype (95% confidence interval: 1.41, 2.38). The maternal genotypes of several variants in the glutathione-S-transferase (GST) family of genes and the fetal genotypes of the variants in the GCLC gene interacted with tobacco exposures to increase the risk of CTDs. Our study suggests that the genetic basis underlying susceptibility of the developing heart to the adverse effects of maternal obesity and tobacco use involve both maternal and embryonic genetic variants. These results may provide insights into the underlying pathophysiology of CTDs, and ultimately lead to novel prevention strategies.

  6. Effects of taurine supplementation on hepatic markers of inflammation and lipid metabolism in mothers and offspring in the setting of maternal obesity.

    Science.gov (United States)

    Li, Minglan; Reynolds, Clare M; Sloboda, Deborah M; Gray, Clint; Vickers, Mark H

    2013-01-01

    Maternal obesity is associated with obesity and metabolic disorders in offspring. However, intervention strategies to reverse or ameliorate the effects of maternal obesity on offspring health are limited. Following maternal undernutrition, taurine supplementation can improve outcomes in offspring, possibly via effects on glucose homeostasis and insulin secretion. The effects of taurine in mediating inflammatory processes as a protective mechanism has not been investigated. Further, the efficacy of taurine supplementation in the setting of maternal obesity is not known. Using a model of maternal obesity, we examined the effects of maternal taurine supplementation on outcomes related to inflammation and lipid metabolism in mothers and neonates. Time-mated Wistar rats were randomised to either: 1) control : control diet during pregnancy and lactation (CON); 2) CON supplemented with 1.5% taurine in drinking water (CT); 3) maternal obesogenic diet (high fat, high fructose) during pregnancy and lactation (MO); or 4) MO supplemented with taurine (MOT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analysed. A MO diet resulted in maternal hyperinsulinemia and hyperleptinemia and increased plasma glucose, glutamate and TNF-α concentrations. Taurine normalised maternal plasma TNF-α and glutamate concentrations in MOT animals. Both MO and MOT mothers displayed evidence of fatty liver accompanied by alterations in key markers of hepatic lipid metabolism. MO neonates displayed a pro-inflammatory hepatic profile which was partially rescued in MOT offspring. Conversely, a pro-inflammatory phenotype was observed in MOT mothers suggesting a possible maternal trade-off to protect the neonate. Despite protective effects of taurine in MOT offspring, neonatal mortality was increased in CT neonates, indicating possible adverse effects of taurine in the setting of normal pregnancy. These data suggest that maternal taurine supplementation may

  7. Maternal obesity and offspring body composition by indirect methods: a systematic review and meta-analysis

    Directory of Open Access Journals (Sweden)

    Helen Castillo-Laura

    2015-10-01

    Full Text Available Abstract This study reviewed the evidence that assessed the association between maternal pre-pregnancy body mass index (BMI and/or gestational weight gain and offspring body composition in childhood. A systematic review was conducted. Cohort studies, case-control studies and randomized controlled trials measuring offspring body composition by indirect methods were included. Meta-analyses of the effect of pre-pregnancy BMI on offspring fat-free mass, body fat percent, and fat mass were conducted through random-effects models. 20 studies were included, most of which reported a positive association of pre-pregnancy BMI with offspring body fat. Standardized mean differences in body fat percent, fat mass and fat-free mass between infants of women with normal pre-pregnancy BMI and those of overweight/obese women were 0.31 percent points (95%CI: 0.19; 0.42, 0.38kg (95%CI: 0.26; 0.50, and 0.18kg (95%CI: -0.07; 0.42, respectively. Evidence so far suggests that pre-pregnancy maternal overweight is associated with higher offspring adiposity.

  8. Maternal obesity during gestation impairs fatty acid oxidation and mitochondrial SIRT3 expression in rat offspring at weaning.

    Directory of Open Access Journals (Sweden)

    Sarah J Borengasser

    Full Text Available In utero exposure to maternal obesity increases the offspring's risk of obesity in later life. We have also previously reported that offspring of obese rat dams develop hepatic steatosis, mild hyperinsulinemia, and a lipogenic gene signature in the liver at postnatal day (PND21. In the current study, we examined systemic and hepatic adaptations in male Sprague-Dawley offspring from lean and obese dams at PND21. Indirect calorimetry revealed decreases in energy expenditure (p<0.001 and increases in RER values (p<0.001, which were further exacerbated by high fat diet (45% kcals from fat consumption indicating an impaired ability to utilize fatty acids in offspring of obese dams as analyzed by PRCF. Mitochondrial function is known to be associated with fatty acid oxidation (FAO in the liver. Several markers of hepatic mitochondrial function were reduced in offspring of obese dams. These included SIRT3 mRNA (p = 0.012 and mitochondrial protein content (p = 0.002, electron transport chain complexes (II, III, and ATPase, and fasting PGC-1α mRNA expression (p<0.001. Moreover, hepatic LCAD, a SIRT3 target, was not only reduced 2-fold (p<0.001 but was also hyperacetylated in offspring of obese dams (p<0.005 suggesting decreased hepatic FAO. In conclusion, exposure to maternal obesity contributes to early perturbations in whole body and liver energy metabolism. Mitochondrial dysfunction may be an underlying event that reduces hepatic fatty acid oxidation and precedes the development of detrimental obesity associated co-morbidities such as insulin resistance and NAFLD.

  9. Differential effects of exposure to maternal obesity or maternal weight loss during the periconceptional period in the sheep on insulin signalling molecules in skeletal muscle of the offspring at 4 months of age.

    Directory of Open Access Journals (Sweden)

    Lisa M Nicholas

    Full Text Available Exposure to maternal obesity before and/or throughout pregnancy may increase the risk of obesity and insulin resistance in the offspring in childhood and adult life, therefore, resulting in its transmission into subsequent generations. We have previously shown that exposure to maternal obesity around the time of conception alone resulted in increased adiposity in female lambs. Changes in the abundance of insulin signalling molecules in skeletal muscle and adipose tissue precede the development of insulin resistance and type 2 diabetes. It is not clear, however, whether exposure to maternal obesity results in insulin resistance in her offspring as a consequence of the impact of increased adiposity on skeletal muscle or as a consequence of the programming of specific changes in the abundance of insulin signalling molecules in this tissue. We have used an embryo transfer model in the sheep to investigate the effects of exposure to either maternal obesity or to weight loss in normal and obese mothers preceding and for one week after conception on the expression and abundance of insulin signalling molecules in muscle in the offspring. We found that exposure to maternal obesity resulted in lower muscle GLUT-4 and Ser 9 phospho-GSK3α and higher muscle GSK3α abundance in lambs when compared to lambs conceived in normally nourished ewes. Exposure to maternal weight loss in normal or obese mothers, however, resulted in lower muscle IRS1, PI3K, p110β, aPKCζ, Thr 642 phospho-AS160 and GLUT-4 abundance in the offspring. In conclusion, maternal obesity or weight loss around conception have each programmed specific changes on subsets of molecules in the insulin signalling, glucose transport and glycogen synthesis pathways in offspring. There is a need for a stronger evidence base to ensure that weight loss regimes in obese women seeking to become pregnant minimize the metabolic costs for the next generation.

  10. Maternal obesity and neonatal mortality according to subtypes of preterm birth

    DEFF Research Database (Denmark)

    Nøhr, Ellen Aagaard; Vaeth, Michael; Bech, Bodil H

    2007-01-01

    : Compared with infants of mothers who were at a normal weight before pregnancy (BMI of 18.5 or more but less than 25), neonatal mortality was increased in infants of mothers who were overweight (BMI of 25 or more but less than 30) or obese (BMI of 30 or more) (adjusted hazard ratios 1.7, CI 1.2-2.5, and 1.......6, CI 1.0-2.4, respectively). For preterm infants (n=3,934, 136 deaths), neonatal mortality in infants born after preterm premature rupture of membranes (PROM) was significantly increased if they were born to an overweight or obese mother (adjusted hazard ratios 3.5, CI 1.4-8.7, and 5.7, CI 2.......2-14.8). There were no associations between high BMI and neonatal mortality in infants born after spontaneous preterm birth without preterm PROM or in infants born after induced preterm delivery. CONCLUSION: High maternal weight seems to increase the risk of neonatal mortality, especially in infants born after...

  11. Maternal Perceptions Related to Eating and Obesity Risk Among Low-Income African American Preschoolers.

    Science.gov (United States)

    Porter, Lauren; Shriver, Lenka H; Ramsay, Samantha

    2016-12-01

    Objectives Health disparities are prevalent in the U.S., with low-income African American children suffering from high rates of obesity and related conditions. Better understanding of parental attitudes and barriers related to healthy eating and obesity risk is needed to suggest more effective intervention foci for this at-risk population. Methods African American caregivers of 3-5 year old children were recruited for focus groups and a questionnaire completion from two Head Start programs in a southeastern state of the U.S. The Social Cognitive Theory was utilized to develop a focus group guide. Focus group recordings were transcribed verbatim and analyzed using the comparative content analysis. Results Eight focus groups (all participants were mothers) yielded the following main themes: (1) general nutrition knowledge but common misconceptions about foods/beverages; (2) beliefs that meals have to include meat and starch and be home-cooked to be healthy; (3) desire to feed children better than their own parents; (4) lack of family support and child pickiness perceived as the greatest barriers to healthy eating; (5) awareness of family history of diseases; and (6) low concern about children's current diet and weight status. Over 25 % of mothers underestimated their child weight status. Conclusions Our findings highlight the importance of understanding maternal perspectives related to food, eating, and weight among low-income African American mothers of preschoolers. Nutrition educators should be aware of misconceptions and recognize that mothers might not perceive diet quality in early childhood as having strong impact on the child's future health and/or obesity risks.

  12. Differential hypothalamic leptin sensitivity in obese rat offspring exposed to maternal and postnatal intake of chocolate and soft drink.

    Science.gov (United States)

    Kjaergaard, M; Nilsson, C; Secher, A; Kildegaard, J; Skovgaard, T; Nielsen, M O; Grove, K; Raun, K

    2017-01-16

    Intake of high-energy foods and maternal nutrient overload increases the risk of metabolic diseases in the progeny such as obesity and diabetes. We hypothesized that maternal and postnatal intake of chocolate and soft drink will affect leptin sensitivity and hypothalamic astrocyte morphology in adult rat offspring. Pregnant Sprague-Dawley rats were fed ad libitum chow diet only (C) or with chocolate and high sucrose soft drink supplement (S). At birth, litter size was adjusted into 10 male offspring per mother. After weaning, offspring from both dietary groups were assigned to either S or C diet, giving four groups until the end of the experiment at 26 weeks of age. As expected, adult offspring fed the S diet post weaning became obese (body weight: Peffect of leptin than energy expenditure, suggesting differential programming of leptin sensitivity in ARC in SS offspring. Effects of the maternal S diet were normalized when offspring were fed a chow diet after weaning. Maternal intake of chocolate and soft drink had long-term consequences for the metabolic phenotype in the offspring if they continued on the S diet in postnatal life. These offspring displayed obesity despite lowered energy intake associated with alterations in hypothalamic leptin signalling.

  13. Maternal BMI as a predictor of methylation of obesity-related genes in saliva samples from preschool-age Hispanic children at-risk for obesity.

    Science.gov (United States)

    Oelsner, Kathryn Tully; Guo, Yan; To, Sophie Bao-Chieu; Non, Amy L; Barkin, Shari L

    2017-01-09

    The study of epigenetic processes and mechanisms present a dynamic approach to assess complex individual variation in obesity susceptibility. However, few studies have examined epigenetic patterns in preschool-age children at-risk for obesity despite the relevance of this developmental stage to trajectories of weight gain. We hypothesized that salivary DNA methylation patterns of key obesogenic genes in Hispanic children would 1) correlate with maternal BMI and 2) allow for identification of pathways associated with children at-risk for obesity. Genome-wide DNA methylation was conducted on 92 saliva samples collected from Hispanic preschool children using the Infinium Illumina HumanMethylation 450 K BeadChip (Illumina, San Diego, CA, USA), which interrogates >484,000 CpG sites associated with ~24,000 genes. The analysis was limited to 936 genes that have been associated with obesity in a prior GWAS Study. Child DNA methylation at 17 CpG sites was found to be significantly associated with maternal BMI, with increased methylation at 12 CpG sites and decreased methylation at 5 CpG sites. Pathway analysis revealed methylation at these sites related to homocysteine and methionine degradation as well as cysteine biosynthesis and circadian rhythm. Furthermore, eight of the 17 CpG sites reside in genes (FSTL1, SORCS2, NRF1, DLC1, PPARGC1B, CHN2, NXPH1) that have prior known associations with obesity, diabetes, and the insulin pathway. Our study confirms that saliva is a practical human tissue to obtain in community settings and in pediatric populations. These salivary findings indicate potential epigenetic differences in Hispanic preschool children at risk for pediatric obesity. Identifying early biomarkers and understanding pathways that are epigenetically regulated during this critical stage of child development may present an opportunity for prevention or early intervention for addressing childhood obesity. The clinical trial protocol is available at Clinical

  14. Association of maternal obesity and depressive symptoms with television-viewing time in low-income preschool children.

    Science.gov (United States)

    Burdette, Hillary L; Whitaker, Robert C; Kahn, Robert S; Harvey-Berino, Jean

    2003-09-01

    Decreasing television (TV)-viewing time may improve child health and well-being. These viewing patterns are shaped during the preschool years. Because mothers play an important role in determining how much TV their preschool children watch, a better understanding is needed of the maternal factors that influence children's TV viewing. To examine the relationship of depressive symptoms and obesity in low-income mothers with TV-viewing time in their preschool children. Cross-sectional, self-administered survey of 295 low-income mothers of 3- and 4-year-old children (92% white) enrolled in the Vermont Special Supplemental Nutrition Program for Women, Infants, and Children. Mothers reported children's usual weekday and weekend-day TV-viewing time. Maternal depressive symptoms were measured with the Center for Epidemiologic Studies Depression Scale (CES-D). Maternal body mass index was calculated from self-reported height and weight measurements (weight in kilograms divided by height in meters squared). Children watched a mean of 2.2 +/-1.2 hours of TV per day. Those in the upper quartile of TV-viewing time (high TV viewers) watched 3 or more hours of TV per day. Of the mothers, 12% had both obesity (BMI > or =30) and depressive symptoms (CES-D score > or =16), 19% were obese only, and 18% had depressive symptoms only. Children were more likely to be high TV viewers if their mothers had clinically significant depressive symptoms (35% vs 23%; P =.03) or if their mothers were obese (35% vs 22%; P =.03). Forty-two percent of children were high TV viewers if the mother had both depressive symptoms and obesity, 30% if the mother had only depressive symptoms, 29% if the mother had only obesity, and 20% if the mother had neither depressive symptoms nor obesity (P =.06 overall; P for trend =.009 using the chi2 test). Among low-income preschool children, those whose mothers had either depressive symptoms or obesity were more likely to watch 3 or more hours of TV a day. Strategies

  15. Maternal obesity-impaired insulin signaling in sheep and induced lipid accumulation and fibrosis in skeletal muscle of offspring.

    Science.gov (United States)

    Yan, Xu; Huang, Yan; Zhao, Jun-Xing; Long, Nathan M; Uthlaut, Adam B; Zhu, Mei-Jun; Ford, Stephen P; Nathanielsz, Peter W; Du, Min

    2011-07-01

    The prevalence of maternal obesity is increasing rapidly in recent decades. We previously showed that maternal obesity affected skeletal muscle development during the fetal stage. The objective of this study was to evaluate the effects of maternal obesity on the skeletal muscle properties of offspring. Ewes were fed a control diet (100% energy requirement, Con) or an obesogenic diet (150% energy requirement, OB) from 2 mo before pregnancy to weaning. After weaning, the offspring lambs were fed a maintenance diet until 19 mo of age and then ad libitum for 12 wk to measure feed intake. At 22 mo old, the longissimus dorsi (LD) muscle was biopsied. The downstream insulin signaling was lower in OB than Con lambs as shown by reduction in the phosphorylation of protein kinase B, mammalian target of rapamycin, and 4-E binding protein 1. On the other hand, the phosphorylation of protein kinase C and insulin receptor substrate 1 was higher in OB compared to Con lambs. More intramuscular adipocytes were observed in OB compared to Con offspring muscle, and the expression of peroxisome proliferator-activated receptor gamma, an adipocyte marker, was also higher, which was consistent with the higher intramuscular triglyceride content. Both fatty acid transport protein 1 and cluster of differentiation 36 (also known as fatty acid translocase) were increased in the OB group. In addition, higher collagen content was also detected in OB compared to Con offspring. In conclusion, our data show that offspring from obese mothers had impaired insulin signaling in muscle compared with control lambs, which correlates with increased intramuscular triglycerides and higher expression of fatty acid transporters. These data clearly show that maternal obesity impairs the function of the skeletal muscle of offspring, supporting the fetal programming of adult metabolic diseases.

  16. The association between maternal serious psychological distress and child obesity at 3 years: a cross-sectional analysis of the UK Millennium Cohort Data.

    Science.gov (United States)

    Ramasubramanian, L; Lane, S; Rahman, A

    2013-01-01

      The prevalence of child obesity is increasing rapidly worldwide. Early childhood has been identified as a critical time period for the development of obesity. Maternal mental health and early life environment are crucial factors and have been linked to adverse child outcomes. The objective of the study was to examine the relationship between maternal serious psychological distress and obesity in early childhood.   A cross-sectional analysis of data from the Millennium Cohort Study was conducted. Subjects consisted of all natural mothers (n= 10 465) who had complete and plausible data for Kessler-6 scores, socio-demographic and anthropometric variables, and their children for whom anthropometric measurements were completed at age 3. Maternal serious psychological distress was defined as a score of 13 or more on the Kessler-6 scale. Obesity was defined as body mass index ≥95th centile of the 1990 reference chart for age and sex in children. The data were analysed using spss 16. Maternal socio-demographic factors that are known to influence maternal mental health and child obesity were identified and adjusted using multivariate logistic regression.   Of the 10 465 mother-child dyads, 3.5% of mothers had serious psychological distress and 5.5% of children were obese at 3 years of age. Logistic regression analysis showed that maternal serious psychological distress was associated with early childhood obesity (P= 0.01; OR 1.62, 95% CI 1.11, 2.37). After adjusting for potential confounding factors using multivariate logistic regression, maternal serious psychological distress remained significantly associated with early childhood obesity (P= 0.01; OR 1.59, 95% CI 1.08, 2.34).   The results show that maternal serious psychological distress is independently associated with early childhood obesity. © 2011 Blackwell Publishing Ltd.

  17. Maternal Obesity Management Using Mobile Technology: A Feasibility Study to Evaluate a Text Messaging Based Complex Intervention during Pregnancy

    Directory of Open Access Journals (Sweden)

    Hora Soltani

    2015-01-01

    Full Text Available Background. Maternal obesity and excessive gestational weight gain (GWG are on the rise with negative impact on pregnancy and birth outcomes. Research into managing GWG using accessible technology is limited. The maternal obesity management using mobile technology (MOMTech study aimed at evaluating the feasibility of text messaging based complex intervention designed to support obese women (BMI ≥ 30 with healthier lifestyles and limit GWG. Methods. Participants received two daily text messages, supported by four appointments with healthy lifestyle midwife, diet and activity goal setting, and self-monitoring diaries. The comparison group were obese mothers who declined to participate but consented for their routinely collected data to be used for comparison. Postnatal interviews and focus groups with participants and the comparison group explored the intervention’s acceptability and suggested improvements. Results. Fourteen women completed the study which did not allow statistical analyses. However, participants had lower mean GWG than the comparison group (6.65 kg versus 9.74 kg and few (28% versus 50% exceeded the Institute of Medicine’s upper limit of 9 kg GWG for obese women. Conclusions. MOMTech was feasible within clinical setting and acceptable intervention to support women to limit GWG. Before further trials, slight modifications are planned to recruitment, text messages, and the logistics of consultation visits.

  18. The effects of dietary and lifestyle interventions among pregnant women who are overweight or obese on longer-term maternal and early childhood outcomes

    DEFF Research Database (Denmark)

    Dodd, Jodie M.; Grivell, Rosalie M.; Louise, Jennie

    2017-01-01

    Background: The aim of this individual participant data meta-analysis (IPDMA) is to evaluate the effects of dietary and lifestyle interventions among pregnant women who are overweight or obese on later maternal and early childhood outcomes at ages 3-5 years. Methods/design: We will build...... or is being undertaken. The primary maternal outcome is a diagnosis of maternal metabolic syndrome. The primary childhood outcome is BMI above 90%. We have identified 7 relevant trials, involving 5425 women who were overweight or obese during pregnancy, with approximately 3544 women and children with follow......-up assessments available for inclusion in the meta-analysis. Discussion: The proposed IPDMA provides an opportunity to evaluate the effect of dietary and lifestyle interventions among pregnant women who are overweight or obese on later maternal and early childhood health outcomes, including risk of obesity...

  19. Antenatal exercise in overweight and obese women and its effects on offspring and maternal health: design and rationale of the IMPROVE (Improving Maternal and Progeny Obesity Via Exercise) randomised controlled trial.

    Science.gov (United States)

    Seneviratne, Sumudu N; Parry, Graham K; McCowan, Lesley Me; Ekeroma, Alec; Jiang, Yannan; Gusso, Silmara; Peres, Geovana; Rodrigues, Raquel O; Craigie, Susan; Cutfield, Wayne S; Hofman, Paul L

    2014-04-26

    Obesity during pregnancy is associated with adverse outcomes for the offspring and mother. Lifestyle interventions in pregnancy such as antenatal exercise, are proposed to improve both short- and long-term health of mother and child. We hypothesise that regular moderate-intensity exercise during the second half of pregnancy will result in improved maternal and offspring outcomes, including a reduction in birth weight and adiposity in the offspring, which may be protective against obesity in later life. The IMPROVE (Improving Maternal and Progeny Risks of Obesity Via Exercise) study is a two-arm parallel randomised controlled clinical trial being conducted in Auckland, New Zealand. Overweight and obese women (BMI ≥25 kg/m2) aged 18-40 years, with a singleton pregnancy of exercise.Participants are randomised with 1:1 allocation ratio to either intervention or control group, using computer-generated randomisation sequences in variable block sizes, stratified on ethnicity and parity, after completion of baseline assessments. The intervention consists of a 16-week structured home-based moderate-intensity exercise programme utilising stationary cycles and heart rate monitors, commencing at 20 weeks of gestation. The control group do not receive any exercise intervention. Both groups undergo regular fetal ultrasonography and receive standard antenatal care. Due to the nature of the intervention, participants are un-blinded to group assignment during the trial.The primary outcome is offspring birth weight. Secondary offspring outcomes include fetal and neonatal body composition and anthropometry, neonatal complications and cord blood metabolic markers. Maternal outcomes include weight gain, pregnancy and delivery complications, aerobic fitness, quality of life, metabolic markers and post-partum body composition. The results of this trial will provide valuable insights on the effects of antenatal exercise on health outcomes in overweight and obese mothers and their

  20. Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes.

    Science.gov (United States)

    Catalano, P; deMouzon, S H

    2015-04-01

    Obesity during pregnancy is associated with an increased risk of short- and long-term metabolic dysfunction in the mother and her offspring. Both higher maternal pregravid body mass index (kg m(-2)) and excessive gestational weight gain (GWG) have been associated with adverse pregnancy outcomes such as gestational diabetes, preeclampsia and fetal adiposity. Multiple lifestyle intervention trials consisting of weight management using various diets, increased physical activity and behavioral modification techniques have been employed to avoid excessive GWG and improve perinatal outcomes. These randomized controlled trials (RCTs) have achieved modest success in decreasing excessive GWG, although the decrease in GWG was often not within the current Institute of Medicine guidelines. RCTs have generally not had any success with decreasing the risk of maternal gestational diabetes (GDM), preeclampsia or excessive fetal growth often referred to as macrosomia. Although the lack of success for these trials has been attributed to lack of statistical power and poor compliance with study protocols, our own research suggests that maternal pregravid and early pregnancy metabolic condition programs early placenta function and gene expression. These alterations in maternal/placental function occur in the first trimester of pregnancy prior to when most intervention trials are initiated. For example, maternal accrural of adipose tissue relies on prior activation of genes controlling lipogenesis and low-grade inflammation in early pregnancy. These metabolic alterations occur prior to any changes in maternal phenotype. Therefore, trials of lifestyle interventions before pregnancy are needed to demonstrate the safety and efficacy for both the mother and her offspring.

  1. Maternal lifestyle characteristics during pregnancy, and the risk of obesity in the offspring: a study of 5,125 children.

    Science.gov (United States)

    Mourtakos, Stamatis P; Tambalis, Konstantinos D; Panagiotakos, Demosthenes B; Antonogeorgos, George; Arnaoutis, Giannis; Karteroliotis, Konstantinos; Sidossis, Labros S

    2015-03-21

    To investigate the association between gestational weight gain, maternal age and lifestyle habits (e.g., physical activity, smoking, and alcohol consumption) during pregnancy, with Body Mass Index of the offspring at the age of 8. Α random sample of 5,125 children was extracted from a national database and matched with their mothers. With the use of a standardised questionnaire, telephone interviews were carried out for the collection of information like: maternal age at pregnancy, gestational weight gain (GWG), exercise levels, smoking and alcohol consumption. The Body Mass Index (BMI) status of the offspring at the age of 8 was calculated from data retrieved from the national database (e.g., height and weight). The odds for being overweight/obese at the age of 8 for 1 kg GWG, for smoking, and for mild exercise during pregnancy compared to sedentary was 1.01 (95%CI: 1.00, 1.02), 1.23 (95%CI: 1.03, 1.47) and 0.77 (95%CI: 0.65, 0.91), respectively. Further analysis revealed that offspring of women who exceeded the Institute of Medicine (IOM) maternal weight gain recommendations were at an increased risk of obesity (OR: 1.45; 95%CI, 1.26, 1.67) compared with offspring of women with GWG within the recommended range. Maternal age and alcohol consumption were not associated with the outcome (p > 0.05). GWG, physical activity and smoking status during pregnancy were significantly associated with obesity for the offspring at the age of 8. Health care professionals should strongly advise women to not smoke and to perform moderate exercise during pregnancy to prevent obesity in the offspring in later life.

  2. Maternal obesity and metabolic risk to the offspring: why lifestyle interventions may have not achieved the desired outcomes

    OpenAIRE

    Catalano, P; deMouzon, SH

    2015-01-01

    Obesity during pregnancy is associated with an increased risk of short- and long-term metabolic dysfunction in the mother and her offspring. Both higher maternal pregravid body mass index (kg m−2) and excessive gestational weight gain (GWG) have been associated with adverse pregnancy outcomes such as gestational diabetes, preeclampsia and fetal adiposity. Multiple lifestyle intervention trials consisting of weight management using various diets, increased physical activity and behavioral modi...

  3. Effect of metformin on maternal and neonatal outcomes in pregnant obese non-diabetic women: A meta-analysis

    Directory of Open Access Journals (Sweden)

    Ahmed Elmaraezy

    2017-09-01

    Full Text Available Background: Metformin reduces maternal and neonatal weight gain in gestational diabetes mellitus; however, this effect is poorly investigated in non-diabetic women. Objective: We performed this meta-analysis to investigate the effect of metformin intake during pregnancy on maternal and neonatal outcomes in obese non-diabetic women. Materials and Methods: We searched Medline, EMBASE, and Cochrane CENTRAL for eligible randomized controlled trials addressing the efficacy of metformin in pregnant obese non-diabetic women. Data were extracted and analyzed using RevMan software (Version 5.3. Neonatal birth weight was the key outcome. Secondary outcomes included maternal weight gain, the incidence of preeclampsia, and neonatal adverse effects (miscarriage, stillbirth and congenital anomalies. Results: Pooled data from two RCTs (n=843 showed that metformin caused a significant reduction in maternal gestational weight gain (MD-1.35, 95% CI: [2.08, -0.630], compared to placebo. The summary effect-estimate did not favor either of the two groups in terms of reduction of neonatal birth weight Z score (MD-0.09, 95% CI: [0.23, 0.06]. Metformin was associated with 41% reduction in the risk of preeclampsia; however, this reduction was not statistically significant [RR 0.59, 95% CI: [0.03, 11.46]. None of the neonatal adverse events including stillbirth [RR 1.14, 95% CI: 0.42, 3.10] and congenital anomalies (RR= 1.36, 95% CI: [0.58, 3.21] differed significantly between the two groups. Conclusion: For obese pregnant women, metformin could decrease gestational weight gain with no significant reduction in neonatal birth weight. In light of the current evidence, metformin should not be used to prevent poor pregnancy outcomes in obese non-diabetic women.

  4. A DRD4 Gene by Maternal Sensitivity Interaction Predicts Risk for Overweight or Obesity in Two Independent Cohorts of Preschool Children

    Science.gov (United States)

    Levitan, Robert D.; Jansen, Pauline; Wendland, Barbara; Tiemeier, Henning; Jaddoe, Vincent W.; Silveira, Patricia P.; Kennedy, James L.; Atkinson, Leslie; Fleming, Alison; Sokolowski, Marla; Gaudreau, Helene; Steiner, Meir; Dubé, Laurette; Hamilton, Jill; Moss, Ellen; Wazana, Ashley; Meaney, Michael

    2017-01-01

    Background: Recent evidence suggests that early exposure to low maternal sensitivity is a risk factor for obesity in children and adolescents. A separate line of study shows that the seven-repeat (7R) allele of the dopamine-4 receptor gene (DRD4) increases susceptibility to environmental factors including maternal sensitivity. The current study…

  5. Effect of Maternal Age at Childbirth on Obesity in Postmenopausal Women

    OpenAIRE

    We, Ji-Sun; Han, Kyungdo; Kwon, Hyuk-Sang; Kil, Kicheol

    2016-01-01

    Abstract The object of this study was to assess the obesity in postmenopausal women, according to age at childbirth. We analyzed the association between age at first childbirth, age at last childbirth, parity, and subject obesity status (general obesity; BMI?>25?kg/m2, nongeneral obesity; BMI ?25?kg/m2, abdominal obesity; waist circumference?>85?cm, nonabdominal obesity; waist circumference ?85?cm), using data from a nationwide population-based survey, the 2010 to 2012 Korean National Health ...

  6. Metabolic syndrome in Spanish adolescents and its association with birth weight, breastfeeding duration, maternal smoking, and maternal obesity: a cross-sectional study.

    Science.gov (United States)

    González-Jiménez, Emilio; Montero-Alonso, Miguel A; Schmidt-RioValle, Jacqueline; García-García, Carmen J; Padez, Cristina

    2015-06-01

    The metabolic syndrome (MetS) in adolescents is a growing problem. The objectives were to verify the association among early predictors such as birth weight, breastfeeding, maternal weight status, smoking during pregnancy, and the development of MetS. A cross-sectional study was performed of 976 children and adolescents, 10-15 years of age, at schools in the provinces of Granada and Almeria (Spain). For this purpose, we analyzed the physical characteristics as well as the biochemical markers of the participants with a view to ascertaining the prevalence of the MetS. Relevant data were also extracted from the clinical histories of their mothers. It was found that 3.85% of the female subjects and 5.38% of the male subjects in the sample population suffered from MetS. In both sexes, there was an association between birth weight and positive MetS diagnosis (OR 1.27). For both males and females, there was an inverse association between the length of time that they had been breastfed and positive MetS diagnosis (OR1-3 months 3.16; OR4-6 months 1.70; OR(>6 months) 0.13). There was also a significant association between maternal weight (OR(overweight )30.79; OR(obesity) 49.36) and cigarette consumption during pregnancy (OR 1.47) and the subsequent development of MetS in the children of these mothers. Those subjects born with a higher than average birth weight had a greater risk of developing MetS in childhood and adolescence. Breastfeeding children for longer than 6 months protected them from MetS in their early years as well as in their teens. Other risk factors for MetS were maternal smoking during pregnancy as well as maternal overweight and obesity.

  7. Identification and comparative analyses of myocardial miRNAs involved in the fetal response to maternal obesity.

    Science.gov (United States)

    Maloyan, Alina; Muralimanoharan, Sribalasubashini; Huffman, Steven; Cox, Laura A; Nathanielsz, Peter W; Myatt, Leslie; Nijland, Mark J

    2013-10-01

    Human and animal studies show that suboptimal intrauterine environments lead to fetal programming, predisposing offspring to disease in later life. Maternal obesity has been shown to program offspring for cardiovascular disease (CVD), diabetes, and obesity. MicroRNAs (miRNAs) are small, noncoding RNA molecules that act as key regulators of numerous cellular processes. Compelling evidence links miRNAs to the control of cardiac development and etiology of cardiac pathology; however, little is known about their role in the fetal cardiac response to maternal obesity. Our aim was to sequence and profile the cardiac miRNAs that are dysregulated in the hearts of baboon fetuses born to high fat/high fructose-diet (HFD) fed mothers for comparison with fetal hearts from mothers eating a regular diet. Eighty miRNAs were differentially expressed. Of those, 55 miRNAs were upregulated and 25 downregulated with HFD. Twenty-two miRNAs were mapped to human; 14 of these miRNAs were previously reported to be dysregulated in experimental or human CVD. We used an Ingenuity Pathway Analysis to integrate miRNA profiling and bioinformatics predictions to determine miRNA-regulated processes and genes potentially involved in fetal programming. We found a correlation between miRNA expression and putative gene targets involved in developmental disorders and CVD. Cellular death, growth, and proliferation were the most affected cellular functions in response to maternal obesity. Thus, the current study reveals significant alterations in cardiac miRNA expression in the fetus of obese baboons. The epigenetic modifications caused by adverse prenatal environment may represent one of the mechanisms underlying fetal programming of CVD.

  8. High fat diet and in utero exposure to maternal obesity disrupts circadian rhythm and leads to metabolic programming of liver in rat offspring.

    Directory of Open Access Journals (Sweden)

    Sarah J Borengasser

    Full Text Available The risk of obesity in adulthood is subject to programming beginning at conception. In animal models, exposure to maternal obesity and high fat diets influences the risk of obesity in the offspring. Among other long-term changes, offspring from obese rats develop hyperinsulinemia, hepatic steatosis, and lipogenic gene expression in the liver at weaning. However, the precise underlying mechanisms leading to metabolic dysregulation in the offspring remains unclear. Using a rat model of overfeeding-induced obesity, we previously demonstrated that exposure to maternal obesity from pre-conception to birth, is sufficient to program increased obesity risk in the offspring. Offspring of obese rat dams gain greater body weight and fat mass when fed high fat diet (HFD as compared to lean dam. Since, disruptions of diurnal circadian rhythm are known to detrimentally impact metabolically active tissues such as liver, we examined the hypothesis that maternal obesity leads to perturbations of core clock components and thus energy metabolism in offspring liver. Offspring from lean and obese dams were examined at post-natal day 35, following a short (2 wk HFD challenge. Hepatic mRNA expression of circadian (CLOCK, BMAL1, REV-ERBα, CRY, PER and metabolic (PPARα, SIRT1 genes were strongly suppressed in offspring exposed to both maternal obesity and HFD. Using a mathematical model, we identified two distinct biological mechanisms that modulate PPARα mRNA expression: i decreased mRNA synthesis rates; and ii increased non-specific mRNA degradation rate. Moreover, our findings demonstrate that changes in PPARα transcription were associated with epigenomic alterations in H3K4me3 and H3K27me3 histone marks near the PPARα transcription start site. Our findings indicated that offspring from obese rat dams have detrimental alternations to circadian machinery that may contribute to impaired liver metabolism in response to HFD, specifically via reduced PPAR

  9. Cumulative incidence of youth obesity is associated with low cardiorespiratory fitness levels and with maternal overweight

    Directory of Open Access Journals (Sweden)

    Anelise Reis Gaya

    2015-12-01

    Full Text Available Abstract This longitudinal study evaluated the association between the incidence of youth overweight/obesity (Ow/Ob and low levels of cardiorespiratory fitness (CRF over 4 years and youths' and their parents' demographic and nutritional characteristics. The randomized sample comprised 398 youth, aged 7-17 years at baseline, from a city in southern Brazil. Subjects were classified as being Ow/Ob according to international body mass index (BMI parameters. Parental weight and height were determined by direct questioning. Youth CRF was measured by a 9-minute walk-and-run test. The cumulative incidences of Ow/Ob and of low CRF levels were 25.1% and 20.5%, respectively. Relative to other youth, youth who were classified as "unhealthy" at baseline (with respect to CRF and by the fourth year were more likely to be classified as Ow/Ob (relative risks: 1.12 and 1.10, respectively. Youth whose mothers were categorized as Ow/Ob were at higher risk of being classified as Ow/Ob than youth whose mothers had normal BMIs (relative risks: 1.19 at baseline and 1.20 in the fourth year. The incidence of Ow/Ob among the former youth was associated with low CRF levels and with maternal Ob.

  10. Experimental Models of Maternal Obesity and Neuroendocrine Programming of Metabolic Disorders in Offspring.

    Science.gov (United States)

    Reynolds, Clare M; Segovia, Stephanie A; Vickers, Mark H

    2017-01-01

    Evidence from epidemiological, clinical, and experimental studies have clearly shown that disease risk in later life is increased following a poor early life environment, a process preferentially termed developmental programming. In particular, this work clearly highlights the importance of the nutritional environment during early development with alterations in maternal nutrition, including both under- and overnutrition, increasing the risk for a range of cardiometabolic and neurobehavioral disorders in adult offspring characterized by both adipokine resistance and obesity. Although the mechanistic basis for such developmental programming is not yet fully defined, a common feature derived from experimental animal models is that of alterations in the wiring of the neuroendocrine pathways that control energy balance and appetite regulation during early stages of developmental plasticity. The adipokine leptin has also received significant attention with clear experimental evidence that normal regulation of leptin levels during the early life period is critical for the normal development of tissues and related signaling pathways that are involved in metabolic and cardiovascular homeostasis. There is also increasing evidence that alterations in the epigenome and other underlying mechanisms including an altered gut-brain axis may contribute to lasting cardiometabolic dysfunction in offspring. Ongoing studies that further define the mechanisms between these associations will allow for identification of early risk markers and implementation of strategies around interventions that will have obvious beneficial implications in breaking a programmed transgenerational cycle of metabolic disorders.

  11. Experimental Models of Maternal Obesity and Neuroendocrine Programming of Metabolic Disorders in Offspring

    Directory of Open Access Journals (Sweden)

    Clare M. Reynolds

    2017-09-01

    Full Text Available Evidence from epidemiological, clinical, and experimental studies have clearly shown that disease risk in later life is increased following a poor early life environment, a process preferentially termed developmental programming. In particular, this work clearly highlights the importance of the nutritional environment during early development with alterations in maternal nutrition, including both under- and overnutrition, increasing the risk for a range of cardiometabolic and neurobehavioral disorders in adult offspring characterized by both adipokine resistance and obesity. Although the mechanistic basis for such developmental programming is not yet fully defined, a common feature derived from experimental animal models is that of alterations in the wiring of the neuroendocrine pathways that control energy balance and appetite regulation during early stages of developmental plasticity. The adipokine leptin has also received significant attention with clear experimental evidence that normal regulation of leptin levels during the early life period is critical for the normal development of tissues and related signaling pathways that are involved in metabolic and cardiovascular homeostasis. There is also increasing evidence that alterations in the epigenome and other underlying mechanisms including an altered gut–brain axis may contribute to lasting cardiometabolic dysfunction in offspring. Ongoing studies that further define the mechanisms between these associations will allow for identification of early risk markers and implementation of strategies around interventions that will have obvious beneficial implications in breaking a programmed transgenerational cycle of metabolic disorders.

  12. Maternal, fetal and perinatal alterations associated with obesity, overweight and gestational diabetes: an observational cohort study (PREOBE

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    Staffan K. Berglund

    2016-03-01

    Full Text Available Abstract Background Maternal overweight, obesity, and gestational diabetes (GD have been negatively associated with offspring development. Further knowledge regarding metabolic and nutritional alterations in these mother and their offspring are warranted. Methods In an observational cohort study we included 331 pregnant women from Granada, Spain. The mothers were categorized into four groups according to BMI and their GD status; overweight (n:56, obese (n:64, GD (n:79, and healthy normal weight controls (n:132. We assessed maternal growth and nutritional biomarkers at 24 weeks (n = 269, 34 weeks (n = 310 and at delivery (n = 310 and the perinatal characteristics including cord blood biomarkers. Results Obese and GD mothers had significantly lower weight gain during pregnancy and infant birth weight, waist circumference, and placental weight were higher in the obese group, including a significantly increased prevalence of macrosomia. Except for differences in markers of glucose metabolism (glucose, HbA1c, insulin and uric acid we found at some measures that overweight and/or obese mothers had lower levels of transferrin saturation, hemoglobin, Vitamin B12 and folate and higher levels of C-reactive protein, erythrocyte sedimentation rate, ferritin, and cortisol. GD mothers had similar differences in hemoglobin and C-reactive protein but higher levels of folate. The latter was seen also in cord blood. Conclusions We identified several metabolic alterations in overweight, obese and GD mothers compared to controls. Together with the observed differences in infant anthropometrics, these may be important biomarkers in future research regarding the programming of health and disease in children. Trial registration The trial was registered at clinicaltrials.gov, identifier ( NCT01634464 .

  13. Existing maternal obesity guidelines may increase inequalities between ethnic groups: a national epidemiological study of 502,474 births in England

    OpenAIRE

    Heslehurst, Nicola; Sattar, Naveed; Rajasingam, Daghni; Wilkinson, John; Summerbell, Carolyn D; Rankin, Judith

    2012-01-01

    Abstract Background Asians are at increased risk of morbidity at a lower body mass index (BMI) than European Whites, particularly relating to metabolic risk. UK maternal obesity guidelines use general population BMI criteria to define obesity, which do not represent the risk of morbidity among Asian populations. This study compares incidence of first trimester obesity using Asian-specific and general population BMI criteria. Method A retrospective epidemiological study of 502,474 births betwe...

  14. Transgenic increase in N-3/n-6 Fatty Acid ratio reduces maternal obesity-associated inflammation and limits adverse developmental programming in mice.

    Science.gov (United States)

    Heerwagen, Margaret J R; Stewart, Michael S; de la Houssaye, Becky A; Janssen, Rachel C; Friedman, Jacob E

    2013-01-01

    Maternal and pediatric obesity has risen dramatically over recent years, and is a known predictor of adverse long-term metabolic outcomes in offspring. However, which particular aspects of obese pregnancy promote such outcomes is less clear. While maternal obesity increases both maternal and placental inflammation, it is still unknown whether this is a dominant mechanism in fetal metabolic programming. In this study, we utilized the Fat-1 transgenic mouse to test whether increasing the maternal n-3/n-6 tissue fatty acid ratio could reduce the consequences of maternal obesity-associated inflammation and thereby mitigate downstream developmental programming. Eight-week-old WT or hemizygous Fat-1 C57BL/6J female mice were placed on a high-fat diet (HFD) or control diet (CD) for 8 weeks prior to mating with WT chow-fed males. Only WT offspring from Fat-1 mothers were analyzed. WT-HFD mothers demonstrated increased markers of infiltrating adipose tissue macrophages (Pmaternal insulin resistance (r = 0.59, Pmaternal protection from excess inflammation corresponded with improved metabolic outcomes in adult WT offspring. While the offspring from WT-HFD mothers weaned onto CD demonstrated increased weight gain (Pmaternal inflammation may be a promising target for preventing adverse fetal metabolic outcomes in pregnancies complicated by maternal obesity.

  15. Maternal obesity and postpartum haemorrhage after vaginal and caesarean delivery among nulliparous women at term: a retrospective cohort study

    Directory of Open Access Journals (Sweden)

    Fyfe Elaine M

    2012-10-01

    Full Text Available Abstract Background Increasing rates of postpartum haemorrhage in developed countries over the past two decades are not explained by corresponding changes in risk factors and conjecture has been raised that maternal obesity may be responsible. Few studies investigating risk factors for PPH have included BMI or investigated PPH risk among nulliparous women. The aim of this study was to determine in a cohort of nulliparous women delivering at term whether overweight and obesity are independent risk factors for major postpartum haemorrhage (PPH ≥1000ml after vaginal and caesarean section delivery. Methods The study population was nulliparous singleton pregnancies delivered at term at National Women’s Hospital, Auckland, New Zealand from 2006 to 2009 (N=11,363. Multivariable logistic regression was adjusted for risk factors for major PPH. Results There were 7238 (63.7% women of normal BMI, 2631 (23.2% overweight and 1494 (13.1% obese. Overall, PPH rates were increased in overweight and obese compared with normal-weight women (n=255 [9.7%], n=233 [15.6%], n=524 [7.2%], p Conclusion Nulliparous obese women have a twofold increase in risk of major PPH compared to women with normal BMI regardless of mode of delivery. Higher rates of PPH among obese women are not attributable to their higher rates of caesarean delivery. Obesity is an important high risk factor for PPH, and the risk following vaginal delivery is emphasised. We recommend in addition to standard practice of active management of third stage of labour, there should be increased vigilance and preparation for PPH management in obese women.

  16. Associations of maternal employment and three-generation families with pre-school children's overweight and obesity in Japan.

    Science.gov (United States)

    Watanabe, E; Lee, J S; Kawakubo, K

    2011-07-01

    Maternal employment has been shown to be associated with childhood overweight and obesity (Ow/Ob), but the presence of family members who care for children in place of the mothers might influence children's Ow/Ob and lifestyles. The influence of maternal employment on children's Ow/Ob should be examined together with the presence of caregivers such as grandparents. The effects of maternal employment and the presence of grandparents on lifestyles and Ow/Ob in Japanese pre-school children were investigated. Cross-sectional study on 2114 children aged 3-6 years who attended all childcare facilities in a city and primary caregivers was conducted. Children's weight and height, family environments (family members, maternal employment, single parent, number of siblings and parental Ow/Ob) and lifestyles (dietary, physical activity and sleeping habits) were surveyed using a self-administered questionnaire. Ow/Ob was defined by the International Obesity Task Force cut-offs. The eligible participants were 1765 children. The prevalence of Ow/Ob was 8.4% in boys and 9.9% in girls. Maternal employment was associated positively with irregular mealtimes, unfixed snacking times, bedtime after 10 p.m. and nighttime sleep duration of less than 10 h, whereas three-generation families were associated negatively with irregular mealtimes after adjustment for children's characteristics and family environments. Irregular mealtimes (OR (95% CI); 2.03 (1.36, 3.06)) and nighttime sleep duration of less than 10 h (1.96 (1.28, 3.01)) were associated with increased risks of being Ow/Ob. Both maternal employment and three-generation families were significantly associated with children's Ow/Ob. However, three-generation families maintained a significant association (1.59 (1.08, 2.35)) after adjustment for maternal employment. These study results suggest that the grandparents who care for pre-school children in place of mothers are more likely to contribute to childhood Ow/Ob than maternal

  17. Behavioral counseling to prevent childhood obesity – study protocol of a pragmatic trial in maternity and child health care

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    Mustila Taina

    2012-07-01

    Full Text Available Abstract Background Prevention is considered effective in combating the obesity epidemic. Prenatal environment may increase offspring's risk for obesity. A child starts to adopt food preferences and other behavioral habits affecting weight gain during preschool years. We report the study protocol of a pragmatic lifestyle intervention aiming at primary prevention of childhood obesity. Methods/Design A non-randomized controlled pragmatic trial in maternity and child health care clinics. The control group was recruited among families who visited the same clinics one year earlier. Eligibility criteria was mother at risk for gestational diabetes: body mass index ≥ 25 kg/m2, macrosomic newborn in any previous pregnancy, immediate family history of diabetes and/or age ≥ 40 years. All maternity clinics in town involved in recruitment. The gestational intervention consisted of individual counseling on diet and physical activity by a public health nurse, and of two group counseling sessions. Intervention continues until offspring’s age of five years. An option to participate a group counseling at child’s age 1 to 2 years was offered. The intervention includes advice on healthy diet, physical activity, sedentary behavior and sleeping pattern. The main outcome measure is offspring BMI z-score and its changes by the age of six years. Discussion Early childhood is a critical time period for prevention of obesity. Pragmatic trials targeting this period are necessary in order to find effective obesity prevention programs feasible in normal health care practice. Trial registration Clinical Trials gov NCT00970710

  18. Maternal pre-pregnancy obesity and achievement of infant motor developmental milestones in the Upstate KIDS Study

    Science.gov (United States)

    Wylie, Amanda; Sundaram, Rajeshwari; Kus, Christopher; Ghassabian, Akhgar; Yeung, Edwina H.

    2015-01-01

    Objective Maternal pre-pregnancy obesity is associated with several poor infant health outcomes; however studies that investigated motor development have been inconsistent. Thus, we examined maternal pre-pregnancy weight status and infants’ gross motor development. Design and Methods Participants consisted of 4,901 mother-infant pairs from the Upstate KIDS study, a longitudinal cohort in New York. Mothers indicated dates when infants achieved each of six gross motor milestones when infants were 4, 8, 12, 18, and 24 months old. Failure time modeling under a Weibull distribution was utilized to compare time to achievement across three levels of maternal pre-pregnancy BMI. Hazard ratios below one indicate a lower “risk” of achieving the milestone and translate to later achievement. Results Compared to infants born to thin and normal weight mothers (BMI obese mothers (BMI>30) were slower to sit without support [HR=0.91, p=0.03] and crawl on hands and knees [HR=0.86, pobesity was associated with a slightly longer time for infant to sit and crawl, potentially due to a compromised intrauterine environment or reduced physically active play. PMID:25755075

  19. Does Insulin Explain the Relation between Maternal Obesity and Poor Lactation Outcomes? An Overview of the Literature.

    Science.gov (United States)

    Nommsen-Rivers, Laurie A

    2016-03-01

    It is well established that obese women are at increased risk of delayed lactogenesis and short breastfeeding duration, but the underlying causal contributors remain unclear. This review summarizes the literature examining the role of insulin in lactation outcomes. Maternal obesity is a strong risk factor for insulin resistance and prediabetes, but until recently a direct role for insulin in milk production had not been elucidated. Over the past 6 y, studies in both animal models and humans have shown insulin-sensitive gene expression to be dramatically upregulated specifically during the lactation cycle. Insulin is now considered to play a direct role in lactation, including essential roles in secretory differentiation, secretory activation, and mature milk production. At the same time, emerging clinical research suggests an important association between suboptimal glucose tolerance and lactation difficulty. To develop effective interventions to support lactation success in obese women further research is needed to identify how, when, and for whom maternal insulin secretion and sensitivity affect lactation ability. © 2016 American Society for Nutrition.

  20. Does Insulin Explain the Relation between Maternal Obesity and Poor Lactation Outcomes? An Overview of the Literature1234

    Science.gov (United States)

    2016-01-01

    It is well established that obese women are at increased risk of delayed lactogenesis and short breastfeeding duration, but the underlying causal contributors remain unclear. This review summarizes the literature examining the role of insulin in lactation outcomes. Maternal obesity is a strong risk factor for insulin resistance and prediabetes, but until recently a direct role for insulin in milk production had not been elucidated. Over the past 6 y, studies in both animal models and humans have shown insulin-sensitive gene expression to be dramatically upregulated specifically during the lactation cycle. Insulin is now considered to play a direct role in lactation, including essential roles in secretory differentiation, secretory activation, and mature milk production. At the same time, emerging clinical research suggests an important association between suboptimal glucose tolerance and lactation difficulty. To develop effective interventions to support lactation success in obese women further research is needed to identify how, when, and for whom maternal insulin secretion and sensitivity affect lactation ability. PMID:26980825

  1. A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta.

    Science.gov (United States)

    Simon, Bailey; Bucher, Matthew; Maloyan, Alina

    2017-09-27

    Maternal obesity is associated with an increased risk of adverse perinatal outcomes that are likely mediated by compromised placental function that can be attributed to, in part, the dysregulation of autophagy. Aberrant changes in the expression of autophagy regulators in the placentas from obese pregnancies may be regulated by inflammatory processes associated with both obesity and pregnancy. Described here is a protocol for sampling of villous tissue and isolation of villous cytotrophoblasts from the term human placenta for primary cell culture. This is followed by a method for simulating the inflammatory milieu in the obese intrauterine environment by treating primary trophoblasts from lean pregnancies with tumor necrosis factor alpha (TNFα), a proinflammatory cytokine that is elevated in obesity and in pregnancy. Through the implementation of the protocol described here, it is found that exposure to exogenous TNFα regulates the expression of Rubicon, a negative regulator of autophagy, in trophoblasts from lean pregnancies with female fetuses. While a variety of biological factors in the obese intrauterine environment maintain the potential to modulate critical pathways in trophoblasts, this ex vivo system is especially useful for determining if expression patterns observed in vivo in human placentas with maternal obesity are a direct result of TNFα signaling. Ultimately, this approach affords the opportunity to parse out the regulatory and molecular implications of inflammation associated with maternal obesity on autophagy and other critical cellular pathways in trophoblasts that have the potential to impact placental function.

  2. Existing maternal obesity guidelines may increase inequalities between ethnic groups: a national epidemiological study of 502,474 births in England.

    Science.gov (United States)

    Heslehurst, Nicola; Sattar, Naveed; Rajasingam, Daghni; Wilkinson, John; Summerbell, Carolyn D; Rankin, Judith

    2012-12-18

    Asians are at increased risk of morbidity at a lower body mass index (BMI) than European Whites, particularly relating to metabolic risk. UK maternal obesity guidelines use general population BMI criteria to define obesity, which do not represent the risk of morbidity among Asian populations. This study compares incidence of first trimester obesity using Asian-specific and general population BMI criteria. A retrospective epidemiological study of 502,474 births between 1995 and 2007, from 34 maternity units across England. Data analyses included a comparison of trends over time between ethnic groups using Asian-specific and general population BMI criteria. Logistic regression estimated odds ratios for first trimester obesity among ethnic groups following adjustment for population demographics. Black and South Asian women have a higher incidence of first trimester obesity compared with White women. This is most pronounced for Pakistani women following adjustment for population structure (OR 2.19, 95% C.I. 2.08, 2.31). There is a twofold increase in the proportion of South Asian women classified as obese when using the Asian-specific BMI criteria rather than general population BMI criteria. The incidence of obesity among Black women is increasing at the most rapid rate over time (p=0.01). The twofold increase in maternal obesity among South Asians when using Asian-specific BMI criteria highlights inequalities among pregnant women. A large proportion of South Asian women are potentially being wrongly assigned to low risk care using current UK guidelines to classify obesity and determine care requirements. Further research is required to identify if there is any improvement in pregnancy outcomes if Asian-specific BMI criteria are utilised in the clinical management of maternal obesity to ensure the best quality of care is provided for women irrespective of ethnicity.

  3. Existing maternal obesity guidelines may increase inequalities between ethnic groups: a national epidemiological study of 502,474 births in England

    Directory of Open Access Journals (Sweden)

    Heslehurst Nicola

    2012-12-01

    Full Text Available Abstract Background Asians are at increased risk of morbidity at a lower body mass index (BMI than European Whites, particularly relating to metabolic risk. UK maternal obesity guidelines use general population BMI criteria to define obesity, which do not represent the risk of morbidity among Asian populations. This study compares incidence of first trimester obesity using Asian-specific and general population BMI criteria. Method A retrospective epidemiological study of 502,474 births between 1995 and 2007, from 34 maternity units across England. Data analyses included a comparison of trends over time between ethnic groups using Asian-specific and general population BMI criteria. Logistic regression estimated odds ratios for first trimester obesity among ethnic groups following adjustment for population demographics. Results Black and South Asian women have a higher incidence of first trimester obesity compared with White women. This is most pronounced for Pakistani women following adjustment for population structure (OR 2.19, 95% C.I. 2.08, 2.31. There is a twofold increase in the proportion of South Asian women classified as obese when using the Asian-specific BMI criteria rather than general population BMI criteria. The incidence of obesity among Black women is increasing at the most rapid rate over time (p=0.01. Conclusion The twofold increase in maternal obesity among South Asians when using Asian-specific BMI criteria highlights inequalities among pregnant women. A large proportion of South Asian women are potentially being wrongly assigned to low risk care using current UK guidelines to classify obesity and determine care requirements. Further research is required to identify if there is any improvement in pregnancy outcomes if Asian-specific BMI criteria are utilised in the clinical management of maternal obesity to ensure the best quality of care is provided for women irrespective of ethnicity.

  4. Maternal depression, stress and feeding styles: towards a framework for theory and research in child obesity

    Science.gov (United States)

    Against the background of rising rates of obesity in children and adults in the USA, and modest effect sizes for obesity interventions, the aim of the present narrative review paper is to extend the UNICEF care model to focus on childhood obesity and its associated risks with an emphasis on the emot...

  5. Maternal-infant relationship quality and risk of obesity at age 5.5 years in a national US cohort

    Science.gov (United States)

    2014-01-01

    Background Poor quality relationships between mothers and toddlers have been associated with higher risk for childhood obesity, but few prospective studies of obesity have assessed maternal-child relationship quality in infancy. In addition it is not known whether the increased risk is associated with the mother’s or the child’s contribution to the relationship quality. Methods We analyzed data (n = 5650) from the Early Childhood Longitudinal Study, Birth Cohort, a national study of U.S. children born in 2001 and followed until they entered kindergarten. At 9 months of age, the Nursing Child Assessment Teaching Scale (NCATS) was used to assess the quality of observed playtime interactions between mothers and infants, yielding separate scores for maternal and infant behaviors. Obesity (BMI ≥95th percentile) at age 5.5 years was based on measured weight and height. Results The prevalence (95% confidence interval) of obesity at 5.5 years of age was higher among children in the lowest quartile of maternal NCATS score (20.2% [95% CI: 17.2%, 23.2%]) than in the highest quartile (13.9% [11.3%, 16.5%]), but maternal NCATS score was not significantly associated with obesity after adjustment for race/ethnicity, maternal education and household income. The prevalence of obesity at 5.5 years of age was similar among children in the lowest quartile of infant NCATS score (17.4% [14.4%, 20.3%]) and in the highest quartile (17.6% 14.4%, 20.8%]), and was not changed with covariate adjustment. Conclusions Maternal-infant relationship quality, assessed by direct observation at 9 months of age in a national sample, was not associated with an increased risk of obesity at age 5.5 years after controlling for sociodemographic characteristics. PMID:24564412

  6. Dietary patterns are associated with child, maternal and household-level characteristics and overweight/obesity among young Samoan children.

    Science.gov (United States)

    Choy, Courtney C; Wang, Dongqing; Baylin, Ana; Soti-Ulberg, Christina; Naseri, Take; Reupena, Muagututia S; Thompson, Avery A; Duckham, Rachel L; Hawley, Nicola L

    2018-05-01

    Among young Samoan children, diet may not be optimal: in 2015, 16·1 % of 24-59-month-olds were overweight/obese, 20·3 % stunted and 34·1 % anaemic. The present study aimed to identify dietary patterns among 24-59-month-old Samoan children and evaluate their association with: (i) child, maternal and household characteristics; and (ii) nutritional status indicators (stunting, overweight/obesity, anaemia). A community-based, cross-sectional study. Principal component analysis on 117 FFQ items was used to identify empirical dietary patterns. Distributions of child, maternal and household characteristics were examined by factor score quintiles. The regression of nutritional status indicators v. these quintiles was performed using logistic regression models. Ten villages on the Samoan island of Upolu. A convenience sample of mother-child pairs (n 305). Two dietary patterns, modern and neo-traditional, emerged. The modern pattern was loaded with 'westernized' foods (red meat, condiments and snacks). The neo-traditional pattern included vegetables, local starches, coconuts, fish and poultry. Following the modern diet was associated with urban residence, greater maternal educational attainment, higher socio-economic status, lower vitamin C intake and higher sugar intake. Following the neo-traditional diet was associated with rural residence, lower socio-economic status, higher vitamin C intake and lower sugar intake. While dietary patterns were not related to stunting or anaemia, following the neo-traditional pattern was positively associated with child overweight/obesity (adjusted OR=4·23, 95 % CI 1·26, 14·17, for the highest quintile, P-trend=0·06). Further longitudinal monitoring and evaluation of early childhood growth and development are needed to understand the influences of early diet on child health in Samoa.

  7. Maternal underweight and obesity and risk of orofacial clefts in a large international consortium of population-based studies.

    Science.gov (United States)

    Kutbi, Hebah; Wehby, George L; Moreno Uribe, Lina M; Romitti, Paul A; Carmichael, Suzan; Shaw, Gary M; Olshan, Andrew F; DeRoo, Lisa; Rasmussen, Sonja A; Murray, Jeffrey C; Wilcox, Allen; Lie, Rolv T; Munger, Ronald G

    2017-02-01

    Evidence on association of maternal pre-pregnancy weight with risk of orofacial clefts is inconsistent. Six large case-control studies of orofacial clefts from Northern Europe and the USA were included in analyses pooling individual-level data. Cases included 4943 mothers of children with orofacial clefts (cleft lip only: 1135, cleft palate with cleft lip: 2081, cleft palate only: 1727) and controls included 10 592 mothers of unaffected children. Association of orofacial cleft risk with pre-pregnancy maternal weight classified by level of body mass index (BMI, kg/m 2 ) was evaluated using logistic regression adjusting for multiple covariates. Cleft palate, both alone and with cleft lip (CP+/-CL), was associated with maternal class II+ pre-pregnancy obesity (≥ 35)compared with normal weight [adjusted odds ratio (aOR) = 1.36; 95% confidence interval (CI) = 1.16, 1.58]. CP+/-CL was marginally associated with maternal underweight (aOR = 1.16; 95% CI = 0.98, 1.36). Cleft lip alone was not associated with BMI. In this largest population-based study to date, we found an increased risk of cleft palate, with or without cleft lip, in class II+ obese mothers compared with normal-weight mothers; underweight mothers may also have an increased risk, but this requires further study. These results also suggest that extremes of weight may have a specific effect on palatal development. © The Author 2016; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association

  8. Changing perspectives in pre-existing diabetes and obesity in pregnancy: maternal and infant short- and long-term outcomes.

    Science.gov (United States)

    Barbour, Linda A

    2014-08-01

    Climbing obesity rates in women have propelled the increasing prevalence of type 2 diabetes mellitus (T2DM) in pregnancy, and an increasing number of women with type 1 diabetes mellitus (T1DM) are also affected by obesity. Increasing recognition that an intrauterine environment characterized by obesity, insulin resistance, nutrient excess, and diabetes may be fueling the obesity epidemic in children has created enormous pressure to re-examine the conventional wisdom of our current approaches. Compelling data in pregnancies complicated by diabetes, in particular those accompanied by insulin resistance and obesity, support a fetal programming effect resulting in increased susceptibility to metabolic disease for the offspring later in life. Recent data also underscore the contribution of obesity, lipids, and lesser degrees of hyperglycemia on fetal fat accretion, challenging the wisdom of current gestational weight gain recommendations with and without diabetes. The risks of adverse pregnancy outcomes in T2DM are at least as high as in T1DM and there remains controversy about the ideal glucose treatment targets, the benefit of different insulin analogues, and the role of continuous glucose monitoring in T1DM and T2DM. It has become unmistakably evident that achieving optimal outcomes in mothers with diabetes is clearly impacted by ideal glycemic control but goes far beyond it. The intrauterine metabolic environment seems to have long-term implications on the future health of the offspring so that the effectiveness of our current approaches can no longer be simply measured by whether or not maternal glucose values are at goal.

  9. An evaluation of the implementation of maternal obesity pathways of care: a mixed methods study with data integration.

    Directory of Open Access Journals (Sweden)

    Nicola Heslehurst

    Full Text Available Maternal obesity has multiple associated risks and requires substantial intervention. This research evaluated the implementation of maternal obesity care pathways from multiple stakeholder perspectives.A simultaneous mixed methods model with data integration was used. Three component studies were given equal priority. 1: Semi-structured qualitative interviews explored obese pregnant women's experiences of being on the pathways. 2: A quantitative and qualitative postal survey explored healthcare professionals' experiences of delivering the pathways. 3: A case note audit quantitatively assessed pathway compliance. Data were integrated using following a thread and convergence coding matrix methods to search for agreement and disagreement between studies.Study 1: Four themes were identified: women's overall (positive and negative views of the pathways; knowledge and understanding of the pathways; views on clinical and weight management advice and support; and views on the information leaflet. Key results included positive views of receiving additional clinical care, negative experiences of risk communication, and weight management support was considered a priority. Study 2: Healthcare professionals felt the pathways were worthwhile, facilitated good practice, and increased confidence. Training was consistently identified as being required. Healthcare professionals predominantly focussed on women's response to sensitive obesity communication. Study 3: There was good compliance with antenatal clinical interventions. However, there was poor compliance with public health and postnatal interventions. There were some strong areas of agreement between component studies which can inform future development of the pathways. However, disagreement between studies included a lack of shared priorities between healthcare professionals and women, different perspectives on communication issues, and different perspectives on women's prioritisation of weight

  10. An Evaluation of the Implementation of Maternal Obesity Pathways of Care: A Mixed Methods Study with Data Integration

    Science.gov (United States)

    Heslehurst, Nicola; Dinsdale, Sarah; Sedgewick, Gillian; Simpson, Helen; Sen, Seema; Summerbell, Carolyn Dawn; Rankin, Judith

    2015-01-01

    Objectives Maternal obesity has multiple associated risks and requires substantial intervention. This research evaluated the implementation of maternal obesity care pathways from multiple stakeholder perspectives. Study Design A simultaneous mixed methods model with data integration was used. Three component studies were given equal priority. 1: Semi-structured qualitative interviews explored obese pregnant women’s experiences of being on the pathways. 2: A quantitative and qualitative postal survey explored healthcare professionals’ experiences of delivering the pathways. 3: A case note audit quantitatively assessed pathway compliance. Data were integrated using following a thread and convergence coding matrix methods to search for agreement and disagreement between studies. Results Study 1: Four themes were identified: women’s overall (positive and negative) views of the pathways; knowledge and understanding of the pathways; views on clinical and weight management advice and support; and views on the information leaflet. Key results included positive views of receiving additional clinical care, negative experiences of risk communication, and weight management support was considered a priority. Study 2: Healthcare professionals felt the pathways were worthwhile, facilitated good practice, and increased confidence. Training was consistently identified as being required. Healthcare professionals predominantly focussed on women’s response to sensitive obesity communication. Study 3: There was good compliance with antenatal clinical interventions. However, there was poor compliance with public health and postnatal interventions. There were some strong areas of agreement between component studies which can inform future development of the pathways. However, disagreement between studies included a lack of shared priorities between healthcare professionals and women, different perspectives on communication issues, and different perspectives on women

  11. Impact of lifestyle intervention for obese women during pregnancy on maternal metabolic and inflammatory markers

    DEFF Research Database (Denmark)

    Renault, K. M.; Carlsen, E. M.; Hædersdal, S.

    2017-01-01

    Background:Offspring of obese mothers have increased risk of developing obesity and related short- and long-term disease. The cause is multifactorial and may partly be explained by the unfavorable intrauterine environment. Intervention during pregnancy leading to a healthier lifestyle among obese...... women can reduce hsCRP representing a marker of inflammation during pregnancy. The effect may partly be mediated by more physical activity and partly by changes in intake of carbohydrates and the glycaemic load....

  12. Impact of maternal obesity on the metabolic profiles of pregnant women and their offspring at birth

    OpenAIRE

    Desert , Romain; Canlet , Cécile; Costet , Nathalie; Cordier , Sylvaine; Bonvallot , Nathalie

    2015-01-01

    International audience; Obesity is currently an increasing public health problem. The intra-uterine environment plays a critical role in foetal development. The objective of this study is to investigate the association of obesity with modifications in the metabolic profiles of pregnant women, and their new-borns. Based on the PELAGIE cohort (Brittany, France), a sample of 321 pregnant women was divided into three groups according to their body mass index (BMI) (normal, over-weight and obese)....

  13. Impact of maternal obesity on inhaled corticosteroid use in childhood: a registry based analysis of first born children and a sibling pair analysis.

    Directory of Open Access Journals (Sweden)

    Adrian J Lowe

    Full Text Available BACKGROUND: It has been proposed that maternal obesity during pregnancy may increase the risk that the child develops allergic disease and asthma, although the mechanisms underpinning this relationship are currently unclear. We sought to assess if this association may be due to confounding by genetic or environmental risk factors that are common to maternal obesity and childhood asthma, using a sibling pair analysis. METHODS: The study population comprised a Swedish national cohort of term children born between 1992 and 2008 to native Swedish parents. Maternal body mass index (BMI was measured at 8-10 weeks gestation. Unconditional logistic regression models were used to determine if maternal obesity was associated with increased risk of inhaled corticosteroid (ICS in 431,718 first-born children, while adjusting for potential confounders. An age-matched discordant sib-pair analysis was performed, taking into account shared genetic and environmental risk factors. RESULTS: Maternal over-weight and obesity were associated with increased risk that the child would require ICS (for BMI≥35 kg/m(2, aOR = 1.30, 95%CI = 1.10-1.52 compared with normal weight mothers in children aged 6-12 years. Similar effects were seen in younger children, but in children aged 13-16 years, maternal obesity (BMI≥30 was related to increased risk of ICS use in girls (aOR = 1.28, 95%CI = 1.07-1.53 but not boys (OR = 1.05, 95%CI = 0.87-1.26. The sib-pair analysis, which included 2,034 sib-pairs older than six years who were discordant for both ICS use and maternal BMI category, failed to find any evidence that increasing maternal weight was related to increased risk of ICS use. CONCLUSION: Maternal obesity is associated with increased risk of childhood ICS use up to approximately 12 years of age, but only in girls after this age. These effects could not be confirmed in a sib pair analysis, suggesting either limited statistical power, or the effects

  14. Maternal malnutrition and offspring sex determine juvenile obesity and metabolic disorders in a swine model of leptin resistance.

    Directory of Open Access Journals (Sweden)

    Alicia Barbero

    Full Text Available The present study aimed to determine, in a swine model of leptin resistance, the effects of type and timing of maternal malnutrition on growth patterns, adiposity and metabolic features of the progeny when exposed to an obesogenic diet during their juvenile development and possible concomitant effects of the offspring sex. Thus, four groups were considered. A CONTROL group involved pigs born from sows fed with a diet fulfilling their daily maintenance requirements for pregnancy. The treated groups involved the progeny of females fed with the same diet but fulfilling either 160% or 50% of pregnancy requirements during the entire gestation (OVERFED and UNDERFED, respectively or 100% of requirements until Day 35 of pregnancy and 50% of such amount from Day 36 onwards (LATE-UNDERFED. OVERFED and UNDERFED offspring were more prone to higher corpulence and fat deposition from early postnatal stages, during breast-feeding; adiposity increased significantly when exposed to obesogenic diets, especially in females. The effects of sex were even more remarkable in LATE-UNDERFED offspring, which had similar corpulence to CONTROL piglets; however, females showed a clear predisposition to obesity. Furthermore, the three groups of pigs with maternal malnutrition showed evidences of metabolic syndrome and, in the case of individuals born from OVERFED sows, even of insulin resistance and the prodrome of type-2 diabetes. These findings support the main role of early nutritional programming in the current rise of obesity and associated diseases in ethnics with leptin resistance.

  15. Pragmatic controlled trial to prevent childhood obesity in maternity and child health care clinics: pregnancy and infant weight outcomes (The VACOPP Study)

    OpenAIRE

    Mustila, Taina; Raitanen, Jani; Keskinen, P?ivi; Saari, Antti; Luoto, Riitta

    2013-01-01

    Background According to current evidence, the prevention of obesity should start early in life. Even the prenatal environment may expose a child to unhealthy weight gain; maternal gestational diabetes is known to be among the prenatal risk factors conducive to obesity. Here we report the effects of antenatal dietary and physical activity counselling on pregnancy and infant weight gain outcomes. Methods The study was a non-randomised controlled pragmatic trial aiming to prevent childhood obesi...

  16. Maternal BMI and migration status as predictors of childhood obesity in Mexico IMC materno y migración como predictor de obesidad infantil de México

    OpenAIRE

    A. Jiménez-Cruz; J. M. Wojcicki; M. Bacardí-Gascón; A. Castellón-Zaragoza; J. L. García-Gallardo; N. Schwartz; M. B. Heyman

    2011-01-01

    Objective: To assess the association of maternal migration to Baja California, body mass index (BMI) status, children's perceived food insecurity, and childhood lifestyle behaviors with overweight (BMI > 85% ile), obesity (BMI > 95% ile) and abdominal obesity (Waist Circumference > 90% ile). Methods: Convenience sampling methods were used to recruit a cross-sectional sample of 4th, 5th and 6th grade children and their parents at Tijuana and Tecate Public Schools. Children's and parents' weigh...

  17. Maternal omega-3 fatty acids regulate offspring obesity through persistent modulation of gut microbiota.

    Science.gov (United States)

    Robertson, Ruairi C; Kaliannan, Kanakaraju; Strain, Conall R; Ross, R Paul; Stanton, Catherine; Kang, Jing X

    2018-05-24

    The early-life gut microbiota plays a critical role in host metabolism in later life. However, little is known about how the fatty acid profile of the maternal diet during gestation and lactation influences the development of the offspring gut microbiota and subsequent metabolic health outcomes. Here, using a unique transgenic model, we report that maternal endogenous n-3 polyunsaturated fatty acid (PUFA) production during gestation or lactation significantly reduces weight gain and markers of metabolic disruption in male murine offspring fed a high-fat diet. However, maternal fatty acid status appeared to have no significant effect on weight gain in female offspring. The metabolic phenotypes in male offspring appeared to be mediated by comprehensive restructuring of gut microbiota composition. Reduced maternal n-3 PUFA exposure led to significantly depleted Epsilonproteobacteria, Bacteroides, and Akkermansia and higher relative abundance of Clostridia. Interestingly, offspring metabolism and microbiota composition were more profoundly influenced by the maternal fatty acid profile during lactation than in utero. Furthermore, the maternal fatty acid profile appeared to have a long-lasting effect on offspring microbiota composition and function that persisted into adulthood after life-long high-fat diet feeding. Our data provide novel evidence that weight gain and metabolic dysfunction in adulthood is mediated by maternal fatty acid status through long-lasting restructuring of the gut microbiota. These results have important implications for understanding the interaction between modern Western diets, metabolic health, and the intestinal microbiome.

  18. Maternal obesity and gestational weight gain are risk factors for infant death.

    Science.gov (United States)

    Bodnar, Lisa M; Siminerio, Lara L; Himes, Katherine P; Hutcheon, Jennifer A; Lash, Timothy L; Parisi, Sara M; Abrams, Barbara

    2016-02-01

    Assessment of the joint and independent relationships of gestational weight gain and prepregnancy body mass index (BMI) on risk of infant mortality was performed. This study used Pennsylvania linked birth-infant death records (2003-2011) from infants without anomalies born to mothers with prepregnancy BMI categorized as underweight (n = 58,973), normal weight (n = 610,118), overweight (n = 296,630), grade 1 obesity (n = 147,608), grade 2 obesity (n = 71,740), and grade 3 obesity (n = 47,277). Multivariable logistic regression models stratified by BMI category were used to estimate dose-response associations between z scores of gestational weight gain and infant death after confounder adjustment. Infant mortality risk was lowest among normal-weight women and increased with rising BMI category. For all BMI groups except for grade 3 obesity, there were U-shaped associations between gestational weight gain and risk of infant death. Weight loss and very low weight gain among women with grades 1 and 2 obesity were associated with high risks of infant mortality. However, even when gestational weight gain in women with obesity was optimized, the predicted risk of infant death remained higher than that of normal-weight women. Interventions aimed at substantially reducing preconception weight among women with obesity and avoiding very low or very high gestational weight gain may reduce risk of infant death. © 2015 The Obesity Society.

  19. Central role for Melanocortin-4 receptors in offspring hypertension arising from maternal obesity

    NARCIS (Netherlands)

    Samuelsson, Anne Maj S; Mullier, Amandine; Maicas, Nuria; Oosterhuis, Nynke R.; Bae, Sung Eun; Novoselova, Tatiana V.; Chan, Li F.; Pombo, Joaquim M.; Taylor, Paul D.; Joles, Jaap A.; Coen, Clive W.; Balthasar, Nina; Poston, Lucilla

    2016-01-01

    Melanocortin-4 receptor (Mc4r)-expressing neurons in the autonomic nervous system, particularly in the paraventricular nucleus of the hypothalamus (PVH), play an essential role in blood pressure (BP) control. Mc4r-deficient (Mc4rKO) mice are severely obese but lack obesity-related hypertension; they

  20. Melatonin protects against maternal obesity-associated oxidative stress and meiotic defects in oocytes via the SIRT3-SOD2-dependent pathway.

    Science.gov (United States)

    Han, Longsen; Wang, Haichao; Li, Ling; Li, Xiaoyan; Ge, Juan; Reiter, Russel J; Wang, Qiang

    2017-10-01

    Maternal obesity in humans is associated with poor outcomes across the reproductive spectrum. Emerging evidence indicates that these defects are likely attributed to factors within the oocyte. Although various molecules and pathways may contribute to impaired oocyte quality, prevention of fertility issues associated with maternal obesity is a challenge. Using mice fed a high-fat diet (HFD) as an obesity model, we document spindle disorganization, chromosome misalignment, and elevated reactive oxygen species (ROS) levels in oocytes from obese mice. Oral administration of melatonin to HFD mice not only reduces ROS generation, but also prevents spindle/chromosome anomalies in oocytes, consequently promoting the developmental potential of early embryos. Consistent with this finding, we find that melatonin supplement during in vitro maturation also markedly attenuates oxidative stress and meiotic defects in HFD oocytes. Finally, by performing morpholino knockdown and acetylation-mimetic mutant overexpression assays, we reveal that melatonin ameliorates maternal obesity-induced defective phenotypes in oocytes through the SIRT3-SOD2-dependent mechanism. In sum, our data uncover the marked beneficial effects of melatonin on oocyte quality from obese females; this opens a new area for optimizing culture system as well as fertility management. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  1. Maternal obesity accelerates fetal pancreatic beta-cell but not alpha-cell development in sheep: prenatal consequences.

    Science.gov (United States)

    Ford, Stephen P; Zhang, Liren; Zhu, Meijun; Miller, Myrna M; Smith, Derek T; Hess, Bret W; Moss, Gary E; Nathanielsz, Peter W; Nijland, Mark J

    2009-09-01

    Maternal obesity affects offspring weight, body composition, and organ function, increasing diabetes and metabolic syndrome risk. We determined effects of maternal obesity and a high-energy diet on fetal pancreatic development. Sixty days prior to breeding, ewes were assigned to control [100% of National Research Council (NRC) recommendations] or obesogenic (OB; 150% NRC) diets. At 75 days gestation, OB ewes exhibited elevated insulin-to-glucose ratios at rest and during a glucose tolerance test, demonstrating insulin resistance compared with control ewes. In fetal studies, ewes ate their respective diets from 60 days before to 75 days after conception when animals were euthanized under general anesthesia. OB and control ewes increased in body weight by approximately 43% and approximately 6%, respectively, from diet initiation until necropsy. Although all organs were heavier in fetuses from OB ewes, only pancreatic weight increased as a percentage of fetal weight. Blood glucose, insulin, and cortisol were elevated in OB ewes and fetuses on day 75. Insulin-positive cells per unit pancreatic area were 50% greater in fetuses from OB ewes as a result of increased beta-cell mitoses rather than decreased programmed cell death. Lambs of OB ewes were born earlier but weighed the same as control lambs; however, their crown-to-rump length was reduced, and their fat mass was increased. We conclude that increased systemic insulin in fetuses from OB ewes results from increased glucose exposure and/or cortisol-induced accelerated fetal beta-cell maturation and may contribute to premature beta-cell function loss and predisposition to obesity and metabolic disease in offspring.

  2. Impact of Maternal Glucose and Gestational Weight Gain on Child Obesity over the First Decade of Life in Normal Birth Weight Infants.

    Science.gov (United States)

    Hillier, Teresa A; Pedula, Kathryn L; Vesco, Kimberly K; Oshiro, Caryn E S; Ogasawara, Keith K

    2016-08-01

    Objective To determine, among children with normal birth weight, if maternal hyperglycemia and weight gain independently increase childhood obesity risk in a very large diverse population. Methods Study population was 24,141 individuals (mothers and their normal birth weight offspring, born 1995-2003) among a diverse population with universal GDM screening [50-g glucose-challenge test (GCT); 3 h. 100 g oral glucose tolerance test (OGTT) if GCT+]. Among the 13,037 full-term offspring with normal birth weight (2500-4000 g), annual measured height/weight was ascertained between ages 2 and 10 years to calculate gender-specific BMI-for-age percentiles using USA norms (1960-1995 standard). Results Among children who began life with normal birth weight, we found a significant trend for developing both childhood overweight (>85 %ile) and obesity (>95 %ile) during the first decade of life with both maternal hyperglycemia (normal GCT, GCT+ but no GDM, GDM) and excessive gestational weight gain [>40 pounds (18.1 kg)]; p maternal glucose and/or weight gain effects to imprint for childhood obesity in the first decade remained after adjustment for potential confounders including maternal age, parity, as well as pre-pregnancy BMI. The attributable risk (%) for childhood obesity was 28.5 % (95 % CI 15.9-41.1) for GDM and 16.4 % (95 % CI 9.4-23.2) for excessive gestational weight gain. Conclusions for Practice Both maternal hyperglycemia and excessive weight gain have independent effects to increase childhood obesity risk. Future research should focus on prevention efforts during pregnancy as a potential window of opportunity to reduce childhood obesity.

  3. A Study on Mediation by Offspring BMI in the Association between Maternal Obesity and Child Respiratory Outcomes in the Amsterdam Born and Their Development Study Cohort.

    Science.gov (United States)

    Harskamp-van Ginkel, Margreet W; London, Stephanie J; Magnus, Maria C; Gademan, Maaike G; Vrijkotte, Tanja G

    2015-01-01

    A causal relationship between maternal obesity and offspring asthma is hypothesized to begin during early development, but no underlying mechanism for the found association is identified. We quantitatively examined mediation by offspring body mass index (BMI) in the association of maternal pre-pregnancy BMI on risk of asthma and wheezing during the first 7-8 years of life in a large Amsterdam born birth cohort. For 3185 mother-child pairs, mothers reported maternal pre-pregnancy BMI and offspring outcomes "ever being diagnosed with asthma" and "wheezing in the past 12 months" on questionnaires. We measured offspring height and weight at age 5-6 years. We performed a multivariate log linear regression comparing outcomes in offspring of mothers with different BMI categories. For each category we quantified and tested mediation by offspring BMI and also investigated interaction by parental asthma. At the age of 7-8 years, 8% of the offspring ever had asthma and 7% had current wheezing. Maternal pre-pregnancy obesity was associated with higher risks of asthma (adjusted RR 2.32 (95% CI: 1.49-3.61) and wheezing (adjusted RR 2.16 (95% CI: 1.28-3.64). Offspring BMI was a mediator in the association between maternal BMI and offspring wheezing, but not for asthma. There was no interaction by parental asthma. Maternal pre-pregnancy obesity was associated with higher risks of offspring asthma and wheezing. The association between maternal obesity and offspring wheezing was both direct and indirect (mediated) through the child's own BMI.

  4. Effect of Maternal Obesity on Foetal Growth and Metabolic Health of the Offspring

    Directory of Open Access Journals (Sweden)

    Claudio Maffeis

    2017-04-01

    Full Text Available Maternal and placental conditions that are unfavourable for the embryo/foetus have long-lasting effects on different tissues and functions of the body, which may persist for life and, potentially, also be transmitted to the offspring. This review resumes current evidence on principle maternal and gestational conditions associated with unfavourable metabolic programming of the offspring, along with their mechanisms of action, either supposed or already proved.

  5. Maternal depression, stress and feeding styles: towards a framework for theory and research in child obesity.

    Science.gov (United States)

    El-Behadli, Ana F; Sharp, Carla; Hughes, Sheryl O; Obasi, Ezemenari M; Nicklas, Theresa A

    2015-01-01

    Against the background of rising rates of obesity in children and adults in the USA, and modest effect sizes for obesity interventions, the aim of the present narrative review paper is to extend the UNICEF care model to focus on childhood obesity and its associated risks with an emphasis on the emotional climate of the parent-child relationship within the family. Specifically, we extended the UNICEF model by applying the systems approach to childhood obesity and by combining previously unintegrated sets of literature across multiple disciplines including developmental psychology, clinical psychology and nutrition. Specifically, we modified the extended care model by explicitly integrating new linkages (i.e. parental feeding styles, stress, depression and mother's own eating behaviour) that have been found to be associated with the development of children's eating behaviours and risk of childhood obesity. These new linkages are based on studies that were not incorporated into the original UNICEF model, but suggest important implications for childhood obesity. In all, this narrative review offers important advancements to the scientific understanding of familial influences on children's eating behaviours and childhood obesity.

  6. Macrophage Populations in Visceral Adipose Tissue from Pregnant Women: Potential Role of Obesity in Maternal Inflammation

    Directory of Open Access Journals (Sweden)

    Eyerahi Bravo-Flores

    2018-04-01

    Full Text Available Obesity is associated with inflammatory changes and accumulation and phenotype polarization of adipose tissue macrophages (ATMs. Obese pregnant women have alterations in adipose tissue composition, but a detailed description of macrophage population is not available. In this study, we characterized macrophage populations in visceral adipose tissue (VAT from pregnant women with normal, overweight, and obese pregestational weight. Immunophenotyping of macrophages from VAT biopsies was performed by flow cytometry using CD45 and CD14 as markers of hematopoietic and monocyte linage, respectively, while HLA-DR, CD11c, CD163, and CD206 were used as pro- and anti-inflammatory markers. Adipocyte number and size were evaluated by light microscopy. The results show that pregnant women that were overweight and obese during the pregestational period had adipocyte hypertrophy. Two different macrophage populations in VAT were identified: recruited macrophages (CD45+CD14+, and a novel population lacking CD45, which was considered to be a resident macrophages subset (CD45−CD14+. The number of resident HLA−DRlow/− macrophages showed a negative correlation with body mass index (BMI. Both resident and recruited macrophages from obese women expressed higher CD206 levels. CD11c expression was higher in resident HLA-DR+ macrophages from obese women. A strong correlation between CD206 and CD11c markers and BMI was observed. Our findings show that being overweight and obese in the pregestational period is associated with adipocyte hypertrophy and specific ATMs populations in VAT.

  7. Severe maternal stress exposure due to bereavement before, during and after pregnancy and risk of overweight and obesity in young adult men: a Danish National Cohort Study.

    Directory of Open Access Journals (Sweden)

    Lena Hohwü

    Full Text Available BACKGROUND: Perinatal stress may programme overweight and obesity. We examined whether maternal pre- and post-natal bereavement was associated with overweight and obesity in young men. METHODS: A cohort study was conducted including 119,908 men born from 1976 to 1993 and examined for military service between 2006 and 2011. Among them, 4,813 conscripts were born to mothers bereaved by death of a close relative from 12 months preconception to birth of the child (exposed group. Median body mass index (BMI and prevalence of overweight and obesity were estimated. Odds ratio of overweight (BMI≥25 kg/m2 and obesity (BMI≥30 kg/m2 were estimated by logistic regression analysis adjusted for maternal educational level. RESULTS: Median BMI was similar in the exposed and the unexposed group but the prevalence of overweight (33.3% versus 30.4%, p = 0.02 and obesity (9.8% versus 8.5%, p = 0.06 was higher in the exposed group. Conscripts exposed 6 to 0 months before conception and during pregnancy had a higher risk of overweight (odds ratio 1.15, 95% confidence interval (CI: 1.03; 1.27 and odds ratio 1.13, 95% CI: 1.03; 1.25, respectively. Conscripts born to mothers who experienced death of the child's biological father before child birth had a two-fold risk of obesity (odds ratio 2.00, 95% CI: 0.93; 4.31. There was no elevated risk in those who experienced maternal bereavement postnatally. CONCLUSION: Maternal bereavement during the prenatal period was associated with increased risk of overweight or obesity in a group of young male conscripts, and this may possibly be reflected to severe stress exposure early in life. However, not all associations were clear, and further studies are warranted.

  8. Severe maternal stress exposure due to bereavement before, during and after pregnancy and risk of overweight and obesity in young adult men: a Danish National Cohort Study.

    Science.gov (United States)

    Hohwü, Lena; Li, Jiong; Olsen, Jørn; Sørensen, Thorkild I A; Obel, Carsten

    2014-01-01

    Perinatal stress may programme overweight and obesity. We examined whether maternal pre- and post-natal bereavement was associated with overweight and obesity in young men. A cohort study was conducted including 119,908 men born from 1976 to 1993 and examined for military service between 2006 and 2011. Among them, 4,813 conscripts were born to mothers bereaved by death of a close relative from 12 months preconception to birth of the child (exposed group). Median body mass index (BMI) and prevalence of overweight and obesity were estimated. Odds ratio of overweight (BMI≥25 kg/m2) and obesity (BMI≥30 kg/m2) were estimated by logistic regression analysis adjusted for maternal educational level. Median BMI was similar in the exposed and the unexposed group but the prevalence of overweight (33.3% versus 30.4%, p = 0.02) and obesity (9.8% versus 8.5%, p = 0.06) was higher in the exposed group. Conscripts exposed 6 to 0 months before conception and during pregnancy had a higher risk of overweight (odds ratio 1.15, 95% confidence interval (CI): 1.03; 1.27 and odds ratio 1.13, 95% CI: 1.03; 1.25, respectively). Conscripts born to mothers who experienced death of the child's biological father before child birth had a two-fold risk of obesity (odds ratio 2.00, 95% CI: 0.93; 4.31). There was no elevated risk in those who experienced maternal bereavement postnatally. Maternal bereavement during the prenatal period was associated with increased risk of overweight or obesity in a group of young male conscripts, and this may possibly be reflected to severe stress exposure early in life. However, not all associations were clear, and further studies are warranted.

  9. Maternal gestational smoking, diabetes, alcohol drinking, pre-pregnancy obesity and the risk of cryptorchidism: a systematic review and meta-analysis of observational studies.

    Directory of Open Access Journals (Sweden)

    Lin Zhang

    Full Text Available Maternal gestational smoking, diabetes, alcohol drinking, and pre-pregnancy obesity are thought to increase the risk of cryptorchidism in newborn males, but the evidence is inconsistent.We conducted a systematic review and meta-analysis of studies on the association between maternal gestational smoking, diabetes, alcohol drinking, and pre-pregnancy obesity and the risk of cryptorchidism. Articles were retrieved by searching PubMed and ScienceDirect, and the meta-analysis was conducted using Stata/SE 12.0 software. Sensitivity analysis was used to evaluate the influence of confounding variables.We selected 32 articles, including 12 case-control, five nested case-control, and 15 cohort studies. The meta-analysis showed that maternal smoking (OR = 1.17, 95% CI: 1.11-1.23 or diabetes (OR = 1.21, 95%CI: 1.00-1.46 during pregnancy were associated with increased risk of cryptorchidism. Overall, the association between maternal alcohol drinking (OR = 0.97, 95% CI: 0.87-1.07, pre-pregnancy body mass index (OR = 1.02, 95% CI: 0.95-1.09 and risk of cryptorchidism were not statistically significant. Additional analysis showed reduced risk (OR = 0.89, 95% CI: 0.82-0.96 of cryptorchidism with moderate alcohol drinking during pregnancy. No dose-response relationship was observed for increments in body mass index in the risk of cryptorchidism. Sensitivity analysis revealed an unstable result for the association between maternal diabetes, alcohol drinking and cryptorchidism. Moderate heterogeneity was detected in studies of the effect of maternal alcohol drinking and diabetes. No publication bias was detected.Maternal gestational smoking, but not maternal pre-pregnancy overweight or obesity, was associated with increased cryptorchidism risk in the offspring. Moderate alcohol drinking may reduce the risk of cryptorchidism while gestational diabetes may be a risk factor, but further studies are needed to verify this.

  10. Maternal gestational smoking, diabetes, alcohol drinking, pre-pregnancy obesity and the risk of cryptorchidism: a systematic review and meta-analysis of observational studies.

    Science.gov (United States)

    Zhang, Lin; Wang, Xing-Huan; Zheng, Xin-Min; Liu, Tong-Zu; Zhang, Wei-Bin; Zheng, Hang; Chen, Mi-Feng

    2015-01-01

    Maternal gestational smoking, diabetes, alcohol drinking, and pre-pregnancy obesity are thought to increase the risk of cryptorchidism in newborn males, but the evidence is inconsistent. We conducted a systematic review and meta-analysis of studies on the association between maternal gestational smoking, diabetes, alcohol drinking, and pre-pregnancy obesity and the risk of cryptorchidism. Articles were retrieved by searching PubMed and ScienceDirect, and the meta-analysis was conducted using Stata/SE 12.0 software. Sensitivity analysis was used to evaluate the influence of confounding variables. We selected 32 articles, including 12 case-control, five nested case-control, and 15 cohort studies. The meta-analysis showed that maternal smoking (OR = 1.17, 95% CI: 1.11-1.23) or diabetes (OR = 1.21, 95%CI: 1.00-1.46) during pregnancy were associated with increased risk of cryptorchidism. Overall, the association between maternal alcohol drinking (OR = 0.97, 95% CI: 0.87-1.07), pre-pregnancy body mass index (OR = 1.02, 95% CI: 0.95-1.09) and risk of cryptorchidism were not statistically significant. Additional analysis showed reduced risk (OR = 0.89, 95% CI: 0.82-0.96) of cryptorchidism with moderate alcohol drinking during pregnancy. No dose-response relationship was observed for increments in body mass index in the risk of cryptorchidism. Sensitivity analysis revealed an unstable result for the association between maternal diabetes, alcohol drinking and cryptorchidism. Moderate heterogeneity was detected in studies of the effect of maternal alcohol drinking and diabetes. No publication bias was detected. Maternal gestational smoking, but not maternal pre-pregnancy overweight or obesity, was associated with increased cryptorchidism risk in the offspring. Moderate alcohol drinking may reduce the risk of cryptorchidism while gestational diabetes may be a risk factor, but further studies are needed to verify this.

  11. Prospective population-based cohort study of maternal obesity as a source of error in gestational age estimation at 11-14weeks

    DEFF Research Database (Denmark)

    Bak, Geske S; Sperling, Lene; Källén, Karin

    2016-01-01

    IntroductionAn impact of maternal obesity on ultrasound dating of pregnancy at 11-14 gestational weeks is possible and was investigated. Material and methodsA prospective cohort study based on the Danish national population during a 4-year period in which we entered all mothers with singleton pre...

  12. Disturbed nitric oxide and homocysteine production are involved in the increased risk of cardiovascular diseases in the F1 offspring of maternal obesity and malnutrition.

    Science.gov (United States)

    Moussa, Y Y; Tawfik, S H; Haiba, M M; Saad, M I; Hanafi, M Y; Abdelkhalek, T M; Oriquat, G A; Kamel, M A

    2017-06-01

    The present study aimed to evaluate the changes in levels of different independent risk factors for vascular diseases in the rat offspring of maternal obesity and malnutrition as maternal health disturbances are thought to have direct consequences on the offspring health. The effect of postnatal diet on the offspring was also assessed. Three groups of female Wistar rats were used (control, obese and malnourished). After the pregnancy and delivery, the offspring were weaned to control diet or high-caloric (HCD) diet and followed up for 30 weeks. Every 5 weeks postnatal, 20 pups (10 males and 10 females) of each subgroup were sacrificed after overnight fasting, the blood sample was obtained, and the rats were dissected out to obtain heart muscle. The following parameters were assessed; lipid profile, NEFA, homocysteine (Hcy), nitric oxide end product (NOx) and myocardial triglyceride content. Maternal obesity and malnutrition caused significant elevation in the body weight, triglycerides, NEFA, Hcy and NOx in the F1 offspring especially those maintained under HCD. Also, the male offspring showed more prominent changes than female offspring. Maternal malnutrition and obesity may increase the risk of the development of cardiovascular diseases in the offspring, especially the male ones.

  13. Maternal overweight and obesity are associated with increased risk of type 1 diabetes in offspring of parents without diabetes regardless of ethnicity.

    Science.gov (United States)

    Hussen, Hozan I; Persson, Martina; Moradi, Tahereh

    2015-07-01

    The incidence of type 1 diabetes in children is increasing in Sweden, as is the prevalence of maternal overweight/obesity. Therefore, the aim of this study was to investigate if maternal overweight/obesity increases the risk of type 1 diabetes in offspring of parents with and without diabetes, and of different ethnicities. The study cohort comprised 1,263,358 children, born in Sweden between 1992 and 2004. Children were followed from birth until diagnosis of type 1 diabetes, emigration, death or end of follow-up in 2009, whichever occurred first. First trimester maternal BMI was calculated (kg/m(2)). Poisson regression was used to calculate incidence rate ratios (IRRs) with 95% CI for type 1 diabetes in the offspring. The risk of type 1 diabetes was increased in offspring of parents with any type of diabetes regardless of parental ethnicity. High first trimester maternal BMI was associated with increased risk of type 1 diabetes only in offspring of parents without diabetes (IRR 1.33 [95% CI 1.20, 1.48]). Increasing incidence of type 1 diabetes in children with non-diabetic parents may partly be explained by increasing prevalence of maternal overweight/obesity.

  14. Screening for pre-eclampsia in the first trimester: role of maternal hemodynamics and bioimpedance in non-obese patients.

    Science.gov (United States)

    Gagliardi, G; Tiralongo, G M; LoPresti, D; Pisani, I; Farsetti, D; Vasapollo, B; Novelli, G P; Andreoli, A; Valensise, H

    2017-11-01

    To test if maternal hemodynamics and bioimpedance, assessed at the time of combined screening for PE, are able to identify in the first trimester of gestation normotensive non-obese patients at risk for pre-eclampsia (PE) and/or intrauterine growth restriction (IUGR). One hundred and fifty healthy nulliparous non-obese women (body mass index < 30 kg/m 2 ) in the first trimester of pregnancy underwent assessment by UltraSonic Cardiac Output Monitor (USCOM) to detect hemodynamic parameters, bioimpedance analysis to characterize body composition, and combined screening for PE (assessment of maternal history, biophysical and maternal biochemical markers). Patients were followed until term, noting the appearance of PE and/or IUGR. One hundred and thirty-eight patients had an uneventful pregnancy (controls), while 12 (8%) developed complications (cases). USCOM showed, in cases compared with controls, lower cardiac output (5.6 ± 0.3 vs 6.7 ± 1.1 L/min, P < 0.001), lower inotropy index (1.54 ± 0.38 vs 1.91 ± 0.32 W/m 2 , P < 0.001) and higher total vascular resistance (1279.8 ± 166.4 vs 1061.4 ± 179.5 dynes × s/cm 5 , P < 0.001). Bioimpedance analysis showed, in cases compared with controls, lower total body water (53.7 ± 3.3% vs 57.2 ± 5.6%, P = 0.037). Combined screening was positive for PE in 8% of the controls and in 50% of the cases (P < 0.001). After identification of cut-off values for USCOM and bioimpedance parameters, forward multivariate logistic regression analysis identified as independent predictors of complications in pregnancy the inotropy index (derived by USCOM), fat mass (derived from bioimpedance analysis) and combined screening. Combined screening for PE and assessment of bioimpedance and maternal hemodynamics can be used to identify early markers of impaired cardiovascular adaptation and body composition that may lead to complications in the third trimester of pregnancy. Copyright

  15. Insatiable insecurity: maternal obesity as a risk factor for mother-child attachment and child weight.

    Science.gov (United States)

    Keitel-Korndörfer, Anja; Sierau, Susan; Klein, Annette M; Bergmann, Sarah; Grube, Matthias; von Klitzing, Kai

    2015-01-01

    Childhood obesity has become a rising health problem, and because parental obesity is a basic risk factor for childhood obesity, biological factors have been especially considered in the complex etiology. Aspects of the family interaction, e.g., mother-child attachment, have not been the main focus. Our study tried to fill this gap by investigating whether there is a difference between children of obese and normal weight mothers in terms of mother-child attachment, and whether mother-child attachment predicts child's weight, in a sample of 31 obese and 31 normal weight mothers with children aged 19 to 58 months. Mother-child attachment was measured with the Attachment Q-Set. We found that (1) children of obese mothers showed a lower quality of mother-child attachment than children of normal weight mothers, which indicates that they are less likely to use their mothers as a secure base; (2) the attachment quality predicted child`s BMI percentile; and (3) the mother-child attachment adds incremental validity to the prediction of child's BMI beyond biological parameters (child's BMI birth percentile, BMI of the parents) and mother's relationship status. Implications of our findings are discussed.

  16. Transgenic increase in N-3/n-6 Fatty Acid ratio reduces maternal obesity-associated inflammation and limits adverse developmental programming in mice.

    Directory of Open Access Journals (Sweden)

    Margaret J R Heerwagen

    Full Text Available Maternal and pediatric obesity has risen dramatically over recent years, and is a known predictor of adverse long-term metabolic outcomes in offspring. However, which particular aspects of obese pregnancy promote such outcomes is less clear. While maternal obesity increases both maternal and placental inflammation, it is still unknown whether this is a dominant mechanism in fetal metabolic programming. In this study, we utilized the Fat-1 transgenic mouse to test whether increasing the maternal n-3/n-6 tissue fatty acid ratio could reduce the consequences of maternal obesity-associated inflammation and thereby mitigate downstream developmental programming. Eight-week-old WT or hemizygous Fat-1 C57BL/6J female mice were placed on a high-fat diet (HFD or control diet (CD for 8 weeks prior to mating with WT chow-fed males. Only WT offspring from Fat-1 mothers were analyzed. WT-HFD mothers demonstrated increased markers of infiltrating adipose tissue macrophages (P<0.02, and a striking increase in 12 serum pro-inflammatory cytokines (P<0.05, while Fat1-HFD mothers remained similar to WT-CD mothers, despite equal weight gain. E18.5 Fetuses from WT-HFD mothers had larger placentas (P<0.02, as well as increased placenta and fetal liver TG deposition (P<0.01 and P<0.02, respectively and increased placental LPL TG-hydrolase activity (P<0.02, which correlated with degree of maternal insulin resistance (r = 0.59, P<0.02. The placentas and fetal livers from Fat1-HFD mothers were protected from this excess placental growth and fetal-placental lipid deposition. Importantly, maternal protection from excess inflammation corresponded with improved metabolic outcomes in adult WT offspring. While the offspring from WT-HFD mothers weaned onto CD demonstrated increased weight gain (P<0.05, body and liver fat (P<0.05 and P<0.001, respectively, and whole body insulin resistance (P<0.05, these were prevented in WT offspring from Fat1-HFD mothers. Our results

  17. Maternal undernutrition and fetal developmental programming of obesity: the glucocorticoid connection.

    Science.gov (United States)

    Correia-Branco, Ana; Keating, Elisa; Martel, Fátima

    2015-02-01

    An adequate maternal nutrition during pregnancy is crucial for the health outcome of offspring in adulthood. Maternal undernutrition during critical periods of fetal development can program the fetus for metabolic syndrome (MetS) later in life, especially when postnatally challenged with a hypernutritive diet. Adipogenesis, which begins in utero and accelerates in neonatal life, is a major candidate for developmental programming. During fetal development, the hypothalamic-pituitary-adrenal (HPA) axis is extremely susceptible to programming, and the HPA tone is increased throughout life in undernourished conditions. As a consequence, an alteration in the expression and function of glucocorticoid (GC) receptors and of the major GC regulatory enzymes (11β-hydroxysteroid dehydrogenase 1 and -2) occurs. In this review, we will give insights into the role of maternoplacental adverse interactions under the specific context of maternal undernutrition, for later-in-life MetS development, with a special emphasis on the role of GCs. © The Author(s) 2014.

  18. Maternal obesity and its effect on labour duration in nulliparous women: a retrospective observational cohort study.

    Science.gov (United States)

    Ellekjaer, Karen Louise; Bergholt, Thomas; Løkkegaard, Ellen

    2017-07-12

    Obesity is increasing among primipara women. We aimed to describe the association between body mass index (BMI) during early-pregnancy and duration of labour in nulliparous women. Retrospective observational cohort study of 1885 nulliparous women with a single cephalic presentation from 37 0/7 to 42 6/7 weeks of completed gestation and spontaneous or induced labour at Nordsjællands Hospital, University of Copenhagen, Denmark, in 2011 and 2012. Total duration of labour and the first and second stages of labour were compared between early-pregnancy normal-weight (BMI women. Proportional hazards and multiple logistic regression models were applied. Early pregnancy BMI classified 1246 (66.1%) women as normal weight, 350 (18.6%) as overweight and 203 (10.8%) as obese. No difference in the duration of total or first stage of active labour was found for overweight (adjusted HR = 1.01, 95% CI 0.88-1.16) or obese (adjusted HR = 1.07, 95% CI 0.90-1.28) compared to normal weight women. Median active labour duration was 5.83 h for normal weight, 6.08 h for overweight and 5.90 h for obese women. The risk of caesarean delivery increased significantly for overweight and obese compared to normal weight women (odds ratios (OR) 1.62; 95%CI 1.18-2.22 and 1.76; 95%CI 1.20-2.58, respectively). Caesarean deliveries were performed earlier in labour in obese than normal-weight women (HR = 1.80, 95%CI 1.28-2.54). BMI had no significant effect on total duration of active labour. Risk of caesarean delivery increased with increasing BMI. Caesarean deliveries are undertaken earlier in obese women compared to normal weight women following the onset of active labour, shortening the total duration of active labour.

  19. Maternal obesity and its effect on labour duration in nulliparous women

    DEFF Research Database (Denmark)

    Ellekjaer, Karen Louise; Bergholt, Thomas; Løkkegaard, Ellen

    2017-01-01

    BACKGROUND: Obesity is increasing among primipara women. We aimed to describe the association between body mass index (BMI) during early-pregnancy and duration of labour in nulliparous women. METHODS: Retrospective observational cohort study of 1885 nulliparous women with a single cephalic......), overweight (BMI 25-29.9 kg/m2), and obese (BMI ≥30 kg/m2) women. Proportional hazards and multiple logistic regression models were applied. RESULTS: Early pregnancy BMI classified 1246 (66.1%) women as normal weight, 350 (18.6%) as overweight and 203 (10.8%) as obese. No difference in the duration of total...... or first stage of active labour was found for overweight (adjusted HR = 1.01, 95% CI 0.88-1.16) or obese (adjusted HR = 1.07, 95% CI 0.90-1.28) compared to normal weight women. Median active labour duration was 5.83 h for normal weight, 6.08 h for overweight and 5.90 h for obese women. The risk...

  20. Excessive Gestational Weight Gain and Subsequent Maternal Obesity at Age 40: A Hypothetical Intervention.

    Science.gov (United States)

    Abrams, Barbara; Coyle, Jeremy; Cohen, Alison K; Headen, Irene; Hubbard, Alan; Ritchie, Lorrene; Rehkopf, David H

    2017-09-01

    To model the hypothetical impact of preventing excessive gestational weight gain on midlife obesity and compare the estimated reduction with the US Healthy People 2020 goal of a 10% reduction of obesity prevalence in adults. We analyzed 3917 women with 1 to 3 pregnancies in the prospective US National Longitudinal Survey of Youth, from 1979 to 2012. We compared the estimated obesity prevalence between 2 scenarios: gestational weight gain as reported and under the scenario of a hypothetical intervention that all women with excessive gestational weight gain instead gained as recommended by the Institute of Medicine (2009). A hypothetical intervention was associated with a significantly reduced estimated prevalence of obesity for first (3.3 percentage points; 95% confidence interval [CI] = 1.0, 5.6) and second (3.0 percentage points; 95% CI = 0.7, 5.2) births, and twice as high in Black as in White mothers, but not significant in Hispanics. The population attributable fraction was 10.7% (95% CI = 3.3%, 18.1%) in first and 9.3% (95% CI = 2.2%, 16.5%) in second births. Development of effective weight-management interventions for childbearing women could lead to meaningful reductions in long-term obesity.

  1. Maternal Pre-Pregnancy Obesity and Risk for Inattention and Negative Emotionality in Children

    Science.gov (United States)

    Rodriguez, Alina

    2010-01-01

    Objective: This study aimed to replicate and extend previous work showing an association between maternal pre-pregnancy adiposity and risk for attention deficit hyperactivity disorder (ADHD) symptoms in children. Methods: A Swedish population-based prospective pregnancy-offspring cohort was followed up when children were 5 years old (N = 1,714).…

  2. Obesity

    Science.gov (United States)

    Obesity means having too much body fat. It is different from being overweight, which means weighing too ... what's considered healthy for his or her height. Obesity happens over time when you eat more calories ...

  3. Risk of major congenital malformations in relation to maternal overweight and obesity severity: cohort study of 1.2 million singletons.

    Science.gov (United States)

    Persson, Martina; Cnattingius, Sven; Villamor, Eduardo; Söderling, Jonas; Pasternak, Björn; Stephansson, Olof; Neovius, Martin

    2017-06-14

    Objective  To estimate the risks of major congenital malformations in the offspring of mothers who are underweight (body mass index (BMI) malformation, and subgroups of organ specific malformations diagnosed during the first year of life. Risk ratios were estimated using generalised linear models adjusted for maternal factors, sex of offspring, and birth year. Results  A total of 43 550 (3.5%) offspring had any major congenital malformation, and the most common subgroup was for congenital heart defects (n=20 074; 1.6%). Compared with offspring of normal weight mothers (risk of malformations 3.4%), the proportions and adjusted risk ratios of any major congenital malformation among the offspring of mothers with higher BMI were: overweight, 3.5% and 1.05 (95% confidence interval 1.02 to 1.07); obesity class I, 3.8% and 1.12 (1.08 to 1.15), obesity class II, 4.2% and 1.23 (1.17 to 1.30), and obesity class III, 4.7% and 1.37 (1.26 to 1.49). The risks of congenital heart defects, malformations of the nervous system, and limb defects also progressively increased with BMI from overweight to obesity class III. The largest organ specific relative risks related to maternal overweight and increasing obesity were observed for malformations of the nervous system. Malformations of the genital and digestive systems were also increased in offspring of obese mothers. Conclusions  Risks of any major congenital malformation and several subgroups of organ specific malformations progressively increased with maternal overweight and increasing severity of obesity. For women who are planning pregnancy, efforts should be encouraged to reduce adiposity in those with a BMI above the normal range. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

  4. Women's and Midwives' Perspectives on the Design of a Text Messaging Support for Maternal Obesity Services: An Exploratory Study

    Directory of Open Access Journals (Sweden)

    H. Soltani

    2012-01-01

    Full Text Available This study was aimed to explore women’s and midwives’ views on the use of mobile technology in supporting obese pregnant women with healthy lifestyle choices. A purposive sample of 14 women and midwives participated in four focus groups in Doncaster, UK. A content analysis of the transcripts from the first focus group led to the emergence of three main constructs with associated subcategories including Benefits (“modernising,” “motivating,” “reminding,” and “reducing” the sense of isolation, Risks and Limitations (possibility of “being offensive,” “creating pressure or guilt,” and “being influenced by mood”, and Service Delivery (making it “available to all pregnant women,” giving attention to the “message tone” and development of “message content”. They also suggested the use of other modalities such as web-based services for weight management during pregnancy. Based on the above results a text messaging service was developed and presented to the 2nd focus group participants who confirmed the positive views from the first focus group on the use of the text messaging as being supportive and informative. The participants also welcomed “women’s engagement and choice” in deciding the content, timing and frequency of messages. The results informed the development of a text messaging service to support maternal obesity management. The implementation and acceptability of this service requires further investigation.

  5. Maternal obesity and offspring dietary patterns at 9 months of age

    DEFF Research Database (Denmark)

    Andersen, Louise Beltoft Borup; Pipper, Christian Bressen; Trolle, Ellen

    2015-01-01

    months. Therefore, the promotion of healthy complementary feeding might be beneficial for the prevention of health implications, such as obesity, later in life for these infants.European Journal of Clinical Nutrition advance online publication, 3 December 2014; doi:10.1038/ejcn.2014.258....

  6. Maternal obesity and development of the preterm newborn at 2 year

    NARCIS (Netherlands)

    van der Burg, J.W.; Allred, E.N.; Kuban, K.; O'Shea, T.M.; Dammann, O.; Leviton, A.

    2015-01-01

    Aim To evaluate to what extent extremely preterm children (<28 weeks' gestational age) of overweight (BMI 25-29) or obese (BMI ≥30) women are at increased risk of adverse development at 2 years measured with the Bayley Scales of Infant Development II in a multicenter prospective cohort study.

  7. Influence of maternal adiposity, preterm birth and birth weight centiles on early childhood obesity in an Indigenous Australian pregnancy-through-to-early-childhood cohort study.

    Science.gov (United States)

    Pringle, K G; Lee, Y Q; Weatherall, L; Keogh, L; Diehm, C; Roberts, C T; Eades, S; Brown, A; Smith, R; Lumbers, E R; Brown, L J; Collins, C E; Rae, K M

    2018-05-16

    Childhood obesity rates are higher among Indigenous compared with non-Indigenous Australian children. It has been hypothesized that early-life influences beginning with the intrauterine environment predict the development of obesity in the offspring. The aim of this paper was to assess, in 227 mother-child dyads from the Gomeroi gaaynggal cohort, associations between prematurity, Gestation Related-Optimal Weight (GROW) centiles, maternal adiposity (percentage body fat, visceral fat area), maternal non-fasting plasma glucose levels (measured at mean gestational age of 23.1 weeks) and offspring BMI and adiposity (abdominal circumference, subscapular skinfold thickness) in early childhood (mean age 23.4 months). Maternal non-fasting plasma glucose concentrations were positively associated with infant birth weight (P=0.005) and GROW customized birth weight centiles (P=0.008). There was a significant association between maternal percentage body fat (P=0.02) and visceral fat area (P=0.00) with infant body weight in early childhood. Body mass index (BMI) in early childhood was significantly higher in offspring born preterm compared with those born at term (P=0.03). GROW customized birth weight centiles was significantly associated with body weight (P=0.01), BMI (P=0.007) and abdominal circumference (P=0.039) at early childhood. Our findings suggest that being born preterm, large for gestational age or exposed to an obesogenic intrauterine environment and higher maternal non-fasting plasma glucose concentrations are associated with increased obesity risk in early childhood. Future strategies should aim to reduce the prevalence of overweight/obesity in women of child-bearing age and emphasize the importance of optimal glycemia during pregnancy, particularly in Indigenous women.

  8. Experimental Models of Maternal Obesity and Neuroendocrine Programming of Metabolic Disorders in Offspring

    OpenAIRE

    Clare M. Reynolds; Stephanie A. Segovia; Mark H. Vickers

    2017-01-01

    Evidence from epidemiological, clinical, and experimental studies have clearly shown that disease risk in later life is increased following a poor early life environment, a process preferentially termed developmental programming. In particular, this work clearly highlights the importance of the nutritional environment during early development with alterations in maternal nutrition, including both under- and overnutrition, increasing the risk for a range of cardiometabolic and neurobehavioral ...

  9. Maternal obesity is the new challenge; a qualitative study of health professionals’ views towards suitable care for pregnant women with a Body Mass Index (BMI ≥30 kg/m2

    Directory of Open Access Journals (Sweden)

    Smith Debbie M

    2012-12-01

    Full Text Available Abstract Background An increase in the number of women with maternal obesity (Body Mass Index [BMI] ≥30 kg/m2 has had a huge impact on the delivery of maternity services. As part of a programme of feasibility work to design an antenatal lifestyle programme for women with a BMI ≥30 kg/m2, the current study explored health professionals’ experiences of caring for women with a BMI ≥30 kg/m2 and their views of the proposed lifestyle programme. Method Semi-structured interviews with 30 health professionals (including midwives, sonographers, anaesthetists and obstetricians were conducted and analysed using thematic analysis. Recruitment occurred in two areas in the North West of England in early 2011. Results Three themes were evident. Firstly, obesity was seen as a conversation stopper; obesity can be a challenge to discuss. Secondly, obesity was seen as a maternity issue; obesity has a direct impact on maternity care and therefore intervention is needed. Finally, the long-term impact of maternal obesity intervention; lifestyle advice in pregnancy has the potential to break the cyclic obesity relationship. The health professionals believed that antenatal lifestyle advice can play a key role in addressing the public health issue of obesity as pregnancy is a time of increased motivation for women with a BMI ≥30 kg/m2. Conclusions Maternal obesity is a challenge and details of the training content required for health professionals to feel confident to approach the issue of maternal obesity with women are presented. Support for the antenatal lifestyle programme for women with a BMI ≥30 kg/m2 highlights the need for further exploration of the impact of interventions on health promotion.

  10. Maternal obesity is the new challenge; a qualitative study of health professionals' views towards suitable care for pregnant women with a Body Mass Index (BMI) ≥ 30 kg/m².

    Science.gov (United States)

    Smith, Debbie M; Cooke, Alison; Lavender, Tina

    2012-12-19

    An increase in the number of women with maternal obesity (Body Mass Index [BMI] ≥30 kg/m2) has had a huge impact on the delivery of maternity services. As part of a programme of feasibility work to design an antenatal lifestyle programme for women with a BMI ≥30 kg/m2, the current study explored health professionals' experiences of caring for women with a BMI ≥30 kg/m2 and their views of the proposed lifestyle programme. Semi-structured interviews with 30 health professionals (including midwives, sonographers, anaesthetists and obstetricians) were conducted and analysed using thematic analysis. Recruitment occurred in two areas in the North West of England in early 2011. Three themes were evident. Firstly, obesity was seen as a conversation stopper; obesity can be a challenge to discuss. Secondly, obesity was seen as a maternity issue; obesity has a direct impact on maternity care and therefore intervention is needed. Finally, the long-term impact of maternal obesity intervention; lifestyle advice in pregnancy has the potential to break the cyclic obesity relationship. The health professionals believed that antenatal lifestyle advice can play a key role in addressing the public health issue of obesity as pregnancy is a time of increased motivation for women with a BMI ≥30 kg/m2. Maternal obesity is a challenge and details of the training content required for health professionals to feel confident to approach the issue of maternal obesity with women are presented. Support for the antenatal lifestyle programme for women with a BMI ≥30 kg/m2 highlights the need for further exploration of the impact of interventions on health promotion.

  11. Unconscious collusion: An interpretative phenomenological analysis of the maternity care experiences of women with obesity (BMI≥30kg/m²).

    Science.gov (United States)

    Atkinson, Sandra; McNamara, Patricia Mannix

    2017-06-01

    obstetric and midwifery literature continually emphasise incidence and consequence of obesity in pregnancy. However, they offer less consensus on how best to support women who are obese. Therefore, this study explores in depth the lived experience of women who have a Body Mass Index (BMI) ≥30kg/m². This exploration provides a bio-psycho-social understanding of the lived experience of women to identify how best to support them throughout their childbirth experience. an Interpretative Phenomenological Analysis (IPA) design was adopted for this qualitative study. Purposive sampling of participants was conducted on the postnatal wards of a maternity hospital in the Republic of Ireland. In total, 15 participants volunteered to take part in semi-structured interviews conducted at six to ten weeks postnatally. Data were analysed utilising the IPA framework. the results indicate that participants were conscious of the problematics of communicating obesity in pregnancy. The narrative data revealed an unconscious collusion between healthcare professionals and women as they navigate obesity related conversations. The behaviours related to unconscious collusion are incorporated in the sub-ordinate themes; 'just recorded and that's all', 'but what's eating healthy? 'pussy footing around' and 'I hate that word obesity. the findings highlight a lack of information received by participants from healthcare professionals regarding increased BMI or weight management. The data suggests that healthcare professionals appeared to collude with women to avoid challenging discussions regarding obesity. This may be related to avoidance on participants' part and/or may be linked with healthcare professionals' reluctance to communicate issues relating to increased BMI. Although participants were generally unhappy with the communication skills of health professionals, they readily acknowledged the sensitive nature of obesity related communications. The findings provide healthcare

  12. Up-regulation of reciprocal inhibition by explosive strength training

    DEFF Research Database (Denmark)

    Geertsen, Svend Sparre; Jensen, Jesper Lundbye; Nielsen, Jens Bo

    of 26 ± 7 years strength trained the ankle dorsiflexor muscles 3 times a week for 4 weeks. Each training session consisted of 4 sets of 16 isometric dorsiflexions with the aim of increasing force as rapidly as possible, separated by 4min rest periods. Test sessions were conducted before, immediately...... in the ankle plantarflexors at the onset of dorsiflexion is larger the quicker the movement, we hypothesized that DRI may be up-regulated when subjects are trained to perform dorsiflexion movements as quickly as possible.   For this purpose, 15 healthy human subjects (7 male, 8 female) with an average age...... after and 2 weeks after the training period. The rate of dorsiflexion force development measured within 30, 50, 100 and 200ms after onset of voluntary explosive isometric dorsiflexion increased by 20-30% (p

  13. Maternal Characteristics and Incidence of Overweight/Obesity in Children: A 13-Year Follow-up Study in an Eastern Mediterranean Population.

    Science.gov (United States)

    Jalali-Farahani, Sara; Amiri, Parisa; Abbasi, Behnood; Karimi, Mehrdad; Cheraghi, Leila; Daneshpour, Maryam Sadat; Azizi, Fereidoun

    2017-05-01

    Objectives To investigate clustering of parental sociobehavioral factors and their relationship with the incidence of overweight and obesity in Iranian children. Methods Demographics, body weight, and certain medical characteristics of the parents of 2999 children were used to categorize parents by cluster; children's weights were assessed for each cluster. Specifically, survival analysis and Cox regression models were used to test the effect of parental clustering on the incidence of childhood overweight and obesity. Results Maternal metabolic syndrome, education level, age, body weight status, and paternal age had important roles in distinguishing clusters with low, moderate, and high risk. Crude incidence rates (per 10,000 person-years) of overweight and obesity were 416.8 (95% confidence interval (CI) 388.2-447.5) and 114.7 (95% CI 101.2-129.9), respectively. Children of parents with certain constellations of demographic and medical characteristics were 37.0 and 41.0% more likely to become overweight and obese, respectively. Conclusions for Practice The current study demonstrated the vital role of maternal characteristics in distinguishing familial clusters, which could be used to predict the incidence of overweight and obesity in children.

  14. Programming maternal and child overweight and obesity in the context of undernutrition: current evidence and key considerations for low- and middle-income countries.

    Science.gov (United States)

    Jaacks, Lindsay M; Kavle, Justine; Perry, Abigail; Nyaku, Albertha

    2017-05-01

    The goals of the present targeted review on maternal and child overweight and obesity were to: (i) understand the current situation in low- and middle-income countries (LMIC) with regard to recent trends and context-specific risk factors; and (ii) building off this, identify entry points for leveraging existing undernutrition programmes to address overweight and obesity in LMIC. Trends reveal that overweight and obesity are a growing problem among women and children in LMIC; as in Ghana, Kenya, Niger, Sierra Leone, Tanzania and Zimbabwe, where the prevalence among urban women is approaching 50 %. Four promising entry points were identified: (i) the integration of overweight and obesity into national nutrition plans; (ii) food systems (integration of food and beverage marketing regulations into existing polices on the marketing of breast-milk substitutes and adoption of policies to promote healthy diets); (iii) education systems (integration of nutrition into school curricula with provision of high-quality foods through school feeding programmes); and (iv) health systems (counselling and social and behaviour change communication to improve maternal diet, appropriate gestational weight gain, and optimal infant and young child feeding practices). We conclude by presenting a step-by-step guide for programme officers and policy makers in LMIC with actionable objectives to address overweight and obesity.

  15. Maternal obesity reduces milk lipid production in lactating mice by inhibiting acetyl-CoA carboxylase and impairing fatty acid synthesis.

    Science.gov (United States)

    Saben, Jessica L; Bales, Elise S; Jackman, Matthew R; Orlicky, David; MacLean, Paul S; McManaman, James L

    2014-01-01

    Maternal metabolic and nutrient trafficking adaptations to lactation differ among lean and obese mice fed a high fat (HF) diet. Obesity is thought to impair milk lipid production, in part, by decreasing trafficking of dietary and de novo synthesized lipids to the mammary gland. Here, we report that de novo lipogenesis regulatory mechanisms are disrupted in mammary glands of lactating HF-fed obese (HF-Ob) mice. HF feeding decreased the total levels of acetyl-CoA carboxylase-1 (ACC), and this effect was exacerbated in obese mice. The relative levels of phosphorylated (inactive) ACC, were elevated in the epithelium, and decreased in the adipose stroma, of mammary tissue from HF-Ob mice compared to those of HF-fed lean (HF-Ln) mice. Mammary gland levels of AMP-activated protein kinase (AMPK), which catalyzes formation of inactive ACC, were also selectively elevated in mammary glands of HF-Ob relative to HF-Ln dams or to low fat fed dams. These responses correlated with evidence of increased lipid retention in mammary adipose, and decreased lipid levels in mammary epithelial cells, of HF-Ob dams. Collectively, our data suggests that maternal obesity impairs milk lipid production, in part, by disrupting the balance of de novo lipid synthesis in the epithelial and adipose stromal compartments of mammary tissue through processes that appear to be related to increased mammary gland AMPK activity, ACC inhibition, and decreased fatty acid synthesis.

  16. Severe Maternal Stress Exposure Due to Bereavement before, during and after Pregnancy and Risk of Overweight and Obesity in Young Adult Men

    DEFF Research Database (Denmark)

    Hohwü, Lena; Li, Jiong; Olsen, Jørn

    2014-01-01

    BACKGROUND: Perinatal stress may programme overweight and obesity. We examined whether maternal pre- and post-natal bereavement was associated with overweight and obesity in young men. METHODS: A cohort study was conducted including 119,908 men born from 1976 to 1993 and examined for military...... service between 2006 and 2011. Among them, 4,813 conscripts were born to mothers bereaved by death of a close relative from 12 months preconception to birth of the child (exposed group). Median body mass index (BMI) and prevalence of overweight and obesity were estimated. Odds ratio of overweight (BMI≥25...... kg/m2) and obesity (BMI≥30 kg/m2) were estimated by logistic regression analysis adjusted for maternal educational level. RESULTS: Median BMI was similar in the exposed and the unexposed group but the prevalence of overweight (33.3% versus 30.4%, p = 0.02) and obesity (9.8% versus 8.5%, p = 0...

  17. Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring.

    Directory of Open Access Journals (Sweden)

    Shona L Kirk

    2009-06-01

    Full Text Available Hypothalamic systems which regulate appetite may be permanently modified during early development. We have previously reported hyperphagia and increased adiposity in the adult offspring of rodents fed an obesogenic diet prior to and throughout pregnancy and lactation. We now report that offspring of obese (OffOb rats display an amplified and prolonged neonatal leptin surge, which is accompanied by elevated leptin mRNA expression in their abdominal white adipose tissue. At postnatal Day 30, before the onset of hyperphagia in these animals, serum leptin is normal, but leptin-induced appetite suppression and phosphorylation of STAT3 in the arcuate nucleus (ARC are attenuated; the level of AgRP-immunoreactivity in the hypothalamic paraventricular nucleus (PVH, which derives from neurones in the ARC and is developmentally dependent on leptin, is also diminished. We hypothesise that prolonged release of abnormally high levels of leptin by neonatal OffOb rats leads to leptin resistance and permanently affects hypothalamic functions involving the ARC and PVH. Such effects may underlie the developmental programming of hyperphagia and obesity in these rats.

  18. Obesity

    Science.gov (United States)

    ... improve or prevent the health problems associated with obesity. Dietary changes, increased physical activity and behavior changes can ... more calories than you burn. And most Americans' diets are too high in calories and are ... factors Obesity usually results from a combination of causes and ...

  19. Up-regulation of melanin synthesis by the antidepressant fluoxetine.

    Science.gov (United States)

    Liao, Sha; Shang, Jing; Tian, Xiaoli; Fan, Xueqi; Shi, Xiupu; Pei, Siran; Wang, Qian; Yu, Boyang

    2012-08-01

    Fluoxetine, a member of the class of selective serotonin reuptake inhibitors, is a potent antidepressant commonly used in clinical practice. Here, we report that fluoxetine increases cellular tyrosinase (TYR) activity, enhances the protein levels of microphthalmia-associated transcription factor (MITF), TYR and tyrosinase-related protein-1 (TRP-1) and eventually leads to a dramatic increase in melanin production in both murine B16F10 melanoma cells and normal human melanocytes (NHMCs). In well-characterized C57BL/6 mouse models, systemic application of fluoxetine increased hair pigmentation by up-regulating hair follicular MITF, TYR, TRP-1 and tyrosinase-related protein-2 (TRP-2) protein levels. Using a serotonin 1A receptor (SR1A) antagonist and RNA interference (RNAi) technique, we revealed that SR1A appears to be one of the involved pathways in the fluoxetine-induced melanogenesis in B16F10 cells. These results suggest that fluoxetine may hold a significant therapeutic potential for treating skin hypopigmentation disorders, and SR1A may serve as a novel target in modulating melanogenesis. © 2012 John Wiley & Sons A/S.

  20. Obesity evaluation and treatment: Expert Committee recommendations. The Maternal and Child Health Bureau, Health Resources and Services Administration and the Department of Health and Human Services.

    Science.gov (United States)

    Barlow, S E; Dietz, W H

    1998-09-01

    The development of recommendations for physicians, nurse practitioners, and nutritionists to guide the evaluation and treatment of overweight children and adolescents. The Maternal and Child Health Bureau, Health Resources and Services Administration, the Department of Health and Human Services convened a committee of pediatric obesity experts to develop the recommendations. The Committee recommended that children with a body mass index (BMI) greater than or equal to the 85th percentile with complications of obesity or with a BMI greater than or equal to the 95th percentile, with or without complications, undergo evaluation and possible treatment. Clinicians should be aware of signs of the rare exogenous causes of obesity, including genetic syndromes, endocrinologic diseases, and psychologic disorders. They should screen for complications of obesity, including hypertension, dyslipidemias, orthopedic disorders, sleep disorders, gall bladder disease, and insulin resistance. Conditions that indicate consultation with a pediatric obesity specialist include pseudotumor cerebri, obesity-related sleep disorders, orthopedic problems, massive obesity, and obesity in children younger than 2 years of age. Recommendations for treatment evaluation included an assessment of patient and family readiness to engage in a weight-management program and a focused assessment of diet and physical activity habits. The primary goal of obesity therapy should be healthy eating and activity. The use of weight maintenance versus weight loss to achieve weight goals depends on each patient's age, baseline BMI percentile, and presence of medical complications. The Committee recommended treatment that begins early, involves the family, and institutes permanent changes in a stepwise manner. Parenting skills are the foundation for successful intervention that puts in place gradual, targeted increases in activity and targeted reductions in high-fat, high-calorie foods. Ongoing support for families

  1. Association between Maternal Fish Consumption and Gestational Weight Gain: Influence of Molecular Genetic Predisposition to Obesity.

    Directory of Open Access Journals (Sweden)

    Sofus C Larsen

    Full Text Available Studies suggest that fish consumption can restrict weight gain. However, little is known about how fish consumption affects gestational weight gain (GWG, and whether this relationship depends on genetic makeup.To examine the association between fish consumption and GWG, and whether this relationship is dependent on molecular genetic predisposition to obesity.A nested case-cohort study based on the Danish National Birth Cohort (DNBC sampling the most obese women (n = 990 and a random sample of the remaining participants (n = 1,128. Replication of statistically significant findings was attempted in the Avon Longitudinal Study of Parents and Children (ALSPAC (n = 4,841. We included 32 body mass index (BMI associated single nucleotide polymorphisms (SNPs and 5 SNPs found associated with GWG. BMI associated SNPs were combined in a genetic risk score (GRS. Associations between consumption of fish, GRS or individual variants and GWG were analysed, and interactions between fish and the GRS or individual variants were examined.In the DNBC, each portion/week (150 g of fatty fish was associated with a higher GWG of 0.58 kg (95% CI: 0.16, 0.99, P<0.01. For total fish and lean fish, similar patterns were observed, but these associations were not statistically significant. We found no association between GRS and GWG, and no interactions between GRS and dietary fish on GWG. However, we found an interaction between the PPARG Pro12Ala variant and dietary fish. Each additional Pro12Ala G-allele was associated with a GWG of -0.83 kg (95% CI: -1.29, -0.37, P<0.01 per portion/week of dietary fish, with the same pattern for both lean and fatty fish. In ALSPAC, we were unable to replicate these findings.We found no consistent evidence of association between fish consumption and GWG, and our results indicate that the association between dietary fish and GWG has little or no dependency on GRS or individual SNPs.

  2. Obesity

    Science.gov (United States)

    ... Peer Support Resources Diseases and Conditions Adrenal Disorders Osteoporosis and Bone Health Children and Teen Health Diabetes Heart Health Men's Health Rare Diseases Pituitary Disorders Thyroid Disorders Transgender Health Obesity and Weight Management Women's Health You and Your ...

  3. Risks of asphyxia-related neonatal complications in offspring of mothers with type 1 or type 2 diabetes: the impact of maternal overweight and obesity.

    Science.gov (United States)

    Cnattingius, Sven; Lindam, Anna; Persson, Martina

    2017-07-01

    We aimed to compare the risks of severe asphyxia-related neonatal complications in the offspring of mothers with type 1 or type 2 diabetes, and to assess the impact of maternal overweight/obesity on these risks. This was a population-based study of 1,343,751 live-born singleton infants in Sweden between 1997 and 2011, including 5941 and 711 infants of mothers with type 1 and type 2 diabetes, respectively. ORs with 95% CIs were calculated for low Apgar score (0-6) at 5 min after birth, hypoxic ischaemic encephalopathy and neonatal seizures. The rates of a low Apgar score were 0.9%, 2.6% and 2.1% in the offspring of mothers without diabetes or with type 1 or type 2 diabetes, respectively. After controlling for maternal confounders (including BMI), the risk of a low Apgar score increased in the offspring of mothers with type 1 diabetes (OR 2.67, 95% CI 2.23, 3.20) but not in the offspring of mothers with type 2 diabetes (OR 1.25, 95% CI 0.66, 2.35). The ORs of hypoxic ischaemic encephalopathy or neonatal seizures were increased in the offspring of mothers with type 1 diabetes (OR 3.41, 95% CI 2.58, 4.49) and type 2 diabetes (OR 2.54, 95% CI 1.13, 5.69). Maternal overweight/obesity was a risk factor for asphyxia-related neonatal complications and low Apgar scores in the offspring of mothers with type 1 diabetes and mothers without diabetes. The risks of a low Apgar score and severe asphyxia-related neonatal complications are increased in the offspring of mothers with type 1 or type 2 diabetes. Maternal overweight/obesity is an important contributing factor.

  4. Maternal-child overweight/obesity and undernutrition in Kenya: a geographic analysis.

    Science.gov (United States)

    Pawloski, Lisa R; Curtin, Kevin M; Gewa, Constance; Attaway, David

    2012-11-01

    The purpose of the study was to examine geographic relationships of nutritional status (BMI), including underweight, overweight and obesity, among Kenyan mothers and children. Spatial relationships were examined concerning BMI of the mothers and BMI-for-age percentiles of their children. These included spatial statistical measures of the clustering of segments of the population, in addition to inspection of co-location of significant clusters. Rural and urban areas of Kenya, including the cities of Nairobi and Mombasa, and the Kisumu region. Mother-child pairs from Demographic and Health Survey data including 1541 observations in 2003 and 1592 observations in 2009. These mother-child pairs were organized into 399 locational clusters. There is extremely strong evidence that high BMI values exhibit strong spatial clustering. There were co-locations of overweight mothers and overweight children only in the Nairobi region, while both underweight mothers and children tended to cluster in rural areas. In Mombasa clusters of overweight mothers were associated with normal-weight children, while in the Kisumu region clusters of overweight children were associated with normal-weight mothers. These findings show there is geographic variability as well as some defined patterns concerning the distribution of malnutrition among mothers and children in Kenya, and suggest the need for further geographic analyses concerning the potential factors which influence nutritional status in this population. In addition, the methods used in this research may be easily applied to other Demographic and Health Survey data in order to begin to understand the geographic determinants of health in low-income countries.

  5. Dog ownership during pregnancy, maternal activity, and obesity: a cross-sectional study.

    Directory of Open Access Journals (Sweden)

    Carri Westgarth

    Full Text Available The Avon Longitudinal Study of Parents and Children (ALSPAC is an observational study of 14,273 UK pregnant singleton mothers in 1990/1991. We examined outcomes of self report of strenuous activity (hours per week at 18 and 32 weeks of gestation, hours spent in leisure-time physical activities and types, and pre-pregnancy body mass index (BMI; overweight status was defined as pre-pregnancy BMI≥25 and obesity BMI≥30. Pet ownership and activity data were reported for 11,466 mothers. Twenty-five percent of mothers owned at least one dog. There was a positive relationship between participation in activity at least once a week and dog ownership (at 18 weeks, Odds ratio 1.27, 95% confidence interval 1.11-1.44, P<0.001. Dog owners were 50% more likely to achieve the recommended 3 hours activity per week, equivalent to 30 minutes per day, most days of the week (1.53, 1.35-1.72, P<0.001. Dog owners were also more likely to participate in brisk walking activity than those who did not have a dog (compared to no brisk walking 2-6 hrs per week 1.43, 1.23 to 1.67, P<0.001; 7+ hrs per week 1.80, 1.43 to 2.27, P<0.001. However, no association was found with any other types of activities and there was no association between dog ownership and weight status. During the time period studied, pregnant women who had dogs were more active, through walking, than those who did not own dogs. As walking is a low-risk exercise, participation of pregnant women in dog walking activities may be a useful context to investigate as part of a broader strategy to improve activity levels in pregnant women.

  6. The Impact of Maternal Obesity and Excessive Gestational Weight Gain on Maternal and Infant Outcomes in Maine: Analysis of Pregnancy Risk Assessment Monitoring System Results from 2000 to 2010.

    Science.gov (United States)

    Baugh, Nancy; Harris, David E; Aboueissa, AbouEl-Makarim; Sarton, Cheryl; Lichter, Erika

    2016-01-01

    The objective of this study is to understand the relationships between prepregnancy obesity and excessive gestational weight gain (GWG) and adverse maternal and fetal outcomes. Pregnancy risk assessment monitoring system (PRAMS) data from Maine for 2000-2010 were used to determine associations between demographic, socioeconomic, and health behavioral variables and maternal and infant outcomes. Multivariate logistic regression analysis was performed on the independent variables of age, race, smoking, previous live births, marital status, education, BMI, income, rurality, alcohol use, and GWG. Dependent variables included maternal hypertension, premature birth, birth weight, infant admission to the intensive care unit (ICU), and length of hospital stay of the infant. Excessive prepregnancy BMI and excessive GWG independently predicted maternal hypertension. A high prepregnancy BMI increased the risk of the infant being born prematurely, having a longer hospital stay, and having an excessive birth weight. Excessive GWG predicted a longer infant hospital stay and excessive birth weight. A low pregnancy BMI and a lower than recommended GWG were also associated with poor outcomes: prematurity, low birth weight, and an increased risk of the infant admitted to ICU. These findings support the importance of preconception care that promotes achievement of a healthy weight to enhance optimal reproductive outcomes.

  7. The Impact of Maternal Obesity and Excessive Gestational Weight Gain on Maternal and Infant Outcomes in Maine: Analysis of Pregnancy Risk Assessment Monitoring System Results from 2000 to 2010

    Directory of Open Access Journals (Sweden)

    Nancy Baugh

    2016-01-01

    Full Text Available The objective of this study is to understand the relationships between prepregnancy obesity and excessive gestational weight gain (GWG and adverse maternal and fetal outcomes. Pregnancy risk assessment monitoring system (PRAMS data from Maine for 2000–2010 were used to determine associations between demographic, socioeconomic, and health behavioral variables and maternal and infant outcomes. Multivariate logistic regression analysis was performed on the independent variables of age, race, smoking, previous live births, marital status, education, BMI, income, rurality, alcohol use, and GWG. Dependent variables included maternal hypertension, premature birth, birth weight, infant admission to the intensive care unit (ICU, and length of hospital stay of the infant. Excessive prepregnancy BMI and excessive GWG independently predicted maternal hypertension. A high prepregnancy BMI increased the risk of the infant being born prematurely, having a longer hospital stay, and having an excessive birth weight. Excessive GWG predicted a longer infant hospital stay and excessive birth weight. A low pregnancy BMI and a lower than recommended GWG were also associated with poor outcomes: prematurity, low birth weight, and an increased risk of the infant admitted to ICU. These findings support the importance of preconception care that promotes achievement of a healthy weight to enhance optimal reproductive outcomes.

  8. A maternal 'junk food' diet in pregnancy and lactation promotes an exacerbated taste for 'junk food' and a greater propensity for obesity in rat offspring.

    Science.gov (United States)

    Bayol, Stéphanie A; Farrington, Samantha J; Stickland, Neil C

    2007-10-01

    Obesity is generally associated with high intake of junk foods rich in energy, fat, sugar and salt combined with a dysfunctional control of appetite and lack of exercise. There is some evidence to suggest that appetite and body mass can be influenced by maternal food intake during the fetal and suckling life of an individual. However, the influence of a maternal junk food diet during pregnancy and lactation on the feeding behaviour and weight gain of the offspring remains largely uncharacterised. In this study, six groups of rats were fed either rodent chow alone or with a junk food diet during gestation, lactation and/or post-weaning. The daily food intakes and body mass were measured in forty-two pregnant and lactating mothers as well as in 216 offspring from weaning up to 10 weeks of age. Results showed that 10 week-old rats born to mothers fed the junk food diet during gestation and lactation developed an exacerbated preference for fatty, sugary and salty foods at the expense of protein-rich foods when compared with offspring fed a balanced chow diet prior to weaning or during lactation alone. Male and female offspring exposed to the junk food diet throughout the study also exhibited increased body weight and BMI compared with all other offspring. This study shows that a maternal junk food diet during pregnancy and lactation may be an important contributing factor in the development of obesity.

  9. Maternal overweight and obesity and risks of severe birth-asphyxia-related complications in term infants: a population-based cohort study in Sweden.

    Science.gov (United States)

    Persson, Martina; Johansson, Stefan; Villamor, Eduardo; Cnattingius, Sven

    2014-05-01

    Maternal overweight and obesity increase risks of pregnancy and delivery complications and neonatal mortality, but the mechanisms are unclear. The objective of the study was to investigate associations between maternal body mass index (BMI) in early pregnancy and severe asphyxia-related outcomes in infants delivered at term (≥37 weeks). A nation-wide Swedish cohort study based on data from the Medical Birth Register included all live singleton term births in Sweden between 1992 and 2010. Logistic regression analyses were used to obtain odds ratios (ORs) with 95% CIs for Apgar scores between 0 and 3 at 5 and 10 minutes, meconium aspiration syndrome, and neonatal seizures, adjusted for maternal height, maternal age, parity, mother's smoking habits, education, country of birth, and year of infant birth. Among 1,764,403 term births, 86% had data on early pregnancy BMI and Apgar scores. There were 1,380 infants who had Apgar score 0-3 at 5 minutes (absolute risk  = 0.8 per 1,000) and 894 had Apgar score 0-3 at 10 minutes (absolute risk  = 0.5 per 1,000). Compared with infants of mothers with normal BMI (18.5-24.9), the adjusted ORs (95% CI) for Apgar scores 0-3 at 10 minutes were as follows: BMI 25-29.9: 1.32 (1.10-1.58); BMI 30-34.9: 1.57 (1.20-2.07); BMI 35-39.9: 1.80 (1.15-2.82); and BMI ≥40: 3.41 (1.91-6.09). The ORs for Apgar scores 0-3 at 5 minutes, meconium aspiration, and neonatal seizures increased similarly with maternal BMI. A study limitation was lack of data on effects of obstetric interventions and neonatal resuscitation efforts. Risks of severe asphyxia-related outcomes in term infants increase with maternal overweight and obesity. Given the high prevalence of the exposure and the severity of the outcomes studied, the results are of potential public health relevance and should be confirmed in other populations. Prevention of overweight and obesity in women of reproductive age is important to improve perinatal health.

  10. Maternal Obesity, Overweight and Gestational Diabetes Affect the Offspring Neurodevelopment at 6 and 18 Months of Age--A Follow Up from the PREOBE Cohort.

    Directory of Open Access Journals (Sweden)

    Francisco J Torres-Espinola

    Full Text Available Brain development in fetal life and early infancy is critical to determine lifelong performance in various neuropsychological domains. Metabolic pathologies such as overweight, obesity, and gestational diabetes in pregnant women are prevalent and increasing risk factors that may adversely affect long-term brain development in their offspring.The objective of this research was to investigate the influence of maternal metabolic pathologies on the neurodevelopment of the offspring at 6 and 18 months of life.This was a prospective case-control study of 331 mother- and child pairs from Granada, Spain. The mothers were included during pregnancy into four groups according to their pre-gestational body mass index and their gestational diabetes status; overweight (n:56, obese (n:64, gestational diabetic (n:79, and healthy normal weight controls (n:132. At 6 months and 18 months we assessed the children with the Bayley III scales of neurodevelopment.At 6 months (n=215, we found significant group differences in cognition composite language, and expressive language. Post hoc test revealed unexpectedly higher scores in the obese group compared to the normal weight group and a similar trend in overweight and diabetic group. The effects on language remained significant after adjusting for confounders with an adjusted odds ratio for a value above median in composite language score of 3.3 (95% CI: 1.1, 10.0; p=0.035 for children of obese mothers. At 18 month (n=197, the offspring born to obese mothers had lost five points in language composite scores and the previous differences in language and cognition was replaced by a suggestive trend of lower gross motor scores in the overweight, obese, and diabetic groups.Infants of obese mothers had a temporary accelerated development of cognition and language, followed by a rapid deceleration until 18 months of age, particularly of language scores. This novel observation prompts further confirmative studies to explore

  11. Obesity

    DEFF Research Database (Denmark)

    Morgen, Camilla Schmidt; Sørensen, Thorkild I A

    2014-01-01

    A new report provides compelling evidence of the high prevalence of overweight and obesity throughout the world. The prevalence has increased since 1980, but at different rates across ages, times and locations. Studies exploring the causes of these differences could aid development of effective...

  12. Early postnatal maternal separation causes alterations in the expression of β3-adrenergic receptor in rat adipose tissue suggesting long-term influence on obesity

    International Nuclear Information System (INIS)

    Miki, Takanori; Liu, Jun-Qian; Ohta, Ken-ichi; Suzuki, Shingo; Kusaka, Takashi; Warita, Katsuhiko; Yokoyama, Toshifumi; Jamal, Mostofa; Ueki, Masaaki; Yakura, Tomiko; Tamai, Motoki; Sumitani, Kazunori; Hosomi, Naohisa; Takeuchi, Yoshiki

    2013-01-01

    Highlights: •High-fat diet intake following maternal separation did not cause body weight gain. •However, levels of metabolism-related molecules in adipose tissue were altered. •Increased levels of prohibitin mRNA in white fat were observed. •Attenuated levels of β3-adrenergic receptor mRNA were observed in brown fat. •Such alterations in adipose tissue may contribute to obesity later in life. -- Abstract: The effects of early postnatal maternal deprivation on the biological characteristics of the adipose tissue later in life were investigated in the present study. Sprague–Dawley rats were classified as either maternal deprivation (MD) or mother-reared control (MRC) groups. MD was achieved by separating the rat pups from their mothers for 3 h each day during the 10–15 postnatal days. mRNA levels of mitochondrial uncoupling protein 1 (UCP-1), β3-adrenergic receptor (β3-AR), and prohibitin (PHB) in the brown and white adipose tissue were determined using real-time RT-PCR analysis. UCP-1, which is mediated through β3-AR, is closely involved in the energy metabolism and expenditure. PHB is highly expressed in the proliferating tissues/cells. At 10 weeks of age, the body weight of the MRC and MD rats was similar. However, the levels of the key molecules in the adipose tissue were substantially altered. There was a significant increase in the expression of PHB mRNA in the white adipose tissue, while the β3-AR mRNA expression decreased significantly, and the UCP-1 mRNA expression remained unchanged in the brown adipose tissue. Given that these molecules influence the mitochondrial metabolism, our study indicates that early postnatal maternal deprivation can influence the fate of adipose tissue proliferation, presumably leading to obesity later in life

  13. Early postnatal maternal separation causes alterations in the expression of β3-adrenergic receptor in rat adipose tissue suggesting long-term influence on obesity

    Energy Technology Data Exchange (ETDEWEB)

    Miki, Takanori, E-mail: mikit@med.kagawa-u.ac.jp [Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University (Japan); Liu, Jun-Qian; Ohta, Ken-ichi; Suzuki, Shingo [Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University (Japan); Kusaka, Takashi [Department of Pediatrics, Faculty of Medicine, Kagawa University (Japan); Warita, Katsuhiko [Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University (Japan); Yokoyama, Toshifumi [Department of Bioresource and Agrobiosciences, Graduate School of Science and Technology, Kobe University (Japan); Jamal, Mostofa [Department of Forensic Medicine, Faculty of Medicine, Kagawa University (Japan); Ueki, Masaaki [Department of Anesthesia, Nishiwaki Municipal Hospital (Japan); Yakura, Tomiko; Tamai, Motoki [Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University (Japan); Sumitani, Kazunori [Department of Medical Education, Faculty of Medicine, Kagawa University (Japan); Hosomi, Naohisa [Department of Clinical Neuroscience and Therapeutics, Hiroshima University Graduate School of Biomedical Sciences (Japan); Takeuchi, Yoshiki [Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University (Japan)

    2013-12-06

    Highlights: •High-fat diet intake following maternal separation did not cause body weight gain. •However, levels of metabolism-related molecules in adipose tissue were altered. •Increased levels of prohibitin mRNA in white fat were observed. •Attenuated levels of β3-adrenergic receptor mRNA were observed in brown fat. •Such alterations in adipose tissue may contribute to obesity later in life. -- Abstract: The effects of early postnatal maternal deprivation on the biological characteristics of the adipose tissue later in life were investigated in the present study. Sprague–Dawley rats were classified as either maternal deprivation (MD) or mother-reared control (MRC) groups. MD was achieved by separating the rat pups from their mothers for 3 h each day during the 10–15 postnatal days. mRNA levels of mitochondrial uncoupling protein 1 (UCP-1), β3-adrenergic receptor (β3-AR), and prohibitin (PHB) in the brown and white adipose tissue were determined using real-time RT-PCR analysis. UCP-1, which is mediated through β3-AR, is closely involved in the energy metabolism and expenditure. PHB is highly expressed in the proliferating tissues/cells. At 10 weeks of age, the body weight of the MRC and MD rats was similar. However, the levels of the key molecules in the adipose tissue were substantially altered. There was a significant increase in the expression of PHB mRNA in the white adipose tissue, while the β3-AR mRNA expression decreased significantly, and the UCP-1 mRNA expression remained unchanged in the brown adipose tissue. Given that these molecules influence the mitochondrial metabolism, our study indicates that early postnatal maternal deprivation can influence the fate of adipose tissue proliferation, presumably leading to obesity later in life.

  14. Maternal inflammation during pregnancy and childhood adiposity

    NARCIS (Netherlands)

    R. Gaillard (Romy); S.L. Rifas-Shiman (Sheryl); W. Perng (Wei); E. Oken (Emily); M.W. Gillman (Matthew W.)

    2016-01-01

    textabstractObjective: Maternal pre-pregnancy obesity is associated with offspring obesity. Underlying mechanisms may involve a maternal obesity-mediated proinflammatory state during pregnancy. Maternal C-reactive protein (CRP) level during pregnancy is a biomarker of low-grade systemic

  15. Obesity.

    OpenAIRE

    Callaway, C W

    1987-01-01

    Obesity is not a single disease, but a variety of conditions resulting from different mechanisms and associated with various types and degrees of risks. To determine who should lose weight, how much weight should be lost, and how to undertake weight loss, the following types of information are needed: personal-demographic data, developmental patterns, family history, energy balance, body composition/fat distribution, psychological/behavioral measures, endocrine/metabolic measures, complicatio...

  16. Retrospective cohort study of the effects of obesity in early pregnancy on maternal weight gain and obstetric outcomes in an obstetric population in Africa

    Directory of Open Access Journals (Sweden)

    Iyoke CA

    2013-08-01

    Full Text Available Chukwuemeka A Iyoke,1 George O Ugwu,1 Frank O Ezugwu,2 Osaheni L Lawani,3 Azubuike K Onyebuchi31Departments of Obstetrics and Gynaecology, University of Nigeria Teaching Hospital, Enugu, 2Departments of Obstetrics and Gynaecology, Enugu State University Teaching Hospital, Enugu, 3Departments of Obstetrics and Gynaecology, Federal Medical Centre, Abakaliki, Ebonyi State, NigeriaObjective: The purpose of this study was to compare maternal weight gain in pregnancy and obstetric outcomes between women with obesity in early pregnancy and those with a normal body mass index (BMI in early pregnancy.Methods: This was a retrospective cohort study of women with obesity in early pregnancy and those with a normal BMI who were seen at three teaching hospitals in South-East Nigeria. Statistical analysis was performed using Statistical Package for the Social Sciences version 17.0 software, with descriptive and inferential statistics at the 95% level of confidence.Results: The study sample consisted of 648 women (324 obese and 324 healthy-weight. The mean age of the obese women was 26.7 ± 5.1 years and that of the healthy-weight women was 26.6 ± 4.9 years. Although both excessive weight gain (odds ratio [OR] 0.35, 95% confidence interval [CI] 0.23–0.54 and inadequate weight gain (OR 0.08, 95% CI 0.04–0.15 were less common in women with early pregnancy obesity than in healthy-weight women, a significantly higher proportion of obese women with excessive weight gain had adverse fetomaternal outcomes. Also, a significantly higher proportion of obese women had specific complications, such as premature rupture of membranes (OR 2.36, 95% CI 1.12–5.04, gestational hypertension/pre-eclampsia (OR 2.31, 95% CI 1.12–5.04, antepartum hemorrhage (OR 2.78, 95% CI 1.02–7.93, gestational diabetes (OR 4.24, 95% CI 1.62–11.74, cesarean delivery (OR 2.3, 95% CI 1.2–5.44, macrosomia (OR 4.08, 95% CI 1.06–8.41, severe birth asphyxia (OR 2.8, 95% CI 1.2–6

  17. Effect of metformin on maternal and fetal outcomes in obese pregnant women (EMPOWaR): a randomised, double-blind, placebo-controlled trial.

    Science.gov (United States)

    Chiswick, Carolyn; Reynolds, Rebecca M; Denison, Fiona; Drake, Amanda J; Forbes, Shareen; Newby, David E; Walker, Brian R; Quenby, Siobhan; Wray, Susan; Weeks, Andrew; Lashen, Hany; Rodriguez, Aryelly; Murray, Gordon; Whyte, Sonia; Norman, Jane E

    2015-10-01

    Maternal obesity is associated with increased birthweight, and obesity and premature mortality in adult offspring. The mechanism by which maternal obesity leads to these outcomes is not well understood, but maternal hyperglycaemia and insulin resistance are both implicated. We aimed to establish whether the insulin sensitising drug metformin improves maternal and fetal outcomes in obese pregnant women without diabetes. We did this randomised, double-blind, placebo-controlled trial in antenatal clinics at 15 National Health Service hospitals in the UK. Pregnant women (aged ≥16 years) between 12 and 16 weeks' gestation who had a BMI of 30 kg/m(2) or more and normal glucose tolerance were randomly assigned (1:1), via a web-based computer-generated block randomisation procedure (block size of two to four), to receive oral metformin 500 mg (increasing to a maximum of 2500 mg) or matched placebo daily from between 12 and 16 weeks' gestation until delivery of the baby. Randomisation was stratified by study site and BMI band (30-39 vs ≥40 kg/m(2)). Participants, caregivers, and study personnel were masked to treatment assignment. The primary outcome was Z score corresponding to the gestational age, parity, and sex-standardised birthweight percentile of liveborn babies delivered at 24 weeks or more of gestation. We did analysis by modified intention to treat. This trial is registered, ISRCTN number 51279843. Between Feb 3, 2011, and Jan 16, 2014, inclusive, we randomly assigned 449 women to either placebo (n=223) or metformin (n=226), of whom 434 (97%) were included in the final modified intention-to-treat analysis. Mean birthweight at delivery was 3463 g (SD 660) in the placebo group and 3462 g (548) in the metformin group. The estimated effect size of metformin on the primary outcome was non-significant (adjusted mean difference -0·029, 95% CI -0·217 to 0·158; p=0·7597). The difference in the number of women reporting the combined adverse outcome of miscarriage

  18. Newborn regional body composition is influenced by maternal obesity, gestational weight gain and the birthweight standard score

    DEFF Research Database (Denmark)

    Carlsen, E M; Renault, Kristina Martha; Nørgaard, K

    2014-01-01

    obese and 80 normal weight mothers and their newborn infants and assessed the babies' body composition using dual-energy X-ray absorptiometry. RESULTS: The total and abdominal fat masses of infants born to mother who were obese before pregnancy were 135 g (p

  19. Peroxisome proliferator-activated receptors-alpha and gamma are targets to treat offspring from maternal diet-induced obesity in mice.

    Directory of Open Access Journals (Sweden)

    D'Angelo Carlo Magliano

    Full Text Available AIM: The aim of the present study was to evaluate whether activation of peroxisome proliferator-activated receptor (PPARalpha and PPARgamma by Bezafibrate (BZ could attenuate hepatic and white adipose tissue (WAT abnormalities in male offspring from diet-induced obese dams. MATERIALS AND METHODS: C57BL/6 female mice were fed a standard chow (SC; 10% lipids diet or a high-fat (HF; 49% lipids diet for 8 weeks before mating and during gestation and lactation periods. Male offspring received SC diet at weaning and were subdivided into four groups: SC, SC/BZ, HF and HF/BZ. Treatment with BZ (100 mg/Kg diet started at 12 weeks of age and was maintained for three weeks. RESULTS: The HF diet resulted in an overweight phenotype and an increase in oral glucose intolerance and fasting glucose of dams. The HF offspring showed increased body mass, higher levels of plasmatic and hepatic triglycerides, higher levels of pro-inflammatory and lower levels of anti-inflammatory adipokines, impairment of glucose metabolism, abnormal fat pad mass distribution, higher number of larger adipocytes, hepatic steatosis, higher expression of lipogenic proteins concomitant to decreased expression of PPARalpha and carnitine palmitoyltransferase I (CPT-1 in liver, and diminished expression of PPARgamma and adiponectin in WAT. Treatment with BZ ameliorated the hepatic and WAT abnormalities generated by diet-induced maternal obesity, with improvements observed in the structural, biochemical and molecular characteristics of the animals' livers and epididymal fat. CONCLUSION: Diet-induced maternal obesity lead to alterations in metabolism, hepatic lipotoxicity and adverse liver and WAT remodeling in the offspring. Targeting PPAR with Bezafibrate has beneficial effects reducing the alterations, mainly through reduction of WAT inflammatory state through PPARgamma activation and enhanced hepatic beta-oxidation due to increased PPARalpha/PPARgamma ratio in liver.

  20. Maternal feeding practices and children's eating behaviours: A comparison of mothers with healthy weight versus overweight/obesity.

    Science.gov (United States)

    Haycraft, Emma; Karasouli, Eleni; Meyer, Caroline

    2017-09-01

    This study aimed to explore differences between mothers with healthy weight versus overweight/obesity in a wide range of their reported child feeding practices and their reports of their children's eating behaviours. Mothers (N = 437) with a 2-6-year-old child participated. They comprised two groups, based on their BMI: healthy weight (BMI of 18.0-24.9, inclusive) or overweight/obese (BMI of 25.0 or more). All mothers provided demographic information and completed self-report measures of their child feeding practices and their child's eating behaviour. In comparison to mothers with healthy weight, mothers with overweight/obesity reported giving their child more control around eating (p obesity reported their children to have a greater desire for drinks (p = 0.003), be more responsive to satiety (p = 0.007), and be slower eaters (p = 0.034). Mothers with overweight/obesity appear to engage in generally less healthy feeding practices with their children than mothers with healthy weight, and mothers with overweight/obesity perceive their children as more avoidant about food but not drinks. Such findings are likely to inform future intervention developments and help health workers and clinicians to better support mothers with overweight/obesity with implementing healthful feeding practices and promoting healthy eating habits in their children. Copyright © 2017 Elsevier Ltd. All rights reserved.

  1. Maternal air pollution exposure induces fetal neuroinflammation and predisposes offspring to obesity in aduthood in a sex-specific manner

    Science.gov (United States)

    Emerging evidence suggests environmental chemical exposures during critical windows of development may contribute to the escalating prevalence of obesity. We tested the hypothesis that prenatal air pollution exposure would predispose the offspring to weight gain in adulthood. Pre...

  2. Influence of Maternal and Child Lifestyle-Related Characteristics on the Socioeconomic Inequality in Overweight and Obesity among 5-year-old Children; The "Be Active, Eat Right" Study

    NARCIS (Netherlands)

    Veldhuis, L.; Vogel, I.; van Rossem, L.; Renders, C.M.; Hirasing, R.A.; Mackenbach, J.P.; Raat, H.

    2013-01-01

    It is unclear whether the socioeconomic inequality in prevalence of overweight and obesity is already present among very young children. This study investigates the association between overweight and socioeconomic status (SES, with maternal educational level as an indicator of SES) among 5-year-old

  3. Influence of maternal and child lifestyle-related characteristics on the socioeconomic inequality in overweight and obesity among 5-year-old children; the "Be Active, Eat Right" Study.

    NARCIS (Netherlands)

    L. Veldhuis (Lydian); I. Vogel (Ineke); L. van Rossem (Lenie); C.M. Renders (Carry); R.A. Hirasing (Remy); J.P. Mackenbach (Johan); H. Raat (Hein)

    2013-01-01

    textabstractIt is unclear whether the socioeconomic inequality in prevalence of overweight and obesity is already present among very young children. This study investigates the association between overweight and socioeconomic status (SES, with maternal educational level as an indicator of SES) among

  4. Influence of maternal and child lifestyle-related characteristics on the socioeconomic inequality in overweight and obesity among 5-year-old children; the "Be active, eat right" study

    NARCIS (Netherlands)

    L. Veldhuis (Lydian); I. Vogel (Ineke); L. van Rossem (Lenie); C.M. Renders (Carry); R.A. Hirasing (Remy); J.P. Mackenbach (Johan); H. Raat (Hein)

    2013-01-01

    textabstractIt is unclear whether the socioeconomic inequality in prevalence of overweight and obesity is already present among very young children. This study investigates the association between overweight and socioeconomic status (SES, with maternal educational level as an indicator of SES) among

  5. [Maternal metabolic diseases related to pre-pregnancy overweight and obesity in mexican women with high risk pregnancy].

    Science.gov (United States)

    Hernández-Higareda, Salvador; Pérez-Pérez, Omar-Alejandro; Balderas-Peña, Luz-Ma-Adriana; Martínez-Herrera, Brenda-Eugenia; Salcedo-Rocha, Ana-Leticia; Ramírez-Conchas, Rosa-Emilia

    Pre-pregnancy obesity has been proposed as a risk factor related to gestational diabetes and hypertensive disorders during pregnancy. Identify pregnancy related diseases associated with pre-pregnancy obesity as a risk factor ina high risk preganancy patient population. 600 patients whose pre-pregnancy obesity had been assessed as a high risk factor were included in the study. The means, standard deviation, median, interquartile intervals, Pearson and Spearman correlation and logistic regression to estimate risk with the odds ratio and 95% confidence intervals were calculated. The mean pre-pregnancy body mass index was 29.59 ± 6.42 kg/m 2 . The mean for recommended pregnancy weight gain was 2.31 ± 1.03 kg, but the mean of real weight gain was 8.91 ± 6.84 kg. A significant correlation between pre-pregnancy obesity and family history of diabetes mellitus (p=0.000), systemic hypertension (p=0.003), cardiac diseases (p=0.000), dyslipidemia (p=0.000) and obesity (p=0.000) was identified. Pre-pregnancy obesity was identified as a risk factor for the development of gestational diabetes (OR: 1.95; IC95%: 1.39 to 2.76; p=0.000) in this kind of patient. 75% of high risk pregnancy women in a high specialty hospital in West Mexico are overweight or obese when they become pregnant. These are risk factors in the development of gestational diabetes. Copyright © 2016 Academia Mexicana de Cirugía A.C. Publicado por Masson Doyma México S.A. All rights reserved.

  6. Longitudinal assessment of maternal endothelial function and markers of inflammation and placental function throughout pregnancy in lean and obese mothers.

    Science.gov (United States)

    Stewart, Frances M; Freeman, Dilys J; Ramsay, Jane E; Greer, Ian A; Caslake, Muriel; Ferrell, William R

    2007-03-01

    Obesity in pregnancy is increasing and is a risk factor for metabolic pathology such as preeclampsia. In the nonpregnant, obesity is associated with dyslipidemia, vascular dysfunction, and low-grade chronic inflammation. Our aim was to measure microvascular endothelial function in lean and obese pregnant women at intervals throughout their pregnancies and at 4 months after delivery. Plasma markers of endothelial function, inflammation, and placental function and their association with microvascular function were also assessed. Women in the 1st trimester of pregnancy were recruited, 30 with a body mass index (BMI) less than 30 kg/m(2) and 30 with a BMI more than or equal to 30 kg/m(2) matched for age, parity, and smoking status. In vivo endothelial-dependent and -independent microvascular function was measured using laser Doppler imaging in the 1st, 2nd, and 3rd trimesters of pregnancy and at 4 months postnatal. Plasma markers of endothelial activation [soluble intercellular cell adhesion molecule-1 (sVCAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), von Willebrand factor (vWF), and plasminogen activator inhibitor (PAI)-1], inflammation (IL-6, TNFalpha, C-reactive protein, and IL-10), and placental function (PAI-1/PAI-2 ratio) were also assessed at each time point. The pattern of improving endothelial function during pregnancy was the same for lean and obese, but endothelial-dependent vasodilation was significantly lower (P lean women but declined to near 1st trimester levels in the obese (lean/obese difference, 115%; P lean response being greater than obese (P = 0.021), and response declined in both groups in the postpartum period. In multivariate analysis, time of sampling had the most impact on endothelial-independent function [18.5% (adjusted sum of squares expressed as a percentage of total means squared), P lean 0.30 (0.21-0.47), P lean counterparts. There was a higher PAI-1/ PAI-2 ratio in the 1st trimester in obese women, which improved later in

  7. Maternal Depressive and Anxiety Symptoms, Self-Esteem, Body Dissatisfaction and Preschooler Obesity: A Cross-Sectional Study

    Science.gov (United States)

    Benton, Pree; Skouteris, Helen; Hayden, Melissa

    2016-01-01

    The primary aim of the present study was to cross-sectionally examine the associations between maternal psychosocial variables, child feeding practices, and preschooler body mass index z-score (BMI-z) in children (aged 2-4 years). A secondary aim was to examine differences in child weight outcomes between mothers scoring above and below specified…

  8. Prenatal programming in an obese swine model: sex-related effects of maternal energy restriction on morphology, metabolism and hypothalamic gene expression.

    Science.gov (United States)

    Óvilo, Cristina; González-Bulnes, Antonio; Benítez, Rita; Ayuso, Miriam; Barbero, Alicia; Pérez-Solana, Maria L; Barragán, Carmen; Astiz, Susana; Fernández, Almudena; López-Bote, Clemente

    2014-02-01

    Maternal energy restriction during pregnancy predisposes to metabolic alterations in the offspring. The present study was designed to evaluate phenotypic and metabolic consequences following maternal undernutrition in an obese pig model and to define the potential role of hypothalamic gene expression in programming effects. Iberian sows were fed a control or a 50 % restricted diet for the last two-thirds of gestation. Newborns were assessed for body and organ weights, hormonal and metabolic status, and hypothalamic expression of genes implicated in energy homeostasis, glucocorticoid function and methylation. Weight and adiposity were measured in adult littermates. Newborns of the restricted sows were lighter (P control newborns of both the sexes (P metabolic stress by nutrient insufficiency. A lower hypothalamic expression of anorexigenic peptides (LEPR and POMC, P controls (Pmetabolic alterations in the offspring. Differences in gene expression at birth and higher growth and adiposity in adulthood suggest a female-specific programming effect for a positive energy balance, possibly due to overexposure to endogenous stress-induced glucocorticoids.

  9. Maternal feeding practices and children's eating behaviours : a comparison of mothers with healthy weight versus overweight/obesity.

    OpenAIRE

    Haycraft, Emma; Karasouli, Eleni; Meyer, Caroline

    2017-01-01

    This study aimed to explore differences between mothers with healthy weight versus overweight/obesity in a wide range of their reported child feeding practices and their reports of their children's eating behaviours. Mothers (N = 437) with a 2-6-year-old child participated. They comprised two groups, based on their BMI: healthy weight (BMI of 18.0–24.9, inclusive) or overweight/obese (BMI of 25.0 or more). All mothers provided demographic information and completed self-report measures of thei...

  10. Maternal prepregnancy obesity and insulin treatment during pregnancy are independently associated with delayed lactogenesis in women with recent gestational diabetes mellitus.

    Science.gov (United States)

    Matias, Susana L; Dewey, Kathryn G; Quesenberry, Charles P; Gunderson, Erica P

    2014-01-01

    The timely onset of stage II lactogenesis (OL) is important for successful breastfeeding and newborn health. Several risk factors for delayed OL are common in women with a history of gestational diabetes mellitus (GDM), which may affect their chances for successful breastfeeding outcomes. We investigated the prevalence and risk factors associated with delayed OL in a racially and ethnically diverse cohort of postpartum women with recent GDM. We analyzed data collected in the Study of Women, Infant Feeding and Type 2 Diabetes After GDM Pregnancy (SWIFT), which is a prospective cohort of women diagnosed with GDM who delivered at Kaiser Permanente Northern California hospitals from 2008 to 2011. At 6-9 wk postpartum, delayed OL was assessed by maternal report of breast fullness and defined as occurring after 72 h postpartum. We obtained data on prenatal course and postdelivery infant feeding practices from electronic medical records and in-person surveys. We used multivariable logistic regression models to estimate associations of delayed OL with prenatal, delivery, and postnatal characteristics. The analysis included 883 SWIFT participants who initiated breastfeeding and did not have diabetes at 6-9 wk postpartum. Delayed OL was reported by 33% of women and was associated with prepregnancy obesity (OR: 1.56; 95% CI: 1.07, 2.29), older maternal age (OR: 1.05; 95% CI: 1.01, 1.08), insulin GDM treatment (OR: 3.11; 95% CI: 1.37, 7.05), and suboptimal in-hospital breastfeeding (OR: 1.65; 95% CI: 1.20, 2.26). A higher gestational age was associated with decreased odds of delayed OL but only in multiparous mothers (OR: 0.79; 95% CI: 0.67, 0.94). One-third of women with recent GDM experienced delayed OL. Maternal obesity, insulin treatment, and suboptimal in-hospital breastfeeding were key risk factors for delayed OL. Early breastfeeding support for GDM women with these risk factors may be needed to ensure successful lactation. This trial was registered at clinicaltrials

  11. Maternal Smoking, Obesity and Male Fetal Sex Predispose to a Large Nuchal Translucency Thickness in Healthy Fetuses

    DEFF Research Database (Denmark)

    Pedersen, Nina Gros; Rode, L; Ekelund, Christer

    2010-01-01

    to multiples of the median (MoM(NT)) using a previously reported linear regression analysis. Results: The odds ratio (OR) for MoM(NT) >95th centile was 1.5 (95% CI 1.2-1.9) for smokers compared to nonsmokers and 1.4 (95% CI 1.1-1.7) for male fetuses compared to female fetuses. Obese women (BMI >/=30) had...... an increased OR for a large NT of 1.7 (95% CI 1.2-2.6) compared to normal weight women. Obese smokers carrying a male fetus had an OR of 4.2 (95% CI 1.7-10.1) of a MoM(NT) >95th centile compared to normal weight nonsmoking women with a female fetus. The effects of smoking, obesity status and fetal sex were...... independent of each other. Conclusions: Smoking, obesity and male sex are associated to a MoM(NT) >95th centile. This may affect screening performance and entail unnecessary anxiety in these women. Further investigations, including fetuses with adverse outcome, are needed....

  12. Maternal Smoking, Obesity and Male Fetal Sex Predispose to a Large Nuchal Translucency Thickness in Healthy Fetuses

    DEFF Research Database (Denmark)

    Pedersen, Nina Gros; Rode, Line; Ekelund, Christer

    2011-01-01

    to multiples of the median (MoM(NT)) using a previously reported linear regression analysis. Results: The odds ratio (OR) for MoM(NT) >95th centile was 1.5 (95% CI 1.2-1.9) for smokers compared to nonsmokers and 1.4 (95% CI 1.1-1.7) for male fetuses compared to female fetuses. Obese women (BMI >/=30) had...... an increased OR for a large NT of 1.7 (95% CI 1.2-2.6) compared to normal weight women. Obese smokers carrying a male fetus had an OR of 4.2 (95% CI 1.7-10.1) of a MoM(NT) >95th centile compared to normal weight nonsmoking women with a female fetus. The effects of smoking, obesity status and fetal sex were...... independent of each other. Conclusions: Smoking, obesity and male sex are associated to a MoM(NT) >95th centile. This may affect screening performance and entail unnecessary anxiety in these women. Further investigations, including fetuses with adverse outcome, are needed....

  13. Newborn regional body composition is influenced by maternal obesity, gestational weight gain and the birthweight standard score.

    Science.gov (United States)

    Carlsen, E M; Renault, K M; Nørgaard, K; Nilas, L; Jensen, J E B; Hyldstrup, L; Michaelsen, K F; Cortes, D; Pryds, O

    2014-09-01

    This study investigated whether newborn body composition is influenced by prepregnancy obesity and gestational weight gain (GWG) and explored any associations between body composition and birthweight standard score (z-score), categorised by size for gestational age. We recruited 231 obese and 80 normal weight mothers and their newborn infants and assessed the babies' body composition using dual-energy X-ray absorptiometry. The total and abdominal fat masses of infants born to mother who were obese before pregnancy were 135 g (p weight mothers. The infants' fat mass increased by 11 g (p gestational age (15.3%) than small for gestational age (5.2%) and appropriate for gestational age (9.8%) (p < 0.001). Lower birthweight z-score was associated with a higher proportion of abdominal fat mass (p = 0.009). Infants born to obese mothers had higher fat mass at birth, with abdominal fat accumulation. Low birthweight was associated with a lower crude abdominal fat mass, but a higher proportion of total fat mass placed abdominally. ©2014 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

  14. Influence of maternal and child lifestyle-related characteristics on the socioeconomic inequality in overweight and obesity among 5-year-old children; the "Be Active, Eat Right" Study.

    Science.gov (United States)

    Veldhuis, Lydian; Vogel, Ineke; van Rossem, Lenie; Renders, Carry M; Hirasing, Remy A; Mackenbach, Johan P; Raat, Hein

    2013-06-06

    It is unclear whether the socioeconomic inequality in prevalence of overweight and obesity is already present among very young children. This study investigates the association between overweight and socioeconomic status (SES, with maternal educational level as an indicator of SES) among 5-year-old children. This cross-sectional study uses baseline data from 5-year-olds of Dutch ethnicity (n = 5,582) and their mothers collected for the "Be active, eat right" study. Compared to children of mothers with the highest educational level, for children of mothers with the lowest educational level the odds ratio (adjusted for demographic characteristics) for having overweight was 2.10 (95% confidence interval: 1.57-2.82), and for having obesity was 4.18 (95% confidence interval: 2.32-7.55). Addition of maternal and child lifestyle-related characteristics decreased the odds ratios for overweight and obesity by 26.4% and 42.1%, respectively. The results show that an inverse SES-overweight/obesity association is already present at elementary school entry, and that watching TV by mother and child, the child consuming breakfast and, especially maternal weight status, are contributing factors in this association. These results should be taken into account when developing policies to reduce inequalities in (childhood) health.

  15. Mechanisms of Hypoxic Up-Regulation of Versican Gene Expression in Macrophages.

    Directory of Open Access Journals (Sweden)

    Fattah Sotoodehnejadnematalahi

    Full Text Available Hypoxia is a hallmark of many pathological tissues. Macrophages accumulate in hypoxic sites and up-regulate a range of hypoxia-inducible genes. The matrix proteoglycan versican has been identified as one such gene, but the mechanisms responsible for hypoxic induction are not fully characterised. Here we investigate the up-regulation of versican by hypoxia in primary human monocyte-derived macrophages (HMDM, and, intriguingly, show that versican mRNA is up-regulated much more highly (>600 fold by long term hypoxia (5 days than by 1 day of hypoxia (48 fold. We report that versican mRNA decay rates are not affected by hypoxia, demonstrating that hypoxic induction of versican mRNA is mediated by increased transcription. Deletion analysis of the promoter identified two regions required for high level promoter activity of luciferase reporter constructs in human macrophages. The hypoxia-inducible transcription factor HIF-1 has previously been implicated as a key potential regulator of versican expression in hypoxia, however our data suggest that HIF-1 up-regulation is unlikely to be principally responsible for the high levels of induction observed in HMDM. Treatment of HMDM with two distinct specific inhibitors of Phosphoinositide 3-kinase (PI3K, LY290042 and wortmannin, significantly reduced induction of versican mRNA by hypoxia and provides evidence of a role for PI3K in hypoxic up-regulation of versican expression.

  16. 7A.06: MATERNAL OBESITY AND THE DEVELOPMENTAL PROGRAMMING OF HYPERTENSION: ALTERED LEPTIN SIGNALLING PATHWAY IN THE CENTRAL NERVOUS SYSTEM.

    Science.gov (United States)

    Lim, J; Burke, S; Head, G A

    2015-06-01

    The prevalence of obesity in women among child baring age is increasing and this has been parallel to the increase in obesity in general population around the world. We investigated the trans-generational 'programming' of leptin signalling in the central nervous system (CNS) to increase blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) following a high fat diet (HFD)feeding in mothers. Female New Zealand White rabbits were fed a high fat (13%) diet (mHFD) or a control diet (mCD) prior mating and during pregnancy. Kittens from mCD rabbits were subdivided and fed HFD for 10days (mCD10dHFD) at 15 weeks of age. All rabbits received an intracerebroventricular (ICV) catheter into the lateral ventricle and a recording electrode on the left renal nerve. Experiments were conducted in conscious rabbits and BP, HR and RSNA was measured. Rabbits received an increasing doses of ICV Melanocortin receptor antagonist (SHU9119),alpha-Melanocortin stimulating hormone (alpha-MSH) and a single dose of Leptin antagonist. ICV SHU9119 reduced BP (-5.8 ± 0.7mmHg and -4.1 ± 0.9mmHg) and RSNA (-2.4 ± 0.3 nu and -0.7 ± 0.3 nu) in mHFD and mCD10dHFD rabbits (P fat was increased (50%) in all rabbits that had HFD. Obesity during pregnancy 'programs' leptin signalling pathway in the CNS of the offspring during development. Leptin via activation of melanocirtin pathway plays a key role in the CNS contributing to the pressor and tachycardic effects as well as renal sympathetic nerve activity in the pathophysiology of obesity.

  17. DMPD: Mechanism of age-associated up-regulation in macrophage PGE2 synthesis. [Dynamic Macrophage Pathway CSML Database

    Lifescience Database Archive (English)

    Full Text Available 15331118 Mechanism of age-associated up-regulation in macrophage PGE2 synthesis. Wu...e-associated up-regulation in macrophage PGE2 synthesis. PubmedID 15331118 Title Mechanism of age-associated... up-regulation in macrophage PGE2 synthesis. Authors Wu D, Meydani SN. Publicatio

  18. Effects of Obesity and Metabolic Syndrome on Steroidogenesis and Folliculogenesis in the Female Ossabaw Mini-Pig.

    Directory of Open Access Journals (Sweden)

    Annie E Newell-Fugate

    Full Text Available The discrete effects of obesity on infertility in females remain undefined to date. To investigate obesity-induced ovarian dysfunction, we characterized metabolic parameters, steroidogenesis, and folliculogenesis in obese and lean female Ossabaw mini-pigs. Nineteen nulliparous, sexually mature female Ossabaw pigs were fed a high fat/cholesterol/fructose diet (n=10 or a control diet (n=9 for eight months. After a three-month diet-induction period, pigs remained on their respective diets and had ovarian ultrasound and blood collection conducted during a five-month study period after which ovaries were collected for histology, cell culture, and gene transcript level analysis. Blood was assayed for steroid and protein hormones. Obese pigs developed abdominal obesity and metabolic syndrome, including hyperglycemia, hypertension, insulin resistance and dyslipidemia. Obese pigs had elongated estrous cycles and hyperandrogenemia with decreased LH, increased FSH and luteal phase progesterone, and increased numbers of medium, ovulatory, and cystic follicles. Theca cells of obese, compared to control, pigs displayed androstenedione hypersecretion in response to in vitro treatment with LH, and up-regulated 3-beta-hydroxysteroid dehydrogenase 1 and 17-beta-hydroxysteroid dehydrogenase 4 transcript levels in response to in vitro treatment with LH or LH + insulin. Granulosa cells of obese pigs had increased 3-beta-hydroxysteroid dehydrogenase 1 transcript levels. In summary, obese Ossabaw pigs have increased transcript levels and function of ovarian enzymes in the delta 4 steroidogenic pathway. Alterations in LH, FSH, and progesterone, coupled with theca cell dysfunction, contribute to the hyperandrogenemia and disrupted folliculogenesis patterns observed in obese pigs. The obese Ossabaw mini-pig is a useful animal model in which to study the effects of obesity and metabolic syndrome on ovarian function and steroidogenesis. Ultimately, this animal model may be

  19. Postpartum maternal fat distribution and its association with offspring body fat through the first year of life

    Science.gov (United States)

    Maternal obesity is known to increase the risk of offspring obesity. Despite the evidence supporting the impact of maternal obesity on infant health, there are no studies examining the effects of maternal fat distribution on the programming of offspring obesity. We hypothesized that increased matern...

  20. Obese pregnant women and complications in relation to pregnancy and birth

    DEFF Research Database (Denmark)

    Vinter, Christina Anne; Tanvig, Mette Honnens; Damm, Peter

    2012-01-01

    One third of the pregnant Danish women are overweight or obese. Maternal obesity is an independent risk factor for adverse maternal and foetal outcomes including infertility, miscarriage, congenital malformations, preeclampsia, gestational diabetes, complicated deliveries, caesarean section......, macrosomia and childhood obesity. This article reviews the effect of maternal obesity on obstetric and neonatal outcomes and provides recommendations for management of obesity in pregnancy....

  1. Feto-Maternal Outcome in Supervised Pregnancies of the ...

    African Journals Online (AJOL)

    obese parturients Materials and Methods 106 obese, pregnant women and an equal number of non–obese matched controls who booked and delivered in LASUTH were studied. Biosocial data as well as feto-maternal parameters were recorded ...

  2. The emerging role of m-TOR up-regulation in brain Astrocytoma.

    Science.gov (United States)

    Ryskalin, Larisa; Limanaqi, Fiona; Biagioni, Francesca; Frati, Alessandro; Esposito, Vincenzo; Calierno, Maria Teresa; Lenzi, Paola; Fornai, Francesco

    2017-05-01

    The present manuscript is an overview of various effects of mTOR up-regulation in astrocytoma with an emphasis on its deleterious effects on the proliferation of Glioblastoma Multiforme. The manuscript reports consistent evidence indicating the occurrence of mTOR up-regulation both in experimental and human astrocytoma. The grading of human astrocytoma is discussed in relationship with mTOR up-regulation. In the second part of the manuscript, the biochemical pathways under the influence of mTOR are translated to cell phenotypes which are generated by mTOR up-regulation and reverted by its inhibition. A special section is dedicated to the prominent role of autophagy in mediating the effects of mTOR in glioblastoma. In detail, autophagy inhibition produced by mTOR up-regulation determines the fate of cancer stem cells. On the other hand, biochemical findings disclose the remarkable effects of autophagy activators as powerful inducers of cell differentiation with a strong prevalence towards neuronal phenotypes. Thus, mTOR modulation acts on the neurobiology of glioblastoma just like it operates in vivo at the level of brain stem cell niches by altering autophagy-dependent cell differentiation. In the light of such a critical role of autophagy we analyzed the ubiquitin proteasome system. The merging between autophagy and proteasome generates a novel organelle, named autophagoproteasome which is strongly induced by mTOR inhibitors in glioblastoma cells. Remarkably, when mTOR is maximally inhibited the proteasome component selectively moves within autophagy vacuoles, thus making the proteasome activity dependent on the entry within autophagy compartment.

  3. Up-regulation of the Neuronal Nicotinic Receptor α7 by HIV Glycoprotein 120

    Science.gov (United States)

    Ballester, Leomar Y.; Capó-Vélez, Coral M.; García-Beltrán, Wilfredo F.; Ramos, Félix M.; Vázquez-Rosa, Edwin; Ríos, Raymond; Mercado, José R.; Meléndez, Roberto I.; Lasalde-Dominicci, José A.

    2012-01-01

    Approximately 30–50% of the >30 million HIV-infected subjects develop neurological complications ranging from mild symptoms to dementia. HIV does not infect neurons, and the molecular mechanisms behind HIV-associated neurocognitive decline are not understood. There are several hypotheses to explain the development of dementia in HIV+ individuals, including neuroinflammation mediated by infected microglia and neuronal toxicity by HIV proteins. A key protein associated with the neurological complications of HIV, gp120, forms part of the viral envelope and can be found in the CSF of infected individuals. HIV-1-gp120 interacts with several receptors including CD4, CCR5, CXCR4, and nicotinic acetylcholine receptors (nAChRs). However, the role of nAChRs in HIV-associated neurocognitive disorder has not been investigated. We studied the effects of gp120IIIB on the expression and function of the nicotinic receptor α7 (α7-nAChR). Our results show that gp120, through activation of the CXCR4 chemokine receptor, induces a functional up-regulation of α7-nAChRs. Because α7-nAChRs have a high permeability to Ca2+, we performed TUNEL staining to investigate the effects of receptor up-regulation on cell viability. Our data revealed an increase in cell death, which was blocked by the selective antagonist α-bungarotoxin. The in vitro data are supported by RT-PCR and Western blot analysis, confirming a remarkable up-regulation of the α7-nAChR in gp120-transgenic mice brains. Specifically, α7-nAChR up-regulation is observed in mouse striatum, a region severely affected in HIV+ patients. In summary, CXCR4 activation induces up-regulation of α7-nAChR, causing cell death, suggesting that α7-nAChR is a previously unrecognized contributor to the neurotoxicity associated with HIV infection. PMID:22084248

  4. Maternal Diet Supplementation with n-6/n-3 Essential Fatty Acids in a 1.2 : 1.0 Ratio Attenuates Metabolic Dysfunction in MSG-Induced Obese Mice

    Directory of Open Access Journals (Sweden)

    Josiane Morais Martin

    2016-01-01

    Full Text Available Essential polyunsaturated fatty acids (PUFAs prevent cardiometabolic diseases. We aimed to study whether a diet supplemented with a mixture of n-6/n-3 PUFAs, during perinatal life, attenuates outcomes of long-term metabolic dysfunction in prediabetic and obese mice. Seventy-day-old virgin female mice were mated. From the conception day, dams were fed a diet supplemented with sunflower oil and flaxseed powder (containing an n-6/n-3 PUFAs ratio of 1.2 : 1.0 throughout pregnancy and lactation, while control dams received a commercial diet. Newborn mice were treated with monosodium L-glutamate (MSG, 4 mg g−1 body weight per day for the first 5 days of age. A batch of weaned pups was sacrificed to quantify the brain and pancreas total lipids; another batch were fed a commercial diet until 90 days of age, where glucose homeostasis and glucose-induced insulin secretion (GIIS as well as retroperitoneal fat and Lee index were assessed. MSG-treated mice developed obesity, glucose intolerance, insulin resistance, pancreatic islet dysfunction, and higher fat stores. Maternal flaxseed diet-supplementation decreased n-6/n-3 PUFAs ratio in the brain and pancreas and blocked glucose intolerance, insulin resistance, GIIS impairment, and obesity development. The n-6/n-3 essential PUFAs in a ratio of 1.2 : 1.0 supplemented in maternal diet during pregnancy and lactation prevent metabolic dysfunction in MSG-obesity model.

  5. Risk factors for obesity and high blood pressure in Chinese American children: maternal acculturation and children's food choices.

    Science.gov (United States)

    Chen, Jyu-Lin; Weiss, Sandra; Heyman, Melvin B; Lustig, Robert

    2011-04-01

    The objective of this study is to explore risk factors associated with overweight and high blood pressure in Chinese American children. Students and their parents were recruited from Chinese language schools in the San Francisco Bay Area. Data were collected on 67 children and their mothers, and included children's weight, height, waist and hip circumferences, blood pressure, level of physical activity, dietary intake, usual food choice, knowledge about nutrition and physical activity, and self-efficacy regarding diet and physical activity. Mothers completed questionnaires on demographic data and acculturation. About 46% of children had a body mass index exceeding the 85th percentile. Lower level of maternal acculturation is a risk factor for overweight and higher waist to hip ratio. Children's unhealthy food choices were predictive of high body mass index and high systolic blood pressure, whereas older age and less physical activity in children were predictors of high diastolic blood pressure. Developing culturally sensitive and developmentally appropriate interventions to reduce overweight and high blood pressure is critical to reduce health disparities among minority children.

  6. Triazophos up-regulated gene expression in the female brown planthopper, Nilaparvata lugens.

    Science.gov (United States)

    Bao, Yan-Yuan; Li, Bao-Ling; Liu, Zhao-Bu; Xue, Jian; Zhu, Zeng-Rong; Cheng, Jia-An; Zhang, Chuan-Xi

    2010-09-01

    The widespread use of insecticides has caused the resurgence of the brown planthopper, Nilaparvata lugens, in Asia. In this study, we investigated an organo-phosphorous insecticide, triazophos, and its ability to induce gene expression variation in female N. lugens nymphs just before emergence. By using the suppression subtractive hybridization method, a triazophos-induced cDNA library was constructed. In total, 402 differentially expressed cDNA clones were obtained. Real-time qPCR analysis confirmed that triazophos up-regulated the expression of six candidate genes at the transcript level in nymphs on day 3 of the 5th instar. These genes encode N. lugens vitellogenin, bystin, multidrug resistance protein (MRP), purine nucleoside phosphorylase (PNP), pyrroline-5-carboxylate reductase (P5CR) and carboxylesterase. Our results imply that the up-regulation of these genes may be involved in the induction of N. lugens female reproduction or resistance to insecticides.

  7. SPARC is up-regulated during skeletal muscle regeneration and inhibits myoblast differentiation

    DEFF Research Database (Denmark)

    Petersson, Stine Juhl; Jørgensen, Louise Helskov; Andersen, Ditte C.

    2013-01-01

    Skeletal muscle repair is mediated primarily by the muscle stem cell, the satellite cell. Several factors, including extracellular matrix, are known to regulate satellite cell function and regeneration. One factor, the matricellular Secreted Protein Acidic and Rich in Cysteine (SPARC) is highly up......-regulated during skeletal muscle disease, but its function remains elusive. In the present study, we demonstrate a prominent yet transient increase in SPARC mRNA and protein content during skeletal muscle regeneration that correlates with the expression profile of specific muscle factors like MyoD, Myf5, Myf6......, Myogenin, NCAM, CD34, and M-Cadherin, all known to be implicated in satellite cell activation/proliferation following muscle damage. This up regulation was detected in more cell types. Ectopic expression of SPARC in the muscle progenitor cell line C2C12 was performed to mimic the high levels of SPARC seen...

  8. Programming of the appetite-regulating neural network: a link between maternal overnutrition and the programming of obesity?

    Science.gov (United States)

    Mühlhäusler, B S

    2007-01-01

    The concept of a functional foetal "appetite regulatory neural network" is a new and potentially critical one. There is a growing body of evidence showing that the nutritional environment to which the foetus is exposed during prenatal and perinatal development has long-term consequences for the function of the appetite-regulating neural network and therefore the way in which an individual regulates energy balance throughout later life. This is of particular importance in the context of evidence obtained from a wide range of epidemiological studies, which have shown that individuals exposed to an elevated nutrient supply before birth have an increased risk of becoming obese as children and adults. This review summarises the key pieces of experimental evidence, by our group and others, that have contributed to our current understanding of the programming of appetite, and highlights the important questions that are yet to be answered. It is clear that this area of research has the potential to generate, within the next few years, interventions that could begin to alleviate the adverse long-term consequences of being exposed to an elevated nutrient supply before birth.

  9. Gene up-regulation in response to predator kairomones in the water flea, Daphnia pulex

    Directory of Open Access Journals (Sweden)

    Okada Yasukazu

    2010-04-01

    Full Text Available Abstract Background Numerous cases of predator-induced polyphenisms, in which alternate phenotypes are produced in response to extrinsic stimuli, have been reported in aquatic taxa to date. The genus Daphnia (Branchiopoda, Cladocera provides a model experimental system for the study of the developmental mechanisms and evolutionary processes associated with predator-induced polyphenisms. In D. pulex, juveniles form neckteeth in response to predatory kairomones released by Chaoborus larvae (Insecta, Diptera. Results Previous studies suggest that the timing of the sensitivity to kairomones in D. pulex can generally be divided into the embryonic and postembryonic developmental periods. We therefore examined which of the genes in the embryonic and first-instar juvenile stages exhibit different expression levels in the presence or absence of predator kairomones. Employing a candidate gene approach and identifying differentially-expressed genes revealed that the morphogenetic factors, Hox3, extradenticle and escargot, were up-regulated by kairomones in the postembryonic stage and may potentially be responsible for defense morph formation. In addition, the juvenile hormone pathway genes, JHAMT and Met, and the insulin signaling pathway genes, InR and IRS-1, were up-regulated in the first-instar stage. It is well known that these hormonal pathways are involved in physiological regulation following morphogenesis in many insect species. During the embryonic stage when morphotypes were determined, one of the novel genes identified by differential display was up-regulated, suggesting that this gene may be related to morphotype determination. Biological functions of the up-regulated genes are discussed in the context of defense morph formation. Conclusions It is suggested that, following the reception of kairomone signals, the identified genes are involved in a series of defensive phenotypic alterations and the production of a defensive phenotype.

  10. Neuropilin 1 Receptor Is Up-Regulated in Dysplastic Epithelium and Oral Squamous Cell Carcinoma.

    Science.gov (United States)

    Shahrabi-Farahani, Shokoufeh; Gallottini, Marina; Martins, Fabiana; Li, Erik; Mudge, Dayna R; Nakayama, Hironao; Hida, Kyoko; Panigrahy, Dipak; D'Amore, Patricia A; Bielenberg, Diane R

    2016-04-01

    Neuropilins are receptors for disparate ligands, including proangiogenic factors such as vascular endothelial growth factor and inhibitory class 3 semaphorin (SEMA3) family members. Differentiated cells in skin epithelium and cutaneous squamous cell carcinoma highly express the neuropilin-1 (NRP1) receptor. We examined the expression of NRP1 in human and mouse oral mucosa. NRP1 was significantly up-regulated in oral epithelial dysplasia and oral squamous cell carcinoma (OSCC). NRP1 receptor localized to the outer suprabasal epithelial layers in normal tongue, an expression pattern similar to the normal skin epidermis. However, dysplastic tongue epithelium and OSCC up-regulated NRP1 in basal and proliferating epithelial layers, a profile unseen in cutaneous squamous cell carcinoma. NRP1 up-regulation is observed in a mouse carcinogen-induced OSCC model and in human tongue OSCC biopsies. Human OSCC cell lines express NRP1 protein in vitro and in mouse tongue xenografts. Sites of capillary infiltration into orthotopic OSCC tumors correlate with high NRP1 expression. HSC3 xenografts, which express the highest NRP1 levels of the cell lines examined, showed massive intratumoral lymphangiogenesis. SEMA3A inhibited OSCC cell migration, suggesting that the NRP1 receptor was bioactive in OSCC. In conclusion, NRP1 is regulated in the oral epithelium and is selectively up-regulated during epithelial dysplasia. NRP1 may function as a reservoir to sequester proangiogenic ligands within the neoplastic compartment, thereby recruiting neovessels toward tumor cells. Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

  11. Catalase activity prevents exercise-induced up-regulation of vasoprotective proteins in venous tissue.

    Science.gov (United States)

    Dao, Vu Thao-Vi; Floeren, Melanie; Kumpf, Stephanie; Both, Charlotte; Peter, Bärbel; Balz, Vera; Suvorava, Tatsiana; Kojda, Georg

    2011-11-01

    Physical activity induces favourable changes of arterial gene expression and protein activity, although little is known about its effect in venous tissue. Although our understanding of the initiating molecular signals is still incomplete, increased expression of endothelial nitric oxide synthase (eNOS) is considered a key event. This study sought to investigate the effects of two different training protocols on the expression of eNOS and extracellular superoxide dismutase (ecSOD) in venous and lung tissue and to evaluate the underlying molecular mechanisms. C57Bl/6 mice underwent voluntary exercise or forced physical activity. Changes of vascular mRNA and protein levels and activity of eNOS, ecSOD and catalase were determined in aorta, heart, lung and vena cava. Both training protocols similarly increased relative heart weight and resulted in up-regulation of aortic and myocardial eNOS. In striking contrast, eNOS expression in vena cava and lung remained unchanged. Likewise, exercise up-regulated ecSOD in the aorta and in left ventricular tissue but remained unchanged in lung tissue. Catalase expression in lung tissue and vena cava of exercised mice exceeded that in aorta by 6.9- and 10-fold, respectively, suggesting a lack of stimulatory effects of hydrogen peroxide. In accordance, treatment of mice with the catalase inhibitor aminotriazole for 6 weeks resulted in significant up-regulation of eNOS and ecSOD in vena cava. These data suggest that physiological venous catalase activity prevents exercise-induced up-regulation of eNOS and ecSOD. Furthermore, therapeutic inhibition of vascular catalase might improve pulmonary rehabilitation. © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.

  12. Mutations in BALB mitochondrial DNA induce CCL20 up-regulation promoting tumorigenic phenotypes

    Energy Technology Data Exchange (ETDEWEB)

    Sligh, James [Department of Medicine—Dermatology Division, University of Arizona, Tucson, AZ 857 24 (United States); University of Arizona Cancer Center, Tucson, AZ 85724 (United States); Janda, Jaroslav [University of Arizona Cancer Center, Tucson, AZ 85724 (United States); Jandova, Jana, E-mail: jjandova@email.arizona.edu [Department of Medicine—Dermatology Division, University of Arizona, Tucson, AZ 857 24 (United States); University of Arizona Cancer Center, Tucson, AZ 85724 (United States)

    2014-11-15

    Highlights: • Alterations in mitochondrial DNA are commonly found in various human cancers. • Mutations in BALB mitochondrial DNA induce up-regulation of chemokine CCL20. • Increased growth and motility of mtBALB cells is associated with CCL20 levels. • mtDNA changes in BALB induce in vivo tumor growth through CCL20 up-regulation. • Mutations in mitochondrial DNA play important roles in keratinocyte neoplasia. - Abstract: mtDNA mutations are common in human cancers and are thought to contribute to the process of neoplasia. We examined the role of mtDNA mutations in skin cancer by generating fibroblast cybrids harboring a mutation in the gene encoding the mitochondrial tRNA for arginine. This somatic mutation (9821insA) was previously reported in UV-induced hyperkeratotic skin tumors in hairless mice and confers specific tumorigenic phenotypes to mutant cybrids. Microarray analysis revealed and RT-PCR along with Western blot analysis confirmed the up-regulation of CCL20 and its receptor CCR6 in mtBALB haplotype containing the mt-Tr 9821insA allele compared to wild type mtB6 haplotype. Based on reported role of CCL20 in cancer progression we examined whether the hyper-proliferation and enhanced motility of mtBALB haplotype would be associated with CCL20 levels. Treatment of both genotypes with recombinant CCL20 (rmCCL20) resulted in enhanced growth and motility of mtB6 cybrids. Furthermore, the acquired somatic alteration increased the in vivo tumor growth of mtBALB cybrids through the up-regulation of CCL20 since neutralizing antibody significantly decreased in vivo tumor growth of these cells; and tumors from anti-CCL20 treated mice injected with mtBALB cybrids showed significantly decreased CCL20 levels. When rmCCL20 or mtBALB cybrids were used as chemotactic stimuli, mtB6 cybrids showed increased motility while anti-CCL20 antibody decreased the migration and in vivo tumor growth of mtBALB cybrids. Moreover, the inhibitors of MAPK signaling and NF

  13. Sobrepeso materno y obesidad en escolares mexicanos: encuesta nacional de nutrición, 1999 Maternal overweight and obesity in Mexican school-age children: national nutrition survey, 1999

    Directory of Open Access Journals (Sweden)

    Mario Flores

    2005-12-01

    Full Text Available OBJETIVO: Evaluar el sobrepeso y la obesidad maternos como factores de riesgo de sobrepeso u obesidad en niños mexicanos de edad escolar (5 a 11 años que participaron en la Encuesta Nacional de Nutrición de 1999 (ENN 99. MATERIAL Y MÉTODOS: Se empleó información recolectada por la ENN 99 para evaluar la relación entre el sobrepeso y obesidad maternos y el sobrepeso u obesidad en niños en edad escolar. Se usó análisis de regresión logística. RESULTADOS: Se estudió a un total de 9 259 niños de 5 a 11 años, de los cuales 19% presentó sobrepeso u obesidad, de acuerdo con la clasificación de Cole. Un 39% de las madres de los niños estudiados tuvo sobrepeso y 26.4% presentó obesidad. Los hijos de madres con sobrepeso tuvieron 1.9 veces más riesgo de ser obesos (IC95% 1.62-2.18, y los hijos de madres con obesidad tuvieron 3.4 veces más riesgo de serlo (IC95% 2.96-4.00, en comparación con los niños cuyas madres tenían un IMC normal, ajustando por edad, sexo, escolaridad de la madre, talla de la madre, residencia urbana o rural, región, condiciones socioeconómicas e indigenismo. CONCLUSIONES: El sobrepeso y la obesidad maternos son factores de riesgo de sobrepeso u obesidad en niños mexicanos en edad escolar. Deben dirigirse intervenciones para promover cambios en los estilos de vida en el ámbito intrafamiliar y modificar ambientes obesigénicos.OBJECTIVE: To assess the effects of maternal overweight and obesity as risk factors for overweight and obesity in Mexican school-age children (5 to 11 years old who participated in the National Nutrition Survey 1999 (NNS-99. MATERIAL AND METHODS: Information obtained by the NNS-99 was used to evaluate the relationship between maternal overweight and obesity and overweight or obesity in school-age children. Multivariate logistic regression analysis was used. RESULTS: A total of 9 259 children were studied. The prevalence of overweight or obesity was 19%, according to the criteria

  14. GestationaL Obesity Weight management: Implementation of National Guidelines (GLOWING): a pilot cluster randomised controlled trial of a guideline implementation intervention for the management of maternal obesity by midwives.

    Science.gov (United States)

    Heslehurst, Nicola; Rankin, Judith; McParlin, Catherine; Sniehotta, Falko F; Howel, Denise; Rice, Stephen; McColl, Elaine

    2018-01-01

    Weight management in pregnancy guidelines exist, although dissemination alone is an ineffective means of implementation. Midwives identify the need for support to overcome complex barriers to practice. An evaluation of an intervention to support midwives' guideline implementation would require a large-scale cluster randomised controlled trial. A pilot study is necessary to explore the feasibility of delivery and evaluation prior to a definitive trial. The GestationaL Obesity Weight management: Implementation of National Guidelines (GLOWING) trial aims to test whether it is feasible and acceptable to deliver a behaviour change intervention to support midwives' implementation of weight management guidelines. GLOWING is a multi-centre parallel group pilot cluster randomised controlled trial comparing the delivery of a behaviour change intervention for midwives versus usual practice. Four NHS Trusts (clusters) will be randomised to intervention and control arms, stratified by size of maternity services. The intervention uses social cognitive theory and consists of face-to-face midwifery training plus information resources for routine practice. The main outcomes are whether the intervention and trial procedures are feasible and acceptable to participants and the feasibility of recruitment and data collection for a definitive trial. Target recruitment involves all eligible midwives in the intervention arm recruited to receive the intervention, 30 midwives and pregnant women per arm for baseline and outcome questionnaire data collection and 20 midwives and women to provide qualitative data. All quantitative and qualitative analyses will be descriptive with the purpose of informing the development of the definitive trial. This pilot study has been developed to support community midwives' implementation of guidelines. Community midwives have been selected as they usually carry out the booking appointment which includes measuring and discussing maternal body mass index. A

  15. A pragmatic controlled trial to prevent childhood obesity within a risk group at maternity and child health-care clinics: results up to six years of age (the VACOPP study).

    Science.gov (United States)

    Mustila, Taina; Raitanen, Jani; Keskinen, Päivi; Luoto, Riitta

    2018-02-27

    Obesity in childhood appears often during the toddler years. The prenatal environment influences obesity risk. Maternal gestational diabetes, the child's diet, and physical activity in the first few years have an important role in subsequent weight gain. A study was conducted to evaluate effectiveness of a primary health-care lifestyle counselling intervention in prevention of childhood obesity up to 6 years of age. The study was a controlled pragmatic trial to prevent childhood obesity and was implemented at maternity and child health-care clinics. The participants (n = 185) were mothers at risk of gestational diabetes mellitus with their offspring born between 2008 and 2010. The prenatal intervention, started at the end of the first trimester of pregnancy, consisted of counselling on diet and physical activity by municipal health-care staff. The intervention continued at yearly appointments with a public health-nurse at child health-care clinics. The paper reports the offspring weight gain results for 2-6 years of age. Weight gain up to 6 years of age was assessed as BMI standard deviation scores (SDS) via a mixed-effect linear regression model. The proportion of children at 6 years with overweight/obesity was assessed as weight-for-height percentage and ISO-BMI. Priority was not given to power calculations, because of the study's pragmatic nature. One hundred forty seven children's (control n = 76/85% and intervention n = 71/56%) weight and height scores were available for analysis at 6 years of age. There was no significant difference in weight gain or overweight/obesity proportions between the groups at 6 years of age, but the proportion of children with obesity in both groups was high (assessed as ISO-BMI 9.9% and 11.8%) relative to prevalence in this age group in Finland. As the authors previously reported, the intervention-group mothers had lower prevalence of gestational diabetes mellitus, but a decrease in obesity incidence before school age

  16. Urban air pollution produces up-regulation of myocardial inflammatory genes and dark chocolate provides cardioprotection.

    Science.gov (United States)

    Villarreal-Calderon, Rodolfo; Reed, William; Palacios-Moreno, Juan; Keefe, Sheyla; Herritt, Lou; Brooks, Diane; Torres-Jardón, Ricardo; Calderón-Garcidueñas, Lilian

    2012-05-01

    Air pollution is a serious environmental problem. Elderly subjects show increased cardiac morbidity and mortality associated with air pollution exposure. Mexico City (MC) residents are chronically exposed to high concentrations of fine particulate matter (PM(2.5)) and PM-associated lipopolysaccharides (PM-LPS). To test the hypothesis that chronic exposure to urban pollution produces myocardial inflammation, female Balb-c mice age 4 weeks were exposed for 16 months to two distinctly different polluted areas within MC: southwest (SW) and northwest (NW). SW mice were given either no treatment or chocolate 2g/9.5 mg polyphenols/3 times per week. Results were compared to mice kept in clean air. Key inflammatory mediator genes: cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and the LPS receptor CD14 (cluster of differentiation antigen 14) were measured by real-time polymerase chain reaction. Also explored were target NFκB (nuclear factor κB), oxidative stress and antioxidant defense genes. TNF-α, IL-6, and COX-2 were significantly increased in both NW and SWMC mice (p=0.0001). CD14 was up-regulated in SW mice in keeping with the high exposures to particulate matter associated endotoxin. Chocolate administration resulted in a significant down-regulation of TNF-α (p<0.0001), IL-6 (p=0.01), and IL-1β (p=0.02). The up-regulation of antioxidant enzymes and the down-regulation of potent oxidases, toll-like receptors, and pro-apoptotic signaling genes completed the protective profile. Exposure to air pollution produces up-regulation of inflammatory myocardial genes and endotoxin plays a key role in the inflammatory response. Regular consumption of dark chocolate may reduce myocardial inflammation and have cardioprotective properties in the setting of air pollution exposures. Copyright © 2010 Elsevier GmbH. All rights reserved.

  17. Up-regulation of CLDN1 in gastric cancer is correlated with reduced survival

    International Nuclear Information System (INIS)

    Eftang, Lars L; Esbensen, Ying; Tannæs, Tone M; Blom, Gustav P; Bukholm, Ida RK; Bukholm, Geir

    2013-01-01

    The genetic changes in gastric adenocarcinoma are extremely complex and reliable tumor markers have not yet been identified. There are also remarkable geographical differences in the distribution of this disease. Our aim was to identify the most differentially regulated genes in 20 gastric adenocarcinomas from a Norwegian selection, compared to matched normal mucosa, and we have related our findings to prognosis, survival and chronic Helicobacter pylori infection. Biopsies from gastric adenocarcinomas and adjacent normal gastric mucosa were obtained from 20 patients immediately following surgical resection of the tumor. Whole genome, cDNA microarray analysis was performed on the RNA isolated from the sample pairs to compare the gene expression profiles between the tumor against matched mucosa. The samples were microscopically examined to classify gastritis. The presence of H. pylori was examined using microscopy and immunohistochemistry. 130 genes showed differential regulation above a predefined cut-off level. Interleukin-8 (IL-8) and Claudin-1 (CLDN1) were the most consistently up-regulated genes in the tumors. Very high CLDN1 expression in the tumor was identified as an independent and significant predictor gene of reduced post-operative survival. There were distinctly different expression profiles between the tumor group and the control mucosa group, and the histological subsets of mixed type, diffuse type and intestinal type cancer demonstrated further sub-clustering. Up-regulated genes were mapped to cell-adhesion, collagen-related processes and angiogenesis, whereas normal intestinal functions such as digestion and excretion were associated with down-regulated genes. We relate the current findings to our previous study on the gene response of gastric epithelial cells to H. pylori infection. CLDN1 was highly up-regulated in gastric cancer, and CLDN1 expression was independently associated with a poor post-operative prognosis, and may have important prognostic

  18. Myostatin signaling is up-regulated in female patients with advanced heart failure.

    Science.gov (United States)

    Ishida, Junichi; Konishi, Masaaki; Saitoh, Masakazu; Anker, Markus; Anker, Stefan D; Springer, Jochen

    2017-07-01

    Myostatin, a negative regulator of skeletal muscle mass, is up-regulated in the myocardium of heart failure (HF) and increased myostatin is associated with weight loss in animal models with HF. Although there are disparities in pathophysiology and epidemiology between male and female patients with HF, it remains unclear whether there is gender difference in myostatin expression and whether it is associated with weight loss in HF patients. Heart tissue samples were collected from patients with advanced heart failure (n=31, female n=5) as well as healthy control donors (n=14, female n=6). Expression levels of myostatin and its related proteins in the heart were evaluated by western blotting analysis. Body mass index was significantly lower in female HF patients than in male counterparts (20.0±4.2 in female vs 25.2±3.8 in male, p=0.04). In female HF patients, both mature myostatin and pSmad2 were significantly up-regulated by 1.9 fold (p=0.05) and 2.5 fold (pmyostatin was not. There was no significant difference in protein expression related to myostatin signaling between male and female patients. In this study, myostatin and pSmad2 were significantly up-regulated in the failing heart of female patients, but not male patients, and female patients displayed lower body mass index. Enhanced myostatin signaling in female failing heart may causally contribute to pathogenesis of HF and cardiac cachexia. Copyright © 2017 Elsevier B.V. All rights reserved.

  19. Up-regulation of the chemokine CCL21 in the skin of subjects exposed to irritants

    Directory of Open Access Journals (Sweden)

    Kuznitzky Raquel

    2004-04-01

    Full Text Available Abstract Background Expression of murine CCL21 by dermal lymphatic endothelial cells (LEC has been demonstrated to be one of the most important steps in Langerhans cell emigration from skin. Previously, our group and others have found that this chemokine is up-regulated in different human inflammatory skin diseases mediated by diverse specific immune responses. This study was carried out to investigate the involvement of CCL21 in human skin after challenge with irritant agents responsible for inducing Irritant Contact Dermatitis (ICD. Results Eleven normal individuals were challenged with different chemical or physical irritants. Two patients with Allergic Contact Dermatitis (ACD were also challenged with the relevant antigen in order to have a positive control for CCL21 expression. Macroscopic as well as microscopic responses were evaluated. We observed typical ICD responses with mostly mononuclear cells in perivascular areas, but a predominance of polymorphonuclear cells away from the inflamed blood vessels and in the epidermis at 24 hours. Immunohistochemical studies showed up-regulation of CCL21 by lymphatic endothelial cells in all the biopsies taken from ICD and ACD lesions compared to normal skin. Kinetic study at 10, 48, 96 and 168 hours after contact with a classical irritant (sodium lauryl sulphate showed that the expression of CCL21 was increased in lymphatic vessels at 10 hours, peaked at 48 hours, and then gradually declined. There was a strong correlation between CCL21 expression and the macroscopic response (r = 0.69; p = 0.0008, but not between CCL21 and the number of infiltrating cells in the lesions. Conclusions These results provide new evidence for the role of CCL21 in inflammatory processes. Since the up-regulation of this chemokine was observed in ICD and ACD, it is tempting to speculate that this mechanism operates independently of the type of dermal insult, facilitating the emigration of CCR7+ cells.

  20. Erbb2 up-regulation of ADAM12 expression accelerates skin cancer progression.

    Science.gov (United States)

    Rao, Velidi H; Vogel, Kristen; Yanagida, Jodi K; Marwaha, Nitin; Kandel, Amrit; Trempus, Carol; Repertinger, Susan K; Hansen, Laura A

    2015-10-01

    Solar ultraviolet (UV) radiation can cause severe damage to the skin and is the primary cause of most skin cancer. UV radiation causes DNA damage leading to mutations and also activates the Erbb2/HER2 receptor through indirect mechanisms involving reactive oxygen species. We hypothesized that Erbb2 activation accelerates the malignant progression of UV-induced skin cancer. Following the induction of benign squamous papillomas by UV exposure of v-ras(Ha) transgenic Tg.AC mice, mice were treated topically with the Erbb2 inhibitor AG825 and tumor progression monitored. AG825 treatment reduced tumor volume, increased tumor regression, and delayed the development of malignant squamous cell carcinoma (SCC). Progression to malignancy was associated with increased Erbb2 and ADAM12 (A Disintegin And Metalloproteinase 12) transcripts and protein, while inhibition of Erbb2 blocked the increase in ADAM12 message upon malignant progression. Similarly, human SCC and SCC cell lines had increased ADAM12 protein and transcripts when compared to normal controls. To determine whether Erbb2 up-regulation of ADAM12 contributed to malignant progression of skin cancer, Erbb2 expression was modulated in cultured SCC cells using forced over-expression or siRNA targeting, demonstrating up-regulation of ADAM12 by Erbb2. Furthermore, ADAM12 transfection or siRNA targeting revealed that ADAM12 increased both the migration and invasion of cutaneous SCC cells. Collectively, these results suggest Erbb2 up-regulation of ADAM12 as a novel mechanism contributing to the malignant progression of UV-induced skin cancer. Inhibition of Erbb2/HER2 reduced tumor burden, increased tumor regression, and delayed the progression of benign skin tumors to malignant SCC in UV-exposed mice. Inhibition of Erbb2 suppressed the increase in metalloproteinase ADAM12 expression in skin tumors, which in turn increased migration and tumor cell invasiveness. © 2014 Wiley Periodicals, Inc.

  1. The Natural Antimicrobial Enzyme Lysozyme is Up-Regulated in Gastrointestinal Inflammatory Conditions

    Directory of Open Access Journals (Sweden)

    Carlos A. Rubio

    2014-01-01

    Full Text Available The cells that line the mucosa of the human gastrointestinal tract (GI, that is, oral cavity, oesophagus, stomach, small intestine, large intestine, and rectum are constantly challenged by adverse micro-environmental factors, such as different pH, enzymes, and bacterial flora. With exception of the oral cavity, these microenvironments also contain remnant cocktails of secreted enzymes and bacteria from upper organs along the tract. The density of the GI bacteria varies, from 103/mL near the gastric outlet, to 1010/mL at the ileocecal valve, to 1011 to 1012/mL in the colon. The total microbial population (ca. 1014 exceeds the total number of cells in the tract. It is, therefore, remarkable that despite the prima facie inauspicious mixture of harmful secretions and bacteria, the normal GI mucosa retains a healthy state of cell renewal. To counteract the hostile microenvironment, the GI epithelia react by speeding cell exfoliation (the GI mucosa has a turnover time of two to three days, by increasing peristalsis, by eliminating bacteria through secretion of plasma cell-immunoglobulins and by increasing production of natural antibacterial compounds, such as defensin-5 and lysozyme. Only recently, lysozyme was found up-regulated in Barrett’s oesophagitis, chronic gastritis, gluten-induced atrophic duodenitis (coeliac disease, collagenous colitis, lymphocytic colitis, and Crohn’s colitis. This up-regulation is a response directed to the special types of bacteria recently detected in these diseases. The aim of lysozyme up-regulation is to protect individual mucosal segments to chronic inflammation. The molecular mechanisms connected to the crosstalk between the intraluminal bacterial flora and the production of lysozyme released by the GI mucosae, are discussed. Bacterial resistance continues to exhaust our supply of commercial antibiotics. The potential use of lysozyme to treat infectious diseases is receiving much attention.

  2. Up-regulation of ALG-2 in hepatomas and lung cancer tissue

    DEFF Research Database (Denmark)

    la Cour, Jonas Marstrand; Mollerup, Jens; Winding, Pernille

    2003-01-01

    , a result confirmed by immunohistochemical analysis. Staining of four different lung cancer tissue microarrays including specimens of 263 patients showed that ALG-2 is mainly localized to epithelial cells and significantly up-regulated in small-cell lung cancers and in non-small-cell lung cancers. Our...... using Western blot analysis and immunohistochemistry. Western blot analysis of 15 different adult mouse tissues demonstrated that ALG-2 is ubiquitously expressed. We found that ALG-2 was more than threefold overexpressed in rat liver hepatoma compared to normal rat liver using Western blot analysis...

  3. Maternal correlates of maternal child feeding practices: a systematic review.

    Science.gov (United States)

    McPhie, Skye; Skouteris, Helen; Daniels, Lynne; Jansen, Elena

    2014-01-01

    Establishing healthy eating habits early in life is one important strategy to combat childhood obesity. Given that early maternal child feeding practices have been linked to child food intake and weight, identifying the maternal correlates of maternal child feeding practices is important in order to understand the determinants of childhood obesity; this was the overall aim of the current review. Academic databases were searched for studies examining the relationship between maternal child feeding practices and parenting, personal characteristics and psychopathology of mothers with preschoolers. Papers were limited to those published in English, between January 2000 and June 2012. Only studies with mothers of normally developing children between the ages of 2 and 6 years were included. There were no restrictions regarding the inclusion of maternal nationality or socioeconomic status (SES). Seventeen eligible studies were sourced. Information on the aim, sample, measures and findings of these was summarised into tables. The findings of this review support a relationship between maternal controlling parenting, general and eating psychopathology, and SES and maternal child feeding practices. The main methodological issues of the studies reviewed included inconsistency in measures of maternal variables across studies and cross-sectional designs. We conclude that the maternal correlates associated with maternal child feeding practices are complex, and the pathways by which maternal correlates impact these feeding practices require further investigation. © 2012 John Wiley & Sons Ltd.

  4. Leptin and insulin up-regulate miR-4443 to suppress NCOA1 and TRAF4, and decrease the invasiveness of human colon cancer cells

    International Nuclear Information System (INIS)

    Meerson, Ari; Yehuda, Hila

    2016-01-01

    Obesity is a risk factor for colorectal cancer (CRC). Normal and tumor cells respond to metabolic hormones, such as leptin and insulin. Thus, obesity-associated resistance to these hormones likely leads to changes in gene expression and behavior of tumor cells. However, the mechanisms affected by leptin and insulin signaling in CRC cells remain mostly unknown. We hypothesized that microRNAs (miRNAs) are involved in the regulation of tumorigenesis-related gene expression in CRC cells by leptin and insulin. To test this hypothesis, miRNA levels in the CRC-derived cell lines HCT-116, HT-29 and DLD-1 were profiled, following leptin and insulin treatment. Candidate miRNAs were validated by RT-qPCR. Predicted miRNA targets with known roles in cancer, were validated by immunoblots and reporter assays in HCT-116 cells. Transfection of HCT-116 cells with candidate miRNA mimic was used to test in vitro effects on proliferation and invasion. Of ~800 miRNAs profiled, miR-4443 was consistently up-regulated by leptin and insulin in HCT-116 and HT-29, but not in DLD-1, which lacked normal leptin receptor expression. Dose response experiments showed that leptin at 100 ng/ml consistently up-regulated miR-4443 in HCT-116 cells, concomitantly with a significant decrease in cell invasion ability. Transfection with miR-4443 mimic decreased invasion and proliferation of HCT-116 cells. Moreover, leptin and miR-4443 transfection significantly down-regulated endogenous NCOA1 and TRAF4, both predicted targets of miR-4443 with known roles in cancer metastasis. miR-4443 was found to directly regulate TRAF4 and NCOA1, as validated by a reporter assay. The up-regulation of miR-4443 by leptin or insulin was attenuated by the inhibition of MEK1/2. Our findings suggest that miR-4443 acts in a tumor-suppressive manner by down-regulating TRAF4 and NCOA1 downstream of MEK-C/EBP-mediated leptin and insulin signaling, and that insulin and/or leptin resistance (e.g. in obesity) may suppress this pathway

  5. Hypothalamic L-Histidine Decarboxylase Is Up-Regulated During Chronic REM Sleep Deprivation of Rats.

    Directory of Open Access Journals (Sweden)

    Gloria E Hoffman

    Full Text Available A competition of neurobehavioral drives of sleep and wakefulness occurs during sleep deprivation. When enforced chronically, subjects must remain awake. This study examines histaminergic neurons of the tuberomammillary nucleus of the posterior hypothalamus in response to enforced wakefulness in rats. We tested the hypothesis that the rate-limiting enzyme for histamine biosynthesis, L-histidine decarboxylase (HDC, would be up-regulated during chronic rapid eye movement sleep deprivation (REM-SD because histamine plays a major role in maintaining wakefulness. Archived brain tissues of male Sprague Dawley rats from a previous study were used. Rats had been subjected to REM-SD by the flowerpot paradigm for 5, 10, or 15 days. For immunocytochemistry, rats were transcardially perfused with acrolein-paraformaldehyde for immunodetection of L-HDC; separate controls used carbodiimide-paraformaldehyde for immunodetection of histamine. Immunolocalization of histamine within the tuberomammillary nucleus was validated using carbodiimide. Because HDC antiserum has cross-reactivity with other decarboxylases at high antibody concentrations, titrations localized L-HDC to only tuberomammillary nucleus at a dilution of ≥ 1:300,000. REM-SD increased immunoreactive HDC by day 5 and it remained elevated in both dorsal and ventral aspects of the tuberomammillary complex. Our results suggest that up-regulation of L-HDC within the tuberomammillary complex during chronic REM-SD may be responsible for maintaining wakefulness.

  6. Honey constituents up-regulate detoxification and immunity genes in the western honey bee Apis mellifera.

    Science.gov (United States)

    Mao, Wenfu; Schuler, Mary A; Berenbaum, May R

    2013-05-28

    As a managed pollinator, the honey bee Apis mellifera is critical to the American agricultural enterprise. Recent colony losses have thus raised concerns; possible explanations for bee decline include nutritional deficiencies and exposures to pesticides and pathogens. We determined that constituents found in honey, including p-coumaric acid, pinocembrin, and pinobanksin 5-methyl ether, specifically induce detoxification genes. These inducers are primarily found not in nectar but in pollen in the case of p-coumaric acid (a monomer of sporopollenin, the principal constituent of pollen cell walls) and propolis, a resinous material gathered and processed by bees to line wax cells. RNA-seq analysis (massively parallel RNA sequencing) revealed that p-coumaric acid specifically up-regulates all classes of detoxification genes as well as select antimicrobial peptide genes. This up-regulation has functional significance in that that adding p-coumaric acid to a diet of sucrose increases midgut metabolism of coumaphos, a widely used in-hive acaricide, by ∼60%. As a major component of pollen grains, p-coumaric acid is ubiquitous in the natural diet of honey bees and may function as a nutraceutical regulating immune and detoxification processes. The widespread apicultural use of honey substitutes, including high-fructose corn syrup, may thus compromise the ability of honey bees to cope with pesticides and pathogens and contribute to colony losses.

  7. Genes up-regulated during red coloration in UV-B irradiated lettuce leaves.

    Science.gov (United States)

    Park, Jong-Sug; Choung, Myoung-Gun; Kim, Jung-Bong; Hahn, Bum-Soo; Kim, Jong-Bum; Bae, Shin-Chul; Roh, Kyung-Hee; Kim, Yong-Hwan; Cheon, Choong-Ill; Sung, Mi-Kyung; Cho, Kang-Jin

    2007-04-01

    Molecular analysis of gene expression differences between green and red lettuce leaves was performed using the SSH method. BlastX comparisons of subtractive expressed sequence tags (ESTs) indicated that 7.6% of clones encoded enzymes involved in secondary metabolism. Such clones had a particularly high abundance of flavonoid-metabolism proteins (6.5%). Following SSH, 566 clones were rescreened for differential gene expression using dot-blot hybridization. Of these, 53 were found to overexpressed during red coloration. The up-regulated expression of six genes was confirmed by Northern blot analyses. The expression of chalcone synthase (CHS), flavanone 3-hydroxylase (F3H), and dihydroflavonol 4-reductase (DFR) genes showed a positive correlation with anthocyanin accumulation in UV-B-irradiated lettuce leaves; flavonoid 3',5'-hydroxylase (F3',5'H) and anthocyanidin synthase (ANS) were expressed continuously in both samples. These results indicated that the genes CHS, F3H, and DFR coincided with increases in anthocyanin accumulation during the red coloration of lettuce leaves. This study show a relationship between red coloration and the expression of up-regulated genes in lettuce. The subtractive cDNA library and EST database described in this study represent a valuable resource for further research for secondary metabolism in the vegetable crops.

  8. TRX is up-regulated by fibroblast growth factor-2 in lung carcinoma.

    Science.gov (United States)

    Deng, Zheng-Hao; Cao, Hui-Qiu; Hu, Yong-Bin; Wen, Ji-Fang; Zhou, Jian-Hua

    2011-01-01

    We have previously shown that exogenous fibroblast growth factor-2 (FGF-2) inhibits apoptosis of the small-cell lung cancer (SCLC) cell line NCI-H446, but the underlying mechanism remains unknown. In this study, the protein profiles of FGF-2-treated and untreated NCI-H446 cells were determined by 2-D gel electrophoresis combined with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and bioinformatics. Differential expression analysis of the protein profiles after FGF-2 treatment identified a total of 24 protein spots, of which nine were up-regulated and 15 were down-regulated. Four proteins were identified by MALDI-TOF-MS: thioredoxin (TRX), visfatin, ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) and Cu/Zn superoxide dismutase (CuZn-SOD). Western blotting revealed that TRX was up-regulated in NCI-H446 and A549 cells treated with FGF-2. Furthermore, immunohistochemical staining confirmed that both FGF-2 and TRX were overexpressed in lung cancer tissues and could be correlated with both lymph node metastasis and clinical stage. These data indicate that TRX may be involved in the FGF-2 signaling pathway. © 2010 The Authors. APMIS © 2010 APMIS.

  9. Artemisia Extract Improves Insulin Sensitivity in Women With Gestational Diabetes Mellitus by Up-Regulating Adiponectin.

    Science.gov (United States)

    Sun, Xia; Sun, Hong; Zhang, Jing; Ji, Xianghong

    2016-12-01

    Gestational diabetes mellitus (GDM) has affected a great number of pregnant women worldwide. Artemisia extracts have been found to exhibit a potent antidiabetic effect in the treatment of type 2 diabetes mellitus. We aimed to examine the effects of Artemisia extract on insulin resistance and lipid profiles in pregnant GDM patients. Patients in their second trimester were randomly assigned to the Artemisia extract group (AE) or to a placebo group (PO). They were instructed to consume either AE or PO daily for a period of 10 weeks. Glucose and insulin profiles and adiponectin level were assessed at baseline (week 0) and after the treatment (week 10). Compared to the PO group, fasting plasma glucose, serum insulin levels, homeostasis model of assessment of insulin resistance (HOMA-IR), and β-cell function (HOMA-B) were significantly reduced in the AE group participants. Moreover, levels of circulating adiponectin were also significantly up-regulated in the AE group, which also positively contributed to improved insulin sensitivity. Daily administration of Artemisia extract improves insulin sensitivity by up-regulating adiponectin in women with gestational diabetes mellitus. © 2016, The American College of Clinical Pharmacology.

  10. Neural cell 3D microtissue formation is marked by cytokines' up-regulation.

    Directory of Open Access Journals (Sweden)

    Yinzhi Lai

    Full Text Available Cells cultured in three dimensional (3D scaffolds as opposed to traditional two-dimensional (2D substrates have been considered more physiologically relevant based on their superior ability to emulate the in vivo environment. Combined with stem cell technology, 3D cell cultures can provide a promising alternative for use in cell-based assays or biosensors in non-clinical drug discovery studies. To advance 3D culture technology, a case has been made for identifying and validating three-dimensionality biomarkers. With this goal in mind, we conducted a transcriptomic expression comparison among neural progenitor cells cultured on 2D substrates, 3D porous polystyrene scaffolds, and as 3D neurospheres (in vivo surrogate. Up-regulation of cytokines as a group in 3D and neurospheres was observed. A group of 13 cytokines were commonly up-regulated in cells cultured in polystyrene scaffolds and neurospheres, suggesting potential for any or a combination from this list to serve as three-dimensionality biomarkers. These results are supportive of further cytokine identification and validation studies with cells from non-neural tissue.

  11. Utrophin up-regulation by an artificial transcription factor in transgenic mice.

    Directory of Open Access Journals (Sweden)

    Elisabetta Mattei

    2007-08-01

    Full Text Available Duchenne Muscular Dystrophy (DMD is a severe muscle degenerative disease, due to absence of dystrophin. There is currently no effective treatment for DMD. Our aim is to up-regulate the expression level of the dystrophin related gene utrophin in DMD, complementing in this way the lack of dystrophin functions. To this end we designed and engineered several synthetic zinc finger based transcription factors. In particular, we have previously shown that the artificial three zinc finger protein named Jazz, fused with the appropriate effector domain, is able to drive the transcription of a test gene from the utrophin promoter "A". Here we report on the characterization of Vp16-Jazz-transgenic mice that specifically over-express the utrophin gene at the muscular level. A Chromatin Immunoprecipitation assay (ChIP demonstrated the effective access/binding of the Jazz protein to active chromatin in mouse muscle and Vp16-Jazz was shown to be able to up-regulate endogenous utrophin gene expression by immunohistochemistry, western blot analyses and real-time PCR. To our knowledge, this is the first example of a transgenic mouse expressing an artificial gene coding for a zinc finger based transcription factor. The achievement of Vp16-Jazz transgenic mice validates the strategy of transcriptional targeting of endogenous genes and could represent an exclusive animal model for use in drug discovery and therapeutics.

  12. Autophagy activity is up-regulated in adipose tissue of obese individuals and modulates proinflammantory cytokine expression.

    NARCIS (Netherlands)

    Jansen, H.J.; Essen, van P.; Koenen, T.; Joosten, L.A.; Netea, M.G.; Tack, C.J.; Stienstra, R.

    2012-01-01

    Autophagy, an evolutionary conserved process aimed at recycling damaged organelles and protein aggregates in the cell, also modulates proinflammatory cytokine production in peripheral blood mononuclear cells. Because adipose tissue inflammation accompanied by elevated levels of proinflammatory

  13. E2F-1 induces melanoma cell apoptosis via PUMA up-regulation and Bax translocation

    International Nuclear Information System (INIS)

    Hao, Hongying; Dong, Yanbin; Bowling, Maria T; Gomez-Gutierrez, Jorge G; Zhou, H Sam; McMasters, Kelly M

    2007-01-01

    PUMA is a pro-apoptotic Bcl-2 family member that has been shown to be involved in apoptosis in many cell types. We sought to ascertain whether induction of PUMA plays a crucial role in E2F-1-induced apoptosis in melanoma cells. PUMA gene and protein expression levels were detected by real-time PCR and Western blot in SK-MEL-2 and HCT116 cell lines after Ad-E2F-1 infection. Activation of the PUMA promoter by E2F-1 overexpression was detected by dual luciferase reporter assay. E2F-1-induced Bax translocation was shown by immunocytochemistry. The induction of caspase-9 activity was measured by caspase-9 colorimetric assay kit. Up-regulation of the PUMA gene and protein by E2F-1 overexpression was detected by real-time PCR and Western blot analysis in the SK-MEL-2 melanoma cell line. In support of this finding, we found six putative E2F-1 binding sites within the PUMA promoter. Subsequent dual luciferase reporter assay showed that E2F-1 expression could increase the PUMA gene promoter activity 9.3 fold in SK-MEL-2 cells. The role of PUMA in E2F-1-induced apoptosis was further investigated in a PUMA knockout cell line. Cell viability assay showed that the HCT116 PUMA-/- cell line was more resistant to Ad-E2F-1-mediated cell death than the HCT116 PUMA+/+ cell line. Moreover, a 2.2-fold induction of the PUMA promoter was also noted in the HCT116 PUMA+/+ colon cancer cell line after Ad-E2F-1 infection. Overexpression of a truncated E2F-1 protein that lacks the transactivation domain failed to up-regulate PUMA promoter, suggesting that PUMA may be a transcriptional target of E2F-1. E2F-1-induced cancer cell apoptosis was accompanied by Bax translocation from the cytosol to mitochondria and the induction of caspase-9 activity, suggesting that E2F-1-induced apoptosis is mediated by PUMA through the cytochrome C/Apaf-1-dependent pathway. Our studies strongly demonstrated that E2F-1 induces melanoma cell apoptosis via PUMA up-regulation and Bax translocation. The signaling

  14. Lipopolysaccharide-induced Pulpitis Up-regulates TRPV1 in Trigeminal Ganglia

    Science.gov (United States)

    Chung, M.-K.; Lee, J.; Duraes, G.; Ro, J.Y.

    2011-01-01

    Tooth pain often accompanies pulpitis. Accumulation of lipopolysaccharides (LPS), a product of Gram-negative bacteria, is associated with painful clinical symptoms. However, the mechanisms underlying LPS-induced tooth pain are not clearly understood. TRPV1 is a capsaicin- and heat-gated nociceptive ion channel implicated in thermosensation and hyperalgesia under inflammation or injury. Although TRPV1 is expressed in pulpal afferents, it is not known whether the application of LPS to teeth modulates TRPV1 in trigeminal nociceptors. By assessing the levels of protein and transcript of TRPV1 in mouse trigeminal ganglia, we demonstrate that dentinal application of LPS increases the expression of TRPV1. Our results suggest that the up-regulation of TRPV1 in trigeminal nociceptors following bacterial infection could contribute to hyperalgesia under pulpitis conditions. PMID:21712529

  15. Up-regulation of β-adrenoreceptors by drugs which cause depression

    International Nuclear Information System (INIS)

    Brand, L.; Van Rooyen, J.M.; Offermeier, J.

    1988-01-01

    A number of drugs associated with depressive episodes in man were investigated for their effects on rat cortical β-adrenoceptors, in view of the down-regulation of β-adrenoceptors caused by chronic administration of anti-depressant drugs. Scatchard analyses of [ 3 H]dihydro-alprenolol binding data provided B max and K D values for the cortical β-adrenoceptors. Up-regulation of the receptors occurred after daily injections of phenobarbitone for seven days (by 55%), pentobarbitone (by 143%), reserpine (by 82%) and propranolol (by 64%). β-adrenoceptors were not affected by daily injections of clonidine, chlorpromazine and flupenthixol for seven days. This work confirms the up-regulatory effect on β-adrenoceptors of certain drugs which produce depressions in man

  16. Maggot debridement therapy promotes diabetic foot wound healing by up-regulating endothelial cell activity.

    Science.gov (United States)

    Sun, Xinjuan; Chen, Jin'an; Zhang, Jie; Wang, Wei; Sun, Jinshan; Wang, Aiping

    2016-03-01

    To determine the role of maggot debridement therapy (MDT) on diabetic foot wound healing, we compared growth related factors in wounds before and after treatment. Furthermore, we utilized human umbilical vein endothelial cells (HUVECs) to explore responses to maggot excretions/secretions on markers of angiogenesis and proliferation. The results showed that there was neo-granulation and angiogenesis in diabetic foot wounds after MDT. Moreover, significant elevation in CD34 and CD68 levels was also observed in treated wounds. In vitro, ES increased HUVEC proliferation, improved tube formation, and increased expression of vascular endothelial growth factor receptor 2 in a dose dependent manner. These results demonstrate that MDT and maggot ES can promote diabetic foot wound healing by up-regulating endothelial cell activity. Copyright © 2016. Published by Elsevier Inc.

  17. SET protein up-regulated testosterone production in the cultured preantral follicles

    Directory of Open Access Journals (Sweden)

    Xu Boqun

    2013-02-01

    Full Text Available Abstract Background We found previously that the expression of SET gene was up-regulated in polycystic ovaries. Evidences suggested that SET protein was essential for regulating both the promoter activity of CYP17A1 and the biological activity of P450c17. In this study, we explored whether SET regulated androgen production in preantral follicles. Methods The mouse preantral follicles were cultured in vitro. Testosterone secretion and expression of steroidogenic enzymes were observed in the preantral follicles treated in vitro by SET overexpression and knockdown. Results Testosterone levels in the media of the AdCMV-SET infected follicles significantly increased, and the CYP17A1 and HSD3B2 expression also significantly increased (P P  Conclusions SET played a positive role in regulating ovarian androgen biosynthesis by enhancing the transcription of steroidogenic enzymes CYP17A1 and HSD3B2, which maybe contribute to the hyperandrogenism in PCOS.

  18. Rapamycin up-regulates triglycerides in hepatocytes by down-regulating Prox1.

    Science.gov (United States)

    Kwon, Sora; Jeon, Ji-Sook; Kim, Su Bin; Hong, Young-Kwon; Ahn, Curie; Sung, Jung-Suk; Choi, Inho

    2016-02-27

    Although the prolonged use of rapamycin may cause unwanted side effects such as hyperlipidemia, the underlying mechanism remains unknown. Prox1 is a transcription factor responsible for the development of several tissues including lymphatics and liver. There is growing evidences that Prox1 participates in metabolism in addition to embryogenesis. However, whether Prox1 is directly related to lipid metabolism is currently unknown. HepG2 human hepatoma cells were treated with rapamycin and total lipids were analyzed by thin layer chromatography. The effect of rapamycin on the expression of Prox1 was determined by western blotting. To investigate the role of Prox1 in triglycerides regulation, siRNA and overexpression system were employed. Rapamycin was injected into mice for 2 weeks and total lipids and proteins in liver were measured by thin layer chromatography and western blot analysis, respectively. Rapamycin up-regulated the amount of triglyceride and down-regulated the expression of Prox1 in HepG2 cells by reducing protein half-life but did not affect its transcript. The loss-of-function of Prox1 was coincident with the increase of triglycerides in HepG2 cells treated with rapamycin. The up-regulation of triglycerides by rapamycin in HepG2 cells reverted to normal levels by the compensation of Prox1 using the overexpression system. Rapamycin also down-regulated Prox1 expression but increased triglycerides in mouse liver. This study suggests that rapamycin can increase the amount of triglycerides by down-regulating Prox1 expression in hepatocytes, which means that the mammalian target of rapamycin (mTOR) signaling is important for the regulation of triglycerides by maintaining Prox1 expression.

  19. Medicago truncatula SOC1 Genes Are Up-regulated by Environmental Cues That Promote Flowering

    Directory of Open Access Journals (Sweden)

    Jared B. Fudge

    2018-04-01

    Full Text Available Like Arabidopsis thaliana, the flowering of the legume Medicago truncatula is promoted by long day (LD photoperiod and vernalization. However, there are differences in the molecular mechanisms involved, with orthologs of two key Arabidopsis thaliana regulators, FLOWERING LOCUS C (FLC and CONSTANS (CO, being absent or not having a role in flowering time function in Medicago. In Arabidopsis, the MADS-box transcription factor gene, SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (AtSOC1, plays a key role in integrating the photoperiodic and vernalization pathways. In this study, we set out to investigate whether the Medicago SOC1 genes play a role in regulating flowering time. Three Medicago SOC1 genes were identified and characterized (MtSOC1a–MtSOC1c. All three MtSOC1 genes, when heterologously expressed, were able to promote earlier flowering of the late-flowering Arabidopsis soc1-2 mutant. The three MtSOC1 genes have different patterns of expression. However, consistent with a potential role in flowering time regulation, all three MtSOC1 genes are expressed in the shoot apex and are up-regulated in the shoot apex of plants in response to LD photoperiods and vernalization. The up-regulation of MtSOC1 genes was reduced in Medicago fta1-1 mutants, indicating that they are downstream of MtFTa1. Insertion mutant alleles of Medicago soc1b do not flower late, suggestive of functional redundancy among Medicago SOC1 genes in promoting flowering.

  20. Axl receptor tyrosine kinase is up-regulated in metformin resistant prostate cancer cells

    Science.gov (United States)

    Bansal, Nitu; Mishra, Prasun J.; Stein, Mark; DiPaola, Robert S.; Bertino, Joseph R.

    2015-01-01

    Recent epidemiological studies showed that metformin, a widely used anti-diabetic drug might prevent certain cancers. Metformin also has an anti-proliferative effect in preclinical studies of both hematologic malignancies as well as solid cancers and clinical studies testing metformin as an anti-cancer drug are in progress. However, all cancer types do not respond to metformin with the same effectiveness or acquire resistance. To understand the mechanism of acquired resistance and possibly its mechanism of action as an anti-proliferative agent, we developed metformin resistant LNCaP prostate cancer cells. Metformin resistant LNCaP cells had an increased proliferation rate, increased migration and invasion ability as compared to the parental cells, and expressed markers of epithelial-mesenchymal transition (EMT). A detailed gene expression microarray comparing the resistant cells to the wild type cells revealed that Edil2, Ereg, Axl, Anax2, CD44 and Anax3 were the top up-regulated genes and calbindin 2 and TPTE (transmembrane phosphatase with tensin homology) and IGF1R were down regulated. We focused on Axl, a receptor tyrosine kinase that has been shown to be up regulated in several drug resistance cancers. Here, we show that the metformin resistant cell line as well as castrate resistant cell lines that over express Axl were more resistant to metformin, as well as to taxotere compared to androgen sensitive LNCaP and CWR22 cells that do not overexpress Axl. Forced overexpression of Axl in LNCaP cells decreased metformin and taxotere sensitivity and knockdown of Axl in resistant cells increased sensitivity to these drugs. Inhibition of Axl activity by R428, a small molecule Axl kinase inhibitor, sensitized metformin resistant cells that overexpressed Axl to metformin. Inhibitors of Axl may enhance tumor responses to metformin and other chemotherapy in cancers that over express Axl. PMID:26036314

  1. Up-regulation of GTPBP4 in colorectal carcinoma is responsible for tumor metastasis

    International Nuclear Information System (INIS)

    Yu, Haitao; Jin, Sufeng; Zhang, Na; Xu, Qi

    2016-01-01

    GTP binding protein 4(GTPBP4), a member of GTP-binding protein family, was previously characterized as a tumor suppressor that regulates and requires merlin to suppress cell proliferation. However, the role of GTPBP4 in the metastasis of colorectal carcinoma (CRC) remains unelucidated. Here, we observed that GTPBP4 was detected at higher levels in CRC metastatic tissues than that in the primary tumor tissues. Notably, up-regulation of GTPBP4 was closely correlated with tumor metastasis in CRCs. Kaplan-Meier and multivariate Cox regression analysis indicated GTPBP4 as an independent prognostic factor for CRC patients (hazard ratio = 2.693, 95% confident interval: 1.193–6.083, p = 0.017). Functional studies established that knockdown of GTPBP4 impeded, whereas ectopic expression of GTPBP4 enhanced cell motility and tumor metastasis in CRC cells. Interestingly, mechanistic investigations suggested that GTPBP4 may disorganize actin cytoskeleton through repressing RhoA signaling. Taken together, our research uncovered that GTPBP4 promotes CRC metastasis by disrupting actin cytoskeleton, which is mediated by the reduced RhoA activity. Strategies targeting GTPBP4 will be promising for CRC patients with metastases. - Highlights: • Up-regulation of GTPBP4 is detected in CRC metastatic tissues and closely correlated with tumor metastasis. • Increase of GTPBP4 is closely associated with poor prognosis. • GTPBP4 promotes cell motility and tumor metastasis in CRC cells. • GTPBP4 induces filamentous actin rearrangement specifically by repressing the activity of RhoA. • GTPBP4 may be a novel therapeutic target for CRC patients with metastasis.

  2. Biotin deficiency up-regulates TNF-alpha production in murine macrophages.

    Science.gov (United States)

    Kuroishi, Toshinobu; Endo, Yasuo; Muramoto, Koji; Sugawara, Shunji

    2008-04-01

    Biotin, a water-soluble vitamin of the B complex, functions as a cofactor of carboxylases that catalyze an indispensable cellular metabolism. Although significant decreases in serum biotin levels have been reported in patients with chronic inflammatory diseases, the biological roles of biotin in inflammatory responses are unclear. In this study, we investigated the effects of biotin deficiency on TNF-alpha production. Mice were fed a basal diet or a biotin-deficient diet for 8 weeks. Serum biotin levels were significantly lower in biotin-deficient mice than biotin-sufficient mice. After i.v. administration of LPS, serum TNF-alpha levels were significantly higher in biotin-deficient mice than biotin-sufficient mice. A murine macrophage-like cell line, J774.1, was cultured in a biotin-sufficient or -deficient medium for 4 weeks. Cell proliferation and biotinylation of intracellular proteins were decreased significantly in biotin-deficient cells compared with biotin-sufficient cells. Significantly higher production and mRNA expression of TNF-alpha were detected in biotin-deficient J774.1 cells than biotin-sufficient cells in response to LPS and even without LPS stimulation. Intracellular TNF-alpha expression was inhibited by actinomycin D, indicating that biotin deficiency up-regulates TNF-alpha production at the transcriptional level. However, the expression levels of TNF receptors, CD14, and TLR4/myeloid differentiation protein 2 complex were similar between biotin-sufficient and -deficient cells. No differences were detected in the activities of the NF-kappaB family or AP-1. The TNF-alpha induction by biotin deficiency was down-regulated by biotin supplementation in vitro and in vivo. These results indicate that biotin deficiency may up-regulate TNF-alpha production or that biotin excess down-regulates TNF-alpha production, suggesting that biotin status may influence inflammatory diseases.

  3. Radiation induces invasiveness of pancreatic cancer via up-regulation of heparanase

    International Nuclear Information System (INIS)

    Lerner, I.; Bensoussan, E.; Meirovitz, A.; Elkin, M.; Vlodavsky, I.

    2013-01-01

    The full text of the publication follows. Pancreatic cancer is one of the most aggressive neoplasms with an extremely low survival rate. Because most pancreatic carcinoma patients miss the opportunity for complete surgical resection at the time of diagnosis, radiotherapy remains a major component of treatment modalities. However, pancreatic cancer often shows resistance to radiation therapy. Ionizing radiation (IR)-induced aggressiveness is emerging as one of the important mechanisms responsible for the limited benefit of radiation therapy in pancreatic cancer, but the identity of downstream effectors responsible for this effect remains poorly investigated. Here we report that IR promotes pancreatic cancer aggressiveness through up-regulation of the heparanase. Heparanase is a predominant mammalian enzyme capable of degrading heparan sulfate (HS), the main polysaccharide component of the basement membrane and other types of extracellular matrix (ECM). Cleavage of HS by heparanase leads to disassembly of ECM, enables cell invasion, releases HS-bound angiogenic and growth factors from the ECM depots, and generates bioactive HS fragments. We found that clinically relevant doses of IR augment invasive ability of pancreatic cells in vitro and in vivo via induction of heparanase. Our results indicate that the effect of IR on heparanase expression is mediated by Egr1 transcription factor. Moreover, specific inhibitor of heparanase enzymatic activity abolished IR-induced invasiveness of pancreatic carcinoma cells in vitro, while combined treatment with IR and the heparanase inhibitor, but not IR alone, attenuated ortho-topic pancreatic tumor progression in vivo. The proposed up-regulation of heparanase by IR represents a new molecular pathway through which IR may promote pancreatic tumor aggressiveness, providing explanation for the limited benefit from radiation therapy in pancreatic cancer. Our research is expected to offer a new approach to improve the efficacy of

  4. Insecticide-Mediated Up-Regulation of Cytochrome P450 Genes in the Red Flour Beetle (Tribolium castaneum

    Directory of Open Access Journals (Sweden)

    Xiao Liang

    2015-01-01

    Full Text Available Some cytochrome P450 (CYP genes are known for their rapid up-regulation in response to insecticide exposures in insects. To date, however, limited information is available with respect to the relationships among the insecticide type, insecticide concentration, exposure duration and the up-regulated CYP genes. In this study, we examined the transcriptional response of eight selected CYP genes, including CYP4G7, CYP4Q4, CYP4BR3, CYP12H1, CYP6BK11, CYP9D4, CYP9Z5 and CYP345A1, to each of four insecticides in the red flour beetle, Tribolium castaneum. Reverse transcription quantitative PCR (RT-qPCR revealed that CYP4G7 and CYP345A1 can be significantly up-regulated by cypermethrin (1.97- and 2.06-fold, respectively, permethrin (2.00- and 2.03-fold and lambda-cyhalothrin (1.73- and 1.81-fold, whereas CYP4BR3 and CYP345A1 can be significantly up-regulated by imidacloprid (1.99- and 1.83-fold when 20-day larvae were exposed to each of these insecticides at the concentration of LC20 for 24 h. Our studies also showed that similar levels of up-regulation can be achieved for CYP4G7, CYP4BR3 and CYP345A1 by cypermethrin, permethrin, lambda-cyhalothrin or imidacloprid with approximately one fourth of LC20 in 6 h. Our study demonstrated that up-regulation of these CYP genes was rapid and only required low concentrations of insecticides, and the up-regulation not only depended on the CYP genes but also the type of insecticides. Our results along with those from previous studies also indicated that there were no specific patterns for predicting the up-regulation of specific CYP gene families based on the insecticide classification.

  5. Perspectives in obesity and pregnancy

    OpenAIRE

    Mariona, Federico G.

    2016-01-01

    Obesity is currently recognized as a health epidemic worldwide. Its prevalence has doubled in the last three decades. Obesity is a complex clinical picture associated with physical, physiologic, hormonal, genetic, cultural, socioeconomic and environmental factors. The rate of obesity is also increasing in the pregnant women population. Maternal obesity is associated with less than optimal obstetrical, fetal and neonatal outcomes. It is also associated with significant adverse long-term effect...

  6. Maternal high-fat diet modulates brown adipose tissue response to B-adrenergic agonist

    Science.gov (United States)

    Maternal obesity increases offspring risk for several metabolic diseases. We previously showed that offspring of obese dams are predisposed to obesity, liver and adipose tissue anomalies. However, the effect of maternal obesity on developmental programing brown adipose tissue (BAT) is poorly underst...

  7. Maternal smoking, obesity, and risk of venous thromboembolism during pregnancy and the puerperium: a population-based nested case-control study

    DEFF Research Database (Denmark)

    Larsen, Torben Bjerregaard; Sørensen, Henrik Toft; Gislum, Mette

    2007-01-01

    BACKGROUND: Smoking and obesity are associated with adverse pregnancy outcomes. The aim of the present study was to examine the association between smoking, obesity (BMI>30), and risk for venous thromboembolism (VTE) during pregnancy and the puerperium. MATERIALS AND METHODS: In a population......) for VTE as a measure of relative risk. RESULTS: Smoking and obesity were associated with increased risk of VTE during pregnancy and the puerperium (adjusted OR 2.7 (95% CI: 1.5, 4.9) and 5.3 (95% CI: 2.1, 13.5), respectively). Obesity appeared to be associated with a higher risk of pulmonary embolism...... (adjusted OR: 14.9 (95% CI: 3.0, 74.8) than of deep venous thrombosis (adjusted OR: 4.4, 95% CI: 1.6, 11.9). CONCLUSION: Smoking and obesity are risk factors for VTE in pregnancy and the puerperium....

  8. Obese pregnant women and complications in relation to pregnancy and birth

    DEFF Research Database (Denmark)

    Vinter, Christina Anne; Tanvig, Mette Honnens; Damm, Peter

    2012-01-01

    One third of the pregnant Danish women are overweight or obese. Maternal obesity is an independent risk factor for adverse maternal and foetal outcomes including infertility, miscarriage, congenital malformations, preeclampsia, gestational diabetes, complicated deliveries, caesarean section, macr...

  9. Genistein up-regulates tumor suppressor microRNA-574-3p in prostate cancer.

    Directory of Open Access Journals (Sweden)

    Takeshi Chiyomaru

    Full Text Available Genistein has been shown to inhibit cancers both in vitro and in vivo, by altering the expression of several microRNAs (miRNAs. In this study, we focused on tumor suppressor miRNAs regulated by genistein and investigated their function in prostate cancer (PCa and target pathways. Using miRNA microarray analysis and real-time RT-PCR we observed that miR-574-3p was significantly up-regulated in PCa cells treated with genistein compared with vehicle control. The expression of miR-574-3p was significantly lower in PCa cell lines and clinical PCa tissues compared with normal prostate cells (RWPE-1 and adjacent normal tissues. Low expression level of miR-574-3p was correlated with advanced tumor stage and higher Gleason score in PCa specimens. Re-expression of miR-574-3p in PCa cells significantly inhibited cell proliferation, migration and invasion in vitro and in vivo. miR-574-3p restoration induced apoptosis through reducing Bcl-xL and activating caspase-9 and caspase-3. Using GeneCodis software analysis, several pathways affected by miR-574-3p were identified, such as 'Pathways in cancer', 'Jak-STAT signaling pathway', and 'Wnt signaling pathway'. Luciferase reporter assays demonstrated that miR-574-3p directly binds to the 3' UTR of several target genes (such as RAC1, EGFR and EP300 that are components of 'Pathways in cancer'. Quantitative real-time PCR and Western analysis showed that the mRNA and protein expression levels of the three target genes in PCa cells were markedly down-regulated with miR-574-3p. Loss-of-function studies demonstrated that the three target genes significantly affect cell proliferation, migration and invasion in PCa cell lines. Our results show that genistein up-regulates tumor suppressor miR-574-3p expression targeting several cell signaling pathways. These findings enhance understanding of how genistein regulates with miRNA in PCa.

  10. Triethylene Glycol Up-Regulates Virulence-Associated Genes and Proteins in Streptococcus mutans.

    Science.gov (United States)

    Sadeghinejad, Lida; Cvitkovitch, Dennis G; Siqueira, Walter L; Santerre, J Paul; Finer, Yoav

    2016-01-01

    Triethylene glycol dimethacrylate (TEGDMA) is a diluent monomer used pervasively in dental composite resins. Through hydrolytic degradation of the composites in the oral cavity it yields a hydrophilic biodegradation product, triethylene glycol (TEG), which has been shown to promote the growth of Streptococcus mutans, a dominant cariogenic bacterium. Previously it was shown that TEG up-regulated gtfB, an important gene contributing to polysaccharide synthesis function in biofilms. However, molecular mechanisms related to TEG's effect on bacterial function remained poorly understood. In the present study, S. mutans UA159 was incubated with clinically relevant concentrations of TEG at pH 5.5 and 7.0. Quantitative real-time PCR, proteomics analysis, and glucosyltransferase enzyme (GTF) activity measurements were employed to identify the bacterial phenotypic response to TEG. A S. mutans vicK isogenic mutant (SMΔvicK1) and its associated complemented strain (SMΔvicK1C), an important regulatory gene for biofilm-associated genes, were used to determine if this signaling pathway was involved in modulation of the S. mutans virulence-associated genes. Extracted proteins from S. mutans biofilms grown in the presence and absence of TEG were subjected to mass spectrometry for protein identification, characterization and quantification. TEG up-regulated gtfB/C, gbpB, comC, comD and comE more significantly in biofilms at cariogenic pH (5.5) and defined concentrations. Differential response of the vicK knock-out (SMΔvicK1) and complemented strains (SMΔvicK1C) implicated this signalling pathway in TEG-modulated cellular responses. TEG resulted in increased GTF enzyme activity, responsible for synthesizing insoluble glucans involved in the formation of cariogenic biofilms. As well, TEG increased protein abundance related to biofilm formation, carbohydrate transport, acid tolerance, and stress-response. Proteomics data was consistent with gene expression findings for the selected

  11. Nitrous oxide discretely up-regulates nNOS and p53 in neonatal rat brain.

    Science.gov (United States)

    Cattano, D; Valleggi, S; Abramo, A; Forfori, F; Maze, M; Giunta, F

    2010-06-01

    Animal studies suggest that neuronal cell death often results from anesthetic administration during synaptogenesis. Volatile anesthetics are strongly involved in triggering neuronal apoptosis, whereas other inhalational agents (xenon) demonstrate protective effects. Nitrous oxide (N2O) has modest pro-apoptotic effects on its own and potent, synergistic toxic effects when combined with volatile agents. Recent findings suggest that, during periods of rapid brain development, the enhanced neurodegeneration triggered by anesthetic drugs may be caused by a compensatory increase in intracellular free calcium, a potent activator of neuronal nitric oxide synthase (nNOS). Anesthesia-induced neuro-apoptosis is also activated via the intrinsic and the extrinsic apoptotic pathways because both pathways involve p53, a key regulatory gene. The molecular events related to neuronal cell apoptosis are not completely understood. To gain further insight into the events underlying neuro-apoptosis, we analyzed the transcriptional consequences of N2O exposure on nNOS, iNOS and p53 mRNA levels. The study used 2 groups of postnatal day seven Sprague/Dawley rats (N=6 each) that were exposed for 120 minutes to air (75% N2, 25% O2) or N2O (75% N2O, 25% O2; this N2O concentration is commonly used to induce anesthesia and has been demonstrated to trigger neurodegeneration in postnatal day seven rats). Total RNA was isolated from each brain and expression analyses on iNOS and nNOS transcripts were performed using relative Real-Time C-reactive protein PCR (using G3PDH as a housekeeping gene). A semi-quantitative RT-PCR analysis was performed on the p53 transcript (using Ciclophylin A as a housekeeping gene). Statistical analysis (REST 2005) revealed a significant, 11-fold up-regulation (P=0.026) of the nNOS transcript but no significant changes in iNOS transcription. The p53 mRNA was up-regulated almost 2-fold (P=0.0002; Student's t-Test; GraphPad Prism 4.00) in N2O-treated samples relative to

  12. No-observed effect levels are associated with up-regulation of MGMT following MMS exposure.

    Science.gov (United States)

    Doak, Shareen H; Brüsehafer, Katja; Dudley, Ed; Quick, Emma; Johnson, George; Newton, Russell P; Jenkins, Gareth J S

    2008-12-15

    The alkylating agents methyl methanesulphonate (MMS) and ethyl methanesulphonate (EMS) have non-linear dose-response curves, with a no-observed effect level (NOEL) and a lowest observed effect level (LOEL) for both gross chromosomal damage and mutagenicity. However, the biological mechanism responsible for the NOEL has yet to be identified. A strong candidate is DNA repair as it may be able to efficiently remove alkyl adducts at low doses resulting in a NOEL, but at higher doses fails to fully remove all lesions due to saturation of enzymatic activity resulting in a LOEL and subsequent linear increases in mutagenicity. We therefore assessed the transcriptional status of N-methylpurine-DNA glycoslase (MPG) and O(6)-methylguanine DNA methyltransferase (MGMT), which represent the first line of defence following exposure to alkylating agents through the respective enzymatic removal of N7-alkylG and O(6)-alkylG. The relative MPG and MGMT gene expression profiles were assessed by real-time RT-PCR following exposure to 0-2 microg/ml MMS for 1-24h. MPG expression remained fairly steady, but in contrast significant up-regulation of MGMT was observed when cells were treated with 0.5 and 1.0 microg/ml MMS for 4h (2.5- and 6.5-fold increases respectively). These doses lie within the NOEL for MMS mutagenicity (LOEL is 1.25 microg/ml), thus this boost in MGMT expression at low doses may be responsible for efficiently repairing O(6)methylG lesions and creating the non-linear response for mutations. However, as the LOEL for MMS clastogenicity is 0.85 microg/ml, O(6)-alkylG is unlikely to be responsible for the clastogenicity observed at these concentrations. Consequently, at low doses N7-methylG is possibly the predominant cause of MMS clastogenicity, while O(6)-methylG is more likely to be responsible for MMS mutagenicity, with MGMT up-regulation playing a key role in removal of O(6)-alkylG lesions before they are fixed as permanent point mutations, resulting in non-linear dose

  13. Up-regulation of sucrose metabolizing enzymes in Oncidium goldiana grown under elevated carbon dioxide

    Energy Technology Data Exchange (ETDEWEB)

    Chang Run Li; Sun, W.Q.; Choy Sin Hew [National Univ. of Singapore. dept. of Biological Sciences (Singapore)

    2001-07-01

    Experiments were conducted in controlled growth chambers to evaluate how increase in CO{sub 2} concentration affected sucrose metabolizing enzymes, especially sucrose phosphate synthase (SPS; EC 2.4.1.14) and sucrose synthase (SS; EC 2.4.1.13), as well as carbon metabolism and partitioning in a tropical epiphytic orchid species (Oncidium goldiana). Response of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco; EC 4.1.1.39) to elevated CO{sub 2} was determined along with dry mass production, photosynthesis rate, chlorophyll content, total nitrogen and total soluble protein content. After 60 days of growth, there was a 80% and 150% increase in dry mass production in plants grown at 750 and 1100 {mu} l{sup -}1 CO{sub 2}, respectively, compared with those grown at ambient CO{sub 2} (about 370 {mu} l{sup -}1). A similar increase in photosynthesis rate was detected throughout the growth period when measured under growth CO{sub 2} conditions. Concomitantly, there was a decline in leaf Rubisco activity in plants in elevated CO{sub 2} after 10 days of growth. Over the growth period, leaf SPS and SS activities were up-regulated by an average of 20% and 40% for plants grown at 750 and 1100 {mu} l{sup -}1 CO{sub 2}, respectively. Leaf sucrose content and starch content were significantly higher throughout the growth period in plants grown at elevated CO{sub 2} than those at ambient CO{sub 2}. The partitioning of photosynthetically fixed carbon between sucrose and starch appeared to be unaffected by the 750 {mu} l{sup -}1 CO{sub 2} treatment, but it was favored into starch under the 1100 {mu} l{sup -}1 CO{sub 2} condition. The activities of SPS and SS in leaf extracts were closely associated with photosynthetic rates and with partitioning of carbon between starch and sucrose in leaves. The data are consistent with the hypothesis that the up-regulation of leaf SPS and SS might be an acclimation response to optimize the utilization and export of organic carbon with the

  14. Maternal supplementation with conjugated linoleic acid in the setting of diet-induced obesity normalises the inflammatory phenotype in mothers and reverses metabolic dysfunction and impaired insulin sensitivity in offspring.

    Science.gov (United States)

    Segovia, Stephanie A; Vickers, Mark H; Zhang, Xiaoyuan D; Gray, Clint; Reynolds, Clare M

    2015-12-01

    Maternal consumption of a high-fat diet significantly impacts the fetal environment and predisposes offspring to obesity and metabolic dysfunction during adulthood. We examined the effects of a high-fat diet during pregnancy and lactation on metabolic and inflammatory profiles and whether maternal supplementation with the anti-inflammatory lipid conjugated linoleic acid (CLA) could have beneficial effects on mothers and offspring. Sprague-Dawley rats were fed a control (CD; 10% kcal from fat), CLA (CLA; 10% kcal from fat, 1% total fat as CLA), high-fat (HF; 45% kcal from fat) or high fat with CLA (HFCLA; 45% kcal from fat, 1% total fat as CLA) diet ad libitum 10days prior to and throughout gestation and lactation. Dams and offspring were culled at either late gestation (fetal day 20, F20) or early postweaning (postnatal day 24, P24). CLA, HF and HFCLA dams were heavier than CD throughout gestation. Plasma concentrations of proinflammatory cytokines interleukin-1β and tumour necrosis factor-α were elevated in HF dams, with restoration in HFCLA dams. Male and female fetuses from HF dams were smaller at F20 but displayed catch-up growth and impaired insulin sensitivity at P24, which was reversed in HFCLA offspring. HFCLA dams at P24 were protected from impaired insulin sensitivity as compared to HF dams. Maternal CLA supplementation normalised inflammation associated with consumption of a high-fat diet and reversed associated programming of metabolic dysfunction in offspring. This demonstrates that there are critical windows of developmental plasticity in which the effects of an adverse early-life environment can be reversed by maternal dietary interventions. Copyright © 2015 Elsevier Inc. All rights reserved.

  15. The yeast PNC1 longevity gene is up-regulated by mRNA mistranslation.

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    Raquel M Silva

    Full Text Available Translation fidelity is critical for protein synthesis and to ensure correct cell functioning. Mutations in the protein synthesis machinery or environmental factors that increase synthesis of mistranslated proteins result in cell death and degeneration and are associated with neurodegenerative diseases, cancer and with an increasing number of mitochondrial disorders. Remarkably, mRNA mistranslation plays critical roles in the evolution of the genetic code, can be beneficial under stress conditions in yeast and in Escherichia coli and is an important source of peptides for MHC class I complex in dendritic cells. Despite this, its biology has been overlooked over the years due to technical difficulties in its detection and quantification. In order to shed new light on the biological relevance of mistranslation we have generated codon misreading in Saccharomyces cerevisiae using drugs and tRNA engineering methodologies. Surprisingly, such mistranslation up-regulated the longevity gene PNC1. Similar results were also obtained in cells grown in the presence of amino acid analogues that promote protein misfolding. The overall data showed that PNC1 is a biomarker of mRNA mistranslation and protein misfolding and that PNC1-GFP fusions can be used to monitor these two important biological phenomena in vivo in an easy manner, thus opening new avenues to understand their biological relevance.

  16. FOXO3-mediated up-regulation of Bim contributes to rhein-induced cancer cell apoptosis.

    Science.gov (United States)

    Wang, Jiao; Liu, Shu; Yin, Yancun; Li, Mingjin; Wang, Bo; Yang, Li; Jiang, Yangfu

    2015-03-01

    The anthraquinone compound rhein is a natural agent in the traditional Chinese medicine rhubarb. Preclinical studies demonstrate that rhein has anticancer activity. Treatment of a variety of cancer cells with rhein may induce apoptosis. Here, we report that rhein induces atypical unfolded protein response in breast cancer MCF-7 cells and hepatoma HepG2 cells. Rhein induces CHOP expression, eIF2α phosphorylation and caspase cleavage, while it does not induce glucose-regulated protein 78 (GRP78) expression in both MCF-7 and HepG2 cells. Meanwhile, rhein inhibits thapsigargin-induced GRP78 expression and X box-binding protein 1 splicing. In addition, rhein inhibits Akt phosphorylation and stimulates FOXO transactivation activity. Rhein induces Bim expression in MCF-7 and HepG2 cells, which can be abrogated by FOXO3a knockdown. Knockdown of FOXO3a or Bim abrogates rhein-induced caspase cleavage and apoptosis. The chemical chaperone 4-phenylbutyrate acid antagonizes the induction of FOXO activation, Bim expression and caspase cleavage by rhein, indicating that protein misfolding may be involved in triggering these deleterious effects. We conclude that FOXO3a-mediated up-regulation of Bim is a key mechanism underlying rhein-induced cancer cells apoptosis.

  17. MicroRNA-276 promotes egg-hatching synchrony by up-regulating brm in locusts

    Science.gov (United States)

    He, Jing; Chen, Qianquan; Wei, Yuanyuan; Jiang, Feng; Yang, Meiling; Hao, Shuguang; Guo, Xiaojiao; Chen, Dahua; Kang, Le

    2016-01-01

    Developmental synchrony, the basis of uniform swarming, migration, and sexual maturation, is an important strategy for social animals to adapt to variable environments. However, the molecular mechanisms underlying developmental synchrony are largely unexplored. The migratory locust exhibits polyphenism between gregarious and solitarious individuals, with the former displaying more synchronous sexual maturation and migration than the latter. Here, we found that the egg-hatching time of gregarious locusts was more uniform compared with solitarious locusts and that microRNA-276 (miR-276) was expressed significantly higher in both ovaries and eggs of gregarious locusts than in solitarious locusts. Interestingly, inhibiting miR-276 in gregarious females and overexpressing it in solitarious females, respectively, caused more heterochronic and synchronous hatching of progeny eggs. Moreover, miR-276 directly targeted a transcription coactivator gene, brahma (brm), resulting in its up-regulation. Knockdown of brm not only resulted in asynchronous egg hatching in gregarious locusts but also impaired the miR-276–induced synchronous egg hatching in solitarious locusts. Mechanistically, miR-276 mediated brm activation in a manner that depended on the secondary structure of brm, namely, a stem-loop around the binding site of miR-276. Collectively, our results unravel a mechanism by which miR-276 enhances brm expression to promote developmental synchrony and provide insight into regulation of developmental homeostasis and population sustaining that are closely related to biological synchrony. PMID:26729868

  18. Is There an Opportunity for Current Chemotherapeutics to Up-regulate MIC-A/B Ligands?

    Directory of Open Access Journals (Sweden)

    Kendel Quirk

    2017-10-01

    Full Text Available Natural killer (NK cells are critical effectors of the immune system. NK cells recognize unhealthy cells by specific ligands [e.g., MHC- class I chain related protein A or B (MIC-A/B] for further elimination by cytotoxicity. Paradoxically, cancer cells down-regulate MIC-A/B and evade NK cell’s anticancer activity. Recent data indicate that cellular-stress induces MIC-A/B, leading to enhanced sensitivity of cancer cells to NK cell-mediated cytotoxicity. In this Perspective article, we hypothesize that current chemotherapeutics at sub-lethal, non-toxic dose may promote cellular-stress and up-regulate the expression of MIC-A/B ligands to augment cancer’s sensitivity to NK cell-mediated cytotoxicity. Preliminary data from two human breast cancer cell lines, MDA-MB-231 and T47D treated with clinically relevant therapeutics such as doxorubicin, paclitaxel and methotrexate support the hypothesis. The goal of this Perspective is to underscore the prospects of current chemotherapeutics in NK cell immunotherapy, and discuss potential challenges and opportunities to improve cancer therapy.

  19. Glucocorticoid up-regulation of high-affinity interleukin 6 receptors on human epithelial cells

    International Nuclear Information System (INIS)

    Snyers, L.; De Wit, L.; Content, J.

    1990-01-01

    Interleukin 6 (IL-6) is a potent pleiotropic cytokine, known, among others, to stimulate immunoglobulin production by B cells and to trigger acute-phase protein synthesis by hepatocytes. Similar to IL-1, it is produced by monocytes and macrophages following an inflammatory challenge. Analysis of IL-6 receptor (IL-6R) expression on different human cell lines indicates that dexamethasone could up-regulate the number of IL-6R on one epithelial cell line (UAC) and on two hepatoma cell lines (HepG2 and Hep3B). This effect was confirmed by Scatchard analysis of binding experiments, using [ 35 S]methionine and [ 35 S]cysteine metabolically labeled IL-6. It was confirmed at the level of mRNA expression by Northern blot analysis. These results provide evidence for a link between IL-6 and glucocorticoids. They could represent an example of a system in which one role of glucocorticoids is to define more accurately the target of cytokines, and they could explain, at least partly, the frequently observed synergy between IL-6 and glucocorticoids, notably in the case of hepatocytes

  20. Hypoxia promotes Mycobacterium tuberculosis-specific up-regulation of granulysin in human T cells.

    Science.gov (United States)

    Zenk, Sebastian F; Vollmer, Michael; Schercher, Esra; Kallert, Stephanie; Kubis, Jan; Stenger, Steffen

    2016-06-01

    Oxygen tension affects local immune responses in inflammation and infection. In tuberculosis mycobacteria avoid hypoxic areas and preferentially persist and reactivate in the oxygen-rich apex of the lung. Oxygen restriction activates antimicrobial effector mechanisms in macrophages and restricts growth of intracellular Mycobacterium tuberculosis (M.Tb). The effect of oxygen restriction on T cell-mediated antimicrobial effector mechanisms is unknown. Therefore we determined the influence of hypoxia on the expression of granulysin, an antimicrobial peptide of lymphocytes. Hypoxia increased the antigen-specific up-regulation of granulysin mRNA and protein in human CD4(+) and CD8(+) T lymphocytes. This observation was functionally relevant, because oxygen restriction supported the growth-limiting effect of antigen-specific T cells against virulent M.Tb residing in primary human macrophages. Our results provide evidence that oxygen restriction promotes the expression of granulysin and suggest that this effect-in conjunction with additional T cell-mediated immune responses-supports protection against mycobacteria. The therapeutic modulation of oxygen availability may offer a new strategy for the host-directed therapy of infectious diseases with intracellular pathogens.

  1. Radiation up-regulated the expression of VEGF in a canine oral melanoma cell line

    International Nuclear Information System (INIS)

    Flickinger, I.; Rütgen, B.C.; Gerner, W.; Tichy, A.; Saalmüller, A.; Kleiter, M.; Calice, I.

    2013-01-01

    To evaluate radiosensitivity and the effects of radiation on the expression of vascular endothelial growth factor (VEGF) and VEGF receptors in the canine oral melanoma cell line, TLM 1, cells were irradiated with doses of 0, 2, 4, 6, 8 and 10 Gray (Gy). Survival rates were then determined by a MTT assay, while vascular endothelial growth factor receptor (VEGFR)-1 and -2 expression was measured by flow cytometry and apoptotic cell death rates were investigated using an Annexin assay. Additionally, a commercially available canine VEGF ELISA kit was used to measure VEGF. Radiosensitivity was detected in TLM 1 cells, and mitotic and apoptotic cell death was found to occur in a radiation dose dependent manner. VEGF was secreted constitutively and significant up-regulation was observed in the 8 and 10 Gy irradiated cells. In addition, a minor portion of TLM 1 cells expressed vascular endothelial growth factor receptor (VEGFR)-1 intracellularly. VEGFR-2 was detected in the cytoplasm and was down-regulated following radiation with increasing dosages. In TLM 1 cells, apoptosis plays an important role in radiation induced cell death. It has also been suggested that the significantly higher VEGF production in the 8 and 10 Gy group could lead to tumour resistance. (author)

  2. MicroRNA-150 Is up-regulated in extranodal marginal zone lymphoma of MALT type.

    Science.gov (United States)

    Gebauer, Niklas; Kuba, Johannes; Senft, Andrea; Schillert, Arne; Bernard, Veronica; Thorns, Christoph

    2014-01-01

    The mechanisms promoting malignant transformation from chronic Helicobacter pylori-gastritis to gastric extranodal marginal zone lymphoma (MALT lymphoma) are insufficiently characterized. This follow-up study aimed to validate candidate microRNAs (miRs) in the process of neoplastic transformation. MicroRNA expression signatures (n=20) were generated for a total of 60 cases of gastric lesions ranging from Wotherspoon 0-5 employing a quantitative real-time polymerase chain reaction (PCR) approach. Morphological and immunohistochemical characterization of the cohort was supplemented by PCR-based immunoglobulin heavy chain recombination studies. Quantitative expression of miR-150, miR-142.3p, miR-375 and miR-494 was significantly de-regulated in samples from MALT lymphoma compared to those from gastritis. The previously reported up-regulation of miR-150 in marginal zone lymphoma of MALT type was verified in an independent cohort of lymphoma samples employing a modified methodology. This further substantiates the role of miR-150 as a potential oncomiR in MALT lymphoma.

  3. Caffeine Induces the Stress Response and Up-Regulates Heat Shock Proteins in Caenorhabditis elegans.

    Science.gov (United States)

    Al-Amin, Mohammad; Kawasaki, Ichiro; Gong, Joomi; Shim, Yhong-Hee

    2016-02-01

    Caffeine has both positive and negative effects on physiological functions in a dose-dependent manner. C. elegans has been used as an animal model to investigate the effects of caffeine on development. Caffeine treatment at a high dose (30 mM) showed detrimental effects and caused early larval arrest. We performed a comparative proteomic analysis to investigate the mode of action of high-dose caffeine treatment in C. elegans and found that the stress response proteins, heat shock protein (HSP)-4 (endoplasmic reticulum [ER] chaperone), HSP-6 (mitochondrial chaperone), and HSP-16 (cytosolic chaperone), were induced and their expression was regulated at the transcriptional level. These findings suggest that high-dose caffeine intake causes a strong stress response and activates all three stress-response pathways in the worms, including the ER-, mitochondrial-, and cytosolic pathways. RNA interference of each hsp gene or in triple combination retarded growth. In addition, caffeine treatment stimulated a food-avoidance behavior (aversion phenotype), which was enhanced by RNAi depletion of the hsp-4 gene. Therefore, up-regulation of hsp genes after caffeine treatment appeared to be the major responses to alleviate stress and protect against developmental arrest.

  4. Up-regulation of microRNA-1290 impairs cytokinesis and affects the reprogramming of colon cancer cells.

    Science.gov (United States)

    Wu, Jia; Ji, Xiaowei; Zhu, Linlin; Jiang, Qiaoli; Wen, Zhenzhen; Xu, Song; Shao, Wei; Cai, Jianting; Du, Qin; Zhu, Yongliang; Mao, Jianshan

    2013-02-28

    Abnormal cytokinesis increases the possibility of nuclear fusion in tumor cells. However, the role of microRNAs (miRNAs) in abnormal cytokinesis is unclear. Here, we found that miR-1290 was significantly up-regulated in clinical colon cancer tissues. Up-regulation of miR-1290 postponed cytokinesis and led to the formation of multinucleated cells. KIF13B was a target of miR-1290 that was involved in aberrant cytokinesis. Furthermore, enforced expression of miR-1290 activated the Wnt pathway and increased the reprogramming-related transcript factors c-Myc and Nanog. Our results suggest that up-regulation of miR-1290 in colon cancer cells impaired cytokinesis and affected reprogramming. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

  5. Up-regulated expression of l-caldesmon associated with malignancy of colorectal cancer

    International Nuclear Information System (INIS)

    Kim, Kyung-Hee; Kim, Byung Chang; Yoo, Byong Chul; Yeo, Seung-Gu; Kim, Won Ki; Kim, Dae Yong; Yeo, Hyun Yang; Hong, Jun Pyu; Chang, Hee Jin; Park, Ji Won; Kim, Sun Young

    2012-01-01

    Caldesmon (CaD), a major actin-associated protein, is found in smooth muscle and non-muscle cells. Smooth muscle caldesmon, h-CaD, is a multifunctional protein, and non-muscle cell caldesmon, l-CaD, plays a role in cytoskeletal architecture and dynamics. h-CaD is thought to be an useful marker for smooth muscle tumors, but the role(s) of l-CaD has not been examined in tumors. Primary colon cancer and liver metastasis tissues were obtained from colon cancer patients. Prior to chemoradiotherapy (CRT), normal and cancerous tissues were obtained from rectal cancer patients. Whole-tissue protein extracts were analyzed by 2-DE-based proteomics. Expression and phosphorylation level of main cellular signaling proteins were determined by western blot analysis. Cell proliferation after CaD siRNA transfection was monitored by MTT assay. The expression level of l-CaD was significantly increased in primary colon cancer and liver metastasis tissues compared to the level in the corresponding normal tissues. In cancerous tissues obtained from the patients showing poor response to CRT (Dworak grade 4), the expression of l-CaD was increased compared to that of good response group (Dworak grade 1). In line with, l-CaD positive human colon cancer cell lines were more resistant to 5-fluorouracil (5-FU) and radiation treatment compared to l-CaD negative cell lines. Artificial suppression of l-CaD increased susceptibility of colon cancer cells to 5-FU, and caused an increase of p21 and c-PARP, and a decrease of NF-kB and p-mTOR expression. Up-regulated expression of l-CaD may have a role for increasing metastatic property and decreasing CRT susceptibility in colorectal cancer cells

  6. Homeobox A7 stimulates breast cancer cell proliferation by up-regulating estrogen receptor-alpha

    International Nuclear Information System (INIS)

    Zhang, Yu; Cheng, Jung-Chien; Huang, He-Feng; Leung, Peter C.K.

    2013-01-01

    Highlights: •HOXA7 regulates MCF7 cell proliferation. •HOXA7 up-regulates ERα expression. •HOXA7 mediates estrogen-induced MCF7 cell proliferation. -- Abstract: Breast cancer is the most common hormone-dependent malignancy in women. Homeobox (HOX) transcription factors regulate many cellular functions, including cell migration, proliferation and differentiation. The aberrant expression of HOX genes has been reported to be associated with human reproductive cancers. Estradiol (E2) and its nuclear receptors, estrogen receptor (ER)-alpha and ER-beta, are known to play critical roles in the regulation of breast cancer cell growth. However, an understanding of the potential relationship between HOXA7 and ER in breast cancer cells is limited. In this study, our results demonstrate that knockdown of HOXA7 in MCF7 cells significantly decreased cell proliferation and ERα expression. In addition, HOXA7 knockdown attenuated E2-induced cell proliferation as well as progesterone receptor (PR) expression. The stimulatory effects of E2 on cell proliferation and PR expression were abolished by co-treatment with ICI 182780, a selective ERα antagonist. In contrast, overexpression of HOXA7 significantly stimulated cell proliferation and ERα expression. Moreover, E2-induced cell proliferation, as well as PR expression, was enhanced by the overexpression of HOXA7. Neither knockdown nor overexpression of HOXA7 affected the ER-beta levels. Our results demonstrate a novel mechanistic role for HOXA7 in modulating breast cancer cell proliferation via regulation of ERα expression. This finding contributes to our understanding of the role HOXA7 plays in regulating the proliferation of ER-positive cancer cells

  7. Up-regulation of Hsp72 and keratin16 mediates wound healing in streptozotocin diabetic rats

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    Rasha R. Ahmed

    2015-01-01

    Full Text Available BACKGROUND: Impaired wound healing is a complication of diabetes and a serious problem in clinical practice. We previously found that whey protein (WP was able to regulate wound healing normally in streptozotocin (STZ-dia-betic models. This subsequent study was designed to assess the effect of WP on heat shock protein-72 (Hsp72 and keratin16 (Krt16 expression during wound healing in diabetic rats. METHODS: WP at a dosage of 100 mg/kg of body weight was orally administered daily to wounded normal and STZ-diabetic rats for 8 days. RESULTS: At day 4, the WP-treated diabetic wound was significantly reduced compared to that in the corresponding control. Diabetic wounded rats developed severe inflammatory infiltration and moderate capillary dilatation and regeneration. Treated rats had mild necrotic formation, moderate infiltration, moderate to severe capillary dilatation and regeneration, in addition to moderate epidermal formation. Hsp72 and Krt16 densities showed low and dense activity in diabetic wounded and diabetic wounded treated groups, respectively. At day 8, WP-treatment of diabetic wounded animals revealed great amelioration with complete recovery and closure of the wound. Reactivity of Hsp72 and Krt16 was reversed, showing dense and low, or medium and low, activity in the diabetic wounded and diabetic wounded treated groups, respectively. Hsp72 expression in the pancreas was found to show dense reactivity with WP-treated diabetic wound rats. CONCLUSION: This data provides evidence for the potential impact of WP in the up-regulation of Hsp72 and Krt16 in T1D, resulting in an improved wound healing process in diabetic models.

  8. Up-regulation of Toll-like receptors 2, 3 and 4 in allergic rhinitis

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    Uddman Rolf

    2005-09-01

    Full Text Available Abstract Background Toll-like receptors enable the host to recognize a large number of pathogen-associated molecular patterns such as bacterial lipopolysaccharide, viral RNA, CpG-containing DNA and flagellin. Toll-like receptors have also been shown to play a pivotal role in both innate and adaptive immune responses. The role of Toll-like receptors as a primary part of our microbe defense system has been shown in several studies, but their possible function as mediators in allergy and asthma remains to be established. The present study was designed to examine the expression of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with intermittent allergic rhinitis, focusing on changes induced by exposure to pollen. Methods 27 healthy controls and 42 patients with seasonal allergic rhinitis volunteered for the study. Nasal biopsies were obtained before and during pollen season as well as before and after allergen challenge. The seasonal material was used for mRNA quantification of Toll-like receptors 2, 3 and 4 with real-time polymerase chain reaction, whereas specimens achieved in conjunction with allergen challenge were used for immunohistochemical localization and quantification of corresponding proteins. Results mRNA and protein representing Toll-like receptors 2, 3 and 4 could be demonstrated in all specimens. An increase in protein expression for all three receptors could be seen following allergen challenge, whereas a significant increase of mRNA only could be obtained for Toll-like receptor 3 during pollen season. Conclusion The up-regulation of Toll-like receptors 2, 3 and 4 in the nasal mucosa of patients with symptomatic allergic rhinitis supports the idea of a role for Toll-like receptors in allergic airway inflammation.

  9. Expression of proto-oncogene KIT is up-regulated in subset of human meningiomas

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    Saini Masum

    2012-06-01

    Full Text Available Abstract Background KIT is a proto-oncogene involved in diverse neoplastic processes. Aberrant kinase activity of the KIT receptor has been targeted by tyrosine kinase inhibitor (TKI therapy in different neoplasias. In all the earlier studies, KIT expression was reported to be absent in meningiomas. However, we observed KIT mRNA expression in some meningioma cases. This prompted us to undertake its detailed analyses in meningioma tissues resected during 2008–2009. Methods Tumor tissues and matched peripheral blood samples collected from meningioma patients were used for detailed molecular analyses. KIT expression was ascertained immunohistochemically and validated by immunoblotting. KIT and KITLG transcript levels were discerned by reverse transcription quantitative real-time PCR (RT-qPCR. Similarly, KIT amplification and allele loss were assessed by quantitative real-time (qPCR and validated by fluorescence in situ hybridization (FISH on the neoplastic tissues. Possible alterations of the gene at the nucleotide level were analyzed by sequencing. Results Contrary to earlier reports, KIT expression, was detected immunohistochemically in 20.6% meningioma cases (n = 34. Receptor (KIT and ligand (KITLG transcripts monitored by RT-qPCR were found to co-express (p = 0.048 in most of the KIT immunopositive tumors. 1/7 KIT positive meningiomas showed allele loss corroborated by reduced FISH signal in the corresponding neoplastic tissue. Sequence analysis of KIT showed M541L substitution in exon 10, in one of the immunopositive cases. However, its biological consequence remains to be uncovered. Conclusions This study clearly demonstrates KIT over-expression in the human meningiomas. The data suggest that up-regulated KIT transcription (p  0.05, is a likely mechanism responsible for altered KIT expression. Thus, KIT is a potential candidate for detailed investigation in the context of meningioma pathogenesis.

  10. Expression of proto-oncogene KIT is up-regulated in subset of human meningiomas

    International Nuclear Information System (INIS)

    Saini, Masum; Jha, Ajaya Nand; Abrari, Andleeb; Ali, Sher

    2012-01-01

    KIT is a proto-oncogene involved in diverse neoplastic processes. Aberrant kinase activity of the KIT receptor has been targeted by tyrosine kinase inhibitor (TKI) therapy in different neoplasias. In all the earlier studies, KIT expression was reported to be absent in meningiomas. However, we observed KIT mRNA expression in some meningioma cases. This prompted us to undertake its detailed analyses in meningioma tissues resected during 2008–2009. Tumor tissues and matched peripheral blood samples collected from meningioma patients were used for detailed molecular analyses. KIT expression was ascertained immunohistochemically and validated by immunoblotting. KIT and KITLG transcript levels were discerned by reverse transcription quantitative real-time PCR (RT-qPCR). Similarly, KIT amplification and allele loss were assessed by quantitative real-time (qPCR) and validated by fluorescence in situ hybridization (FISH) on the neoplastic tissues. Possible alterations of the gene at the nucleotide level were analyzed by sequencing. Contrary to earlier reports, KIT expression, was detected immunohistochemically in 20.6% meningioma cases (n = 34). Receptor (KIT) and ligand (KITLG) transcripts monitored by RT-qPCR were found to co-express (p = 0.048) in most of the KIT immunopositive tumors. 1/7 KIT positive meningiomas showed allele loss corroborated by reduced FISH signal in the corresponding neoplastic tissue. Sequence analysis of KIT showed M541L substitution in exon 10, in one of the immunopositive cases. However, its biological consequence remains to be uncovered. This study clearly demonstrates KIT over-expression in the human meningiomas. The data suggest that up-regulated KIT transcription (p < 0.001), instead of gene amplification (p > 0.05), is a likely mechanism responsible for altered KIT expression. Thus, KIT is a potential candidate for detailed investigation in the context of meningioma pathogenesis

  11. Suspension state increases reattachment of breast cancer cells by up-regulating lamin A/C.

    Science.gov (United States)

    Zhang, Xiaomei; Lv, Yonggang

    2017-12-01

    Extravasation is a rate-limiting step of tumor metastasis, for which adhesion to endothelium of circulating tumor cells (CTCs) is the prerequisite. The suspension state of CTCs undergoing detachment from primary tumor is a persistent biomechanical cue, which potentially regulates the biophysical characteristics and cellular behaviors of tumor cells. In this study, breast tumor cells MDA-MB-231 in suspension culture condition were used to investigate the effect of suspension state on reattachment of CTCs. Our study demonstrated that suspension state significantly increased the adhesion ability of breast tumor cells. In addition, suspension state markedly promoted the formation of stress fibers and focal adhesions and reduced the motility in reattached breast cancer cells. Moreover, lamin A/C was reversibly accumulated at posttranscriptional level under suspension state, improving the cell stiffness of reattached breast cancer cells. Disruption of actin cytoskeleton by cytochalasin D caused lamin A/C accumulation. Conversely, decreasing actomyosin contraction by ROCK inhibitor Y27632 reduced lamin A/C level. Knocking down lamin A/C weakened the suspension-induced increase of adhesion, and also abolished the suspension-induced decrease of motility and increase of stress fibers and focal adhesion in reattaching tumor cells, suggesting a crucial role of lamin A/C. In conclusion, it was demonstrated that suspension state promoted the reattachment of breast tumor cells by up-regulating lamin A/C via cytoskeleton disruption. These findings highlight the important role of suspension state for tumor cells in tumor metastasis. Copyright © 2017 Elsevier B.V. All rights reserved.

  12. PSG gene expression is up-regulated by lysine acetylation involving histone and nonhistone proteins.

    Directory of Open Access Journals (Sweden)

    Soledad A Camolotto

    Full Text Available BACKGROUND: Lysine acetylation is an important post-translational modification that plays a central role in eukaryotic transcriptional activation by modifying chromatin and transcription-related factors. Human pregnancy-specific glycoproteins (PSG are the major secreted placental proteins expressed by the syncytiotrophoblast at the end of pregnancy and represent early markers of cytotrophoblast differentiation. Low PSG levels are associated with complicated pregnancies, thus highlighting the importance of studying the mechanisms that control their expression. Despite several transcription factors having been implicated as key regulators of PSG gene family expression; the role of protein acetylation has not been explored. METHODOLOGY/PRINCIPAL FINDINGS: Here, we explored the role of acetylation on PSG gene expression in the human placental-derived JEG-3 cell line. Pharmacological inhibition of histone deacetylases (HDACs up-regulated PSG protein and mRNA expression levels, and augmented the amount of acetylated histone H3 associated with PSG 5'regulatory regions. Moreover, PSG5 promoter activation mediated by Sp1 and KLF6, via the core promoter element motif (CPE, -147/-140, was markedly enhanced in the presence of the HDAC inhibitor trichostatin A (TSA. This effect correlated with an increase in Sp1 acetylation and KLF6 nuclear localization as revealed by immunoprecipitation and subcellular fractionation assays. The co-activators PCAF, p300, and CBP enhanced Sp1-dependent PSG5 promoter activation through their histone acetylase (HAT function. Instead, p300 and CBP acetyltransferase domain was dispensable for sustaining co-activation of PSG5 promoter by KLF6. CONCLUSIONS/SIGNIFICANCE: Results are consistent with a regulatory role of lysine acetylation on PSG expression through a relaxed chromatin state and an increase in the transcriptional activity of Sp1 and KLF6 following an augmented Sp1 acetylation and KLF6 nuclear localization.

  13. Intermittent fasting up-regulates Fsp27/Cidec gene expression in white adipose tissue.

    Science.gov (United States)

    Karbowska, Joanna; Kochan, Zdzislaw

    2012-03-01

    Fat-specific protein of 27 kDa (FSP27) is a novel lipid droplet protein that promotes triacylglycerol storage in white adipose tissue (WAT). The regulation of the Fsp27 gene expression in WAT is largely unknown. We investigated the nutritional regulation of FSP27 in WAT. The effects of intermittent fasting (48 d, eight cycles of 3-d fasting and 3-d refeeding), caloric restriction (48 d), fasting-refeeding (3-d fasting and 3-d refeeding), and fasting (3 d) on mRNA expression of FSP27, peroxisome proliferator-activated receptor γ (PPARγ2), CCAAT/enhancer binding protein α (C/EBPα), and M isoform of carnitine palmitoyltransferase 1 (a positive control for PPARγ activation) in epididymal WAT and on serum triacylglycerol, insulin, and leptin levels were determined in Wistar rats. We also determined the effects of PPARγ activation by rosiglitazone or pioglitazone on FSP27 mRNA levels in primary rat adipocytes. Long-term intermittent fasting, in contrast to other dietary manipulations, significantly up-regulated Fsp27 gene expression in WAT. Moreover, in rats subjected to intermittent fasting, serum insulin levels were elevated; PPARγ2 and C/EBPα mRNA expression in WAT was increased, and there was a positive correlation of Fsp27 gene expression with PPARγ2 and C/EBPα mRNA levels. FSP27 mRNA expression was also increased in adipocytes treated with PPARγ agonists. Our study demonstrates that the transcription of the Fsp27 gene in adipose tissue may be induced in response to nutritional stimuli. Furthermore, PPARγ2, C/EBPα, and insulin may be involved in the nutritional regulation of FSP27. Thus intermittent fasting, despite lower caloric intake, may promote triacylglycerol deposition in WAT by increasing the expression of genes involved in lipid storage, such as Fsp27. Copyright © 2012 Elsevier Inc. All rights reserved.

  14. Molecular characterization of Quercus suber MYB1, a transcription factor up-regulated in cork tissues.

    Science.gov (United States)

    Almeida, Tânia; Menéndez, Esther; Capote, Tiago; Ribeiro, Teresa; Santos, Conceição; Gonçalves, Sónia

    2013-01-15

    The molecular processes associated with cork development in Quercus suber L. are poorly understood. A previous molecular approach identified a list of genes potentially important for cork formation and differentiation, providing a new basis for further molecular studies. This report is the first molecular characterization of one of these candidate genes, QsMYB1, coding for an R2R3-MYB transcription factor. The R2R3-MYB gene sub-family has been described as being involved in the phenylpropanoid and lignin pathways, both involved in cork biosynthesis. The results showed that the expression of QsMYB1 is putatively mediated by an alternative splicing (AS) mechanism that originates two different transcripts (QsMYB1.1 and QsMYB1.2), differing only in the 5'-untranslated region, due to retention of the first intron in one of the variants. Moreover, within the retained intron, a simple sequence repeat (SSR) was identified. The upstream regulatory region of QsMYB1 was extended by a genome walking approach, which allowed the identification of the putative gene promoter region. The relative expression pattern of QsMYB1 transcripts determined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) revealed that both transcripts were up-regulated in cork tissues; the detected expression was several times higher in newly formed cork harvested from trees producing virgin, second or reproduction cork when compared with wood. Moreover, the expression analysis of QsMYB1 in several Q. suber organs showed very low expression in young branches and roots, whereas in leaves, immature acorns or male flowers, no expression was detected. These preliminary results suggest that QsMYB1 may be related to secondary growth and, in particular, with the cork biosynthesis process with a possible alternative splicing mechanism associated with its regulatory function. Copyright © 2012 Elsevier GmbH. All rights reserved.

  15. Homeobox A7 stimulates breast cancer cell proliferation by up-regulating estrogen receptor-alpha

    Energy Technology Data Exchange (ETDEWEB)

    Zhang, Yu [Department of Reproductive Endocrinology, Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou 310006 (China); Department of Obstetrics and Gynaecology, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia V5Z 4H4 (Canada); Cheng, Jung-Chien [Department of Obstetrics and Gynaecology, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia V5Z 4H4 (Canada); Huang, He-Feng, E-mail: huanghefg@hotmail.com [Department of Reproductive Endocrinology, Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou 310006 (China); Leung, Peter C.K., E-mail: peter.leung@ubc.ca [Department of Reproductive Endocrinology, Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou 310006 (China); Department of Obstetrics and Gynaecology, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia V5Z 4H4 (Canada)

    2013-11-01

    Highlights: •HOXA7 regulates MCF7 cell proliferation. •HOXA7 up-regulates ERα expression. •HOXA7 mediates estrogen-induced MCF7 cell proliferation. -- Abstract: Breast cancer is the most common hormone-dependent malignancy in women. Homeobox (HOX) transcription factors regulate many cellular functions, including cell migration, proliferation and differentiation. The aberrant expression of HOX genes has been reported to be associated with human reproductive cancers. Estradiol (E2) and its nuclear receptors, estrogen receptor (ER)-alpha and ER-beta, are known to play critical roles in the regulation of breast cancer cell growth. However, an understanding of the potential relationship between HOXA7 and ER in breast cancer cells is limited. In this study, our results demonstrate that knockdown of HOXA7 in MCF7 cells significantly decreased cell proliferation and ERα expression. In addition, HOXA7 knockdown attenuated E2-induced cell proliferation as well as progesterone receptor (PR) expression. The stimulatory effects of E2 on cell proliferation and PR expression were abolished by co-treatment with ICI 182780, a selective ERα antagonist. In contrast, overexpression of HOXA7 significantly stimulated cell proliferation and ERα expression. Moreover, E2-induced cell proliferation, as well as PR expression, was enhanced by the overexpression of HOXA7. Neither knockdown nor overexpression of HOXA7 affected the ER-beta levels. Our results demonstrate a novel mechanistic role for HOXA7 in modulating breast cancer cell proliferation via regulation of ERα expression. This finding contributes to our understanding of the role HOXA7 plays in regulating the proliferation of ER-positive cancer cells.

  16. Maternal obesity in the rat programs male offspring exploratory, learning and motivation behavior: prevention by dietary intervention pre-gestation or in gestation.

    Science.gov (United States)

    Rodriguez, J S; Rodríguez-González, G L; Reyes-Castro, L A; Ibáñez, C; Ramírez, A; Chavira, R; Larrea, F; Nathanielsz, P W; Zambrano, E

    2012-04-01

    We studied the effects of maternal high fat diet (HFD, 25% calories from fat administered before and during pregnancy and lactation) and dietary intervention (switching dams from HFD to control diet) at different periconceptional periods on male offspring anxiety related behavior, exploration, learning, and motivation. From weaning at postnatal day (PND) 21, female subjects produced to be the mothers in the study received either control diet (CTR - 5% calories from fat), HFD through pregnancy and lactation (MO), HFD during PNDs 21-90 followed by CTR diet (pre-gestation (PG) intervention) or HFD from PND 21 to 120 followed by CTR diet (gestation and lactation (G) intervention) and bred at PND 120. At 19 days of gestation maternal serum corticosterone was increased in MO and the PG and G dams showed partial recovery with intermediate levels. In offspring, no effects were found in the elevated plus maze test. In the open field test, MO and G offspring showed increase zone entries, displaying less thigmotaxis; PG offspring showed partial recuperation of this behavior. During initial operant conditioning MO, PG and G offspring displayed decreased approach behavior with subsequent learning impairment during the acquisition of FR-1 and FR-5 operant conditioning for sucrose reinforcement. Motivation during the progressive ratio test increased in MO offspring; PG and G intervention recuperated this behavior. We conclude that dietary intervention can reverse negative effects of maternal HFD and offspring outcomes are potentially due to elevated maternal corticosterone. Copyright © 2012 ISDN. Published by Elsevier Ltd. All rights reserved.

  17. Weight Loss Instead of Weight Gain within the Guidelines in Obese Women during Pregnancy: A Systematic Review and Meta-Analyses of Maternal and Infant Outcomes.

    Directory of Open Access Journals (Sweden)

    Mufiza Zia Kapadia

    Full Text Available Controversy exists about how much, if any, weight obese pregnant women should gain. While the revised Institute of Medicine guidelines on gestational weight gain (GWG in 2009 recommended a weight gain of 5-9 kg for obese pregnant women, many studies suggested even gestational weight loss (GWL for obese women.A systematic review was conducted to summarize pregnancy outcomes in obese women with GWL compared to GWG within the 2009 Institute of Medicine guidelines (5-9 kg.Five databases were searched from 1 January 2009 to 31 July 2014. The Cochrane Handbook for Systematic Reviews of Interventions and the PRISMA Statement were followed. A modified version of the Newcastle-Ottawa scale was used to assess individual study quality. Small for gestational age (SGA, large for gestational age (LGA and preterm birth were our primary outcomes.Six cohort studies were included, none of which assessed preterm birth. Compared to GWG within the guidelines, women with GWL had higher odds of SGA 90th percentile (AOR 0.57; 95% CI 0.52-0.62. There was a trend towards a graded relationship between SGA <10th percentile and each of three obesity classes (I: AOR 1.73; 95% CI 1.53-1.97; II: AOR 1.63; 95% CI 1.44-1.85 and III: AOR 1.39; 95% CI 1.17-1.66, respectively.Despite decreased odds of LGA, increased odds of SGA and a lack of information on preterm birth indicate that GWL should not be advocated in general for obese women.

  18. Up-Regulation of Claudin-6 in the Distal Lung Impacts Secondhand Smoke-Induced Inflammation

    Directory of Open Access Journals (Sweden)

    Joshua B. Lewis

    2016-10-01

    Full Text Available It has long been understood that increased epithelial permeability contributes to inflammation observed in many respiratory diseases. Recently, evidence has revealed that environmental exposure to noxious material such as cigarette smoke reduces tight junction barrier integrity, thus enhancing inflammatory conditions. Claudin-6 (Cldn6 is a tetraspanin transmembrane protein found within the tight junctional complex and is implicated in maintaining lung epithelial barriers. To test the hypothesis that increased Cldn6 ameliorates inflammation at the respiratory barrier, we utilized the Tet-On inducible transgenic system to conditionally over-express Clnd6 in the distal lung. Cldn6 transgenic (TG and control mice were continuously provided doxycycline from postnatal day (PN 30 until euthanasia date at PN90. A subset of Cldn6 TG and control mice were also subjected to daily secondhand tobacco smoke (SHS via a nose only inhalation system from PN30-90 and compared to room air (RA controls. Animals were euthanized on PN90 and lungs were harvested for histological and molecular characterization. Bronchoalveolar lavage fluid (BALF was procured for the assessment of inflammatory cells and molecules. Quantitative RT-PCR and immunoblotting revealed increased Cldn6 expression in TG vs. control animals and SHS decreased Cldn6 expression regardless of genetic up-regulation. Histological evaluations revealed no adverse pulmonary remodeling via Hematoxylin and Eosin (H&E staining or any qualitative alterations in the abundance of type II pneumocytes or proximal non-ciliated epithelial cells via staining for cell specific propeptide of Surfactant Protein-C (proSP-C or Club Cell Secretory Protein (CCSP, respectively. Immunoblotting and qRT-PCR confirmed the differential expression of Cldn6 and the pro-inflammatory cytokines TNF-α and IL-1β. As a general theme, inflammation induced by SHS exposure was influenced by the availability of Cldn6. These data reveal

  19. The measurement of maternal adiposity.

    LENUS (Irish Health Repository)

    Fattah, C

    2012-02-01

    The issue of maternal obesity has become a major public health problem. Internationally, the diagnosis of obesity is based on body mass index (BMI) that is, weight in kg\\/height in m2. While epidemiological associations have been shown between different BMI categories and adverse clinical outcomes, there is also a growing realisation that BMI has significant limitations. In this review, we assess current methods to measure body fat and, in particular, their application in pregnant women.

  20. Histones Induce the Procoagulant Phenotype of Endothelial Cells through Tissue Factor Up-Regulation and Thrombomodulin Down-Regulation.

    Science.gov (United States)

    Kim, Ji Eun; Yoo, Hyun Ju; Gu, Ja Yoon; Kim, Hyun Kyung

    2016-01-01

    The high circulating levels of histones found in various thrombotic diseases may compromise the anticoagulant barrier of endothelial cells. We determined how histones affect endothelial procoagulant tissue factor (TF) and anticoagulant thrombomodulin (TM). Surface antigens, soluble forms, and mRNA levels of TF and TM were measured by flow cytometry, ELISA, and real-time RT-PCR, respectively. TF and TM activity were measured using procoagulant activity, thrombin generation, or chromogenic assays. Involvement of the toll-like receptor (TLR) was assessed using the neutralizing antibodies. Histones dose-dependently induced surface antigens, activity and mRNA levels of endothelial TF. Histone-treated endothelial cells significantly shortened the lag time and enhanced the endogenous thrombin potential of normal plasma, which was normalized by a TF neutralizing antibody. Histones induced phosphatidylserine and protein-disulfide isomerase expression in endothelial cells. Histones also reduced the surface antigen, activity, and mRNA levels of endothelial TM. Polysialic acid and heparin reversed the histone-induced TF up-regulation and TM down-regulation. Activated protein C did not affect the TF up-regulation, but interrupted TM down-regulation. TLR2, and TLR4 inhibitors partially blocked the TF up-regulation. Histones induced the endothelial procoagulant phenotype through TF up-regulation and TM down-regulation. The effects of histones were partly mediated by TLR2, TLR4. Strategies to inhibit the harmful effects of histones in endothelial cells may be required in order to prevent a thrombotic environment.

  1. Sildenafil prevents the up-regulation of transient receptor potential canonical channels in the development of cardiomyocyte hypertrophy

    International Nuclear Information System (INIS)

    Kiso, Hironori; Ohba, Takayoshi; Iino, Kenji; Sato, Kazuhiro; Terata, Yutaka; Murakami, Manabu; Ono, Kyoichi; Watanabe, Hiroyuki; Ito, Hiroshi

    2013-01-01

    Highlights: •Transient receptor potential canonical (TRPC1, 3 and 6) are up-regulated by ET-1. •Sildenafil inhibited hypertrophic responses (BNP, Ca entry, NFAT activation). •Sildenafil suppressed TRPC1, 3 and 6 expression. -- Abstract: Background: Transient receptor potential canonical (TRPCs) channels are up-regulated in the development of cardiac hypertrophy. Sildenafil inhibits TRPC6 activation and expression, leading to the prevention of cardiac hypertrophy. However, the effects of sildenafil on the expression of other TRPCs remain unknown. We hypothesized that in addition to its effects of TRPC6, sildenafil blocks the up-regulation of other TRPC channels to suppress cardiomyocyte hypertrophy. Methods and results: In cultured neonatal rat cardiomyocytes, a 48 h treatment with 10 nM endothelin (ET)-1 induced hypertrophic responses characterized by nuclear factor of activated T cells activation and enhancement of brain natriuretic peptide expression and cell surface area. Co-treatment with sildenafil (1 μM, 48 h) inhibited these ET-1-induced hypertrophic responses. Although ET-1 enhanced the gene expression of TRPCs, sildenafil inhibited the enhanced gene expression of TRPC1, C3 and C6. Moreover, co-treatment with sildenafil abolished the augmentation of SOCE in the hypertrophied cardiomyocytes. Conclusions: These results suggest that sildenafil inhibits cardiomyocyte hypertrophy by suppressing the up-regulation of TRPC expression

  2. PTX3 is up-regulated in epithelial mammary cells during S. aureus intramammary infection in goat

    Directory of Open Access Journals (Sweden)

    Joel Fernando Soares Filipe

    2015-07-01

    PTX3 was up-regulated in epithelial mammary cells and in milk cells after S. aureus infection, demonstrating that it represents a first line of immune defense in goat udder. No modulation was observed in macrophages, in the secretum and in the ductal epithelial cells. Further experiments are needed to elucidate the role of PTX3 in the pathogenesis of S. aureus infection.

  3. Obesity, reproduction and oxidative stress

    Directory of Open Access Journals (Sweden)

    Tamara V. Zhuk

    2017-12-01

    Full Text Available The prevalence of obesity and overweight is one of the most pressing problems nowadays. Obesity as a comorbid condition affects all body systems. Obesity has been reported to be a risk factor not only for cardiovascular diseases and oncopathology, but also for fertility problems, many obstetric and perinatal complications worsening the maternal and infant health. The balance between the oxidative and antioxidant system is one of the indicators of the state of human homeostasis. Today it is proved that obesity is associated with an increase in oxidative stress and a decrease in antioxidant protection. This review reveals a close relationship between obesity, oxidative stress and reproductive problems.

  4. Psychological issues in pediatric obesity

    Directory of Open Access Journals (Sweden)

    Gurvinder Kalra

    2012-01-01

    Full Text Available Pediatric obesity is a major health problem and has reached epidemiological proportions today. The present paper reviews major psychological issues in pediatric obesity from a developmental perspective. Research and literature has shown that a number of developmental, family, maternal and child factors are responsible in the genesis of pediatric obesity. Family food habits, early developmental lifestyle of the child, parenting, early family relationships and harmony all contribute towards the growth and development of a child. The present review focuses on the role of developmental psychological factors in the pathogenesis of pediatric obesity and highlights the developmental factors that must be kept in mind when evaluating a case of pediatric obesity.

  5. Down-regulated miR-448 relieves spinal cord ischemia/reperfusion injury by up-regulating SIRT1

    Directory of Open Access Journals (Sweden)

    Yun Wang

    2018-03-01

    Full Text Available MicroRNAs play a crucial role in the progression of spinal cord ischemia/reperfusion injury (SCII. The role of miR-448 and SIRT1 in SCII was investigated in this study, to provide further insights into prevention and improvement of this disorder. In this study, expressions of miR-448 and SIRT1 protein were determined by qRT-PCR and western blot, respectively. Flow cytometry was used to analyze cell apoptosis. The endogenous expression of genes was modulated by recombinant plasmids and cell transfection. Dual-luciferase reporter assay was performed to determine the interaction between miR-448 and SIRT1. The Basso, Beattie, and Bresnahan score was used to measure the hind-limb function of rat. The spinal cord ischemia reperfusion injury model of adult rats was developed by abdominal aorta clamping, and the nerve function evaluation was completed by motor deficit index score. In SCII tissues and cells treated with hypoxia, miR-448 was up-regulated while SIRT1 was down-regulated. Hypoxia treatment reduced the expression of SIRT1 through up-regulating miR-448 in nerve cells. Up-regulation of miR-448 induced by hypoxia promoted apoptosis of nerve cells through down-regulating SIRT1. Down-regulated miR-448 improved neurological function and hind-limb motor function of rats with SCII by up-regulating SIRT1. Down-regulated miR-448 inhibited apoptosis of nerve cells and improved neurological function by up-regulating SIRT1, which contributes to relieving SCII.