Retinopatia de Purtscher-like e pancreatite aguda Purtscher-like retinopathy and acute pancreatitis

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Kelly Fernandes de Paula Rodrigues

2008-04-01

Full Text Available Retinopatia de Purtscher-like é uma baixa súbita da visão associada à imagem de múltiplas áreas branco-amareladas (manchas algodonosas e hemorragias no pólo posterior de ambos os olhos. O exato mecanismo da injúria ainda não é claro, mas provavelmente seria de natureza embólica.Tem sido descrita em uma variedade de condições, incluindo pancreatite aguda, síndrome de embolia gordurosa, insuficiência renal, nascimento (parto e pós-parto, desordens do tecido conectivo, entre outras. Serão relatados três casos de pancreatite aguda confirmada pelos exames laboratoriais e história clínica, associadas a alterações no exame do fundo de olho, compatíveis com esta retinopatia.Purtscher-like retinopathy is acute loss of vision associated image of the multiple areas of retinal whitening and hemorrhage in the posterior pole of both eyes. The exact mechanism of injury remains unclear, current evidence suggests that it is embolic in nature. In a variety of conditions are been described including acute pancreatitis, fat embolism syndrome, renal failure, childbirth, and connective tissue disorders. Will are related three cases of the acute pancreatitis which was confirmed by complementary laboratory studies and clinical history, associated from exam of the fundus of the eye, similar is this retinopathy.

Changes in the management of patients with severe acute pancreatitis Mudanças no manejo de doentes com pancreatite aguda grave

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Tercio De Campos

2008-09-01

Full Text Available BACKGROUND: Severe acute pancreatitis is present in up to 25% of patients with acute pancreatitis, with considerable mortality. Changes in the management of acute pancreatitis in the last 2 decades contributed to reduce the mortality. AIM: To show the evolution in the management of severe acute pancreatitis, comparing two different approaches. METHODS: All patients with severe acute pancreatitis from 1999 to 2005 were included. We compared the results of a retrospective review from 1999 to 2002 (group A with a prospective protocol, from 2003 to 2005 (group B. In group A severe pancreatitis was defined by the presence of systemic or local complications. In group B the Atlanta criteria were used to define severity. The variables analyzed were: age, gender, etiology, APACHE II, leukocytes, bicarbonate, fluid collections and necrosis on computed tomography, surgical treatment and mortality. RESULTS: Seventy-one patients were classified as severe, 24 in group A and 47 in group B. The mean APACHE II in groups A and B were 10.7 ± 3.5 and 9.3 ± 4.5, respectively. Necrosis was seen in 12 patients (50% in group A and in 21 patients (44.7% in group B. Half of the patients in group A and two (4.3% in group B underwent to pancreatic interventions. Mortality reached 45.8% in group A and 8.5% in group B. CONCLUSION: A specific approach and a prospective protocol can change the results in the treatment of patients with severe acute pancreatitis.RACIONAL: A pancreatite aguda grave está presente em até 25% dos doentes com pancreatite aguda, com mortalidade considerável. Mudanças no tratamento da pancreatite aguda nas últimas duas décadas contribuíram para a redução da mortalidade destes doentes. OBJETIVO: Mostrar a evolução do manejo da pancreatite aguda, comparando duas diferentes abordagens. MÉTODOS: Todos os doentes com pancreatite aguda grave de 1999 a 2005 do Serviço de Emergência da Santa Casa de São Paulo, SP, foram incluídos. Os

Pancreatic adenocarcinoma and diabetes mellitus

International Nuclear Information System (INIS)

Novotna, T.

2015-01-01

Impaired glucose tolerance or frank diabetes mellitus is known to occur more frequently in patients with pancreatic cancer than in the general population. At the time of the diagnosis of pancreatic cancer, more than 70% of patients taking the glucose tolerance test show diabetes or impaired glucose tolerance (1). Relationship among diabetes mellitus and pancreatic cancer is vague but sure, although neither the nature nor the sequence of the possible cause – effect relationship has been established. The reason for the high frequency of glucose intolerance in patients with pancreatic cancer remains controversial. (author)

Pancreatic scintigraphy in diabetes mellitus

International Nuclear Information System (INIS)

Shio, Hiroshi; Ueki, Jyuichi; Nomura, Kozi; Nakamura, Yoshifumi

1983-01-01

Pancreatic scintigraphy was performed on 67 diabetic patients (42 males and 25 females) in order to study exocrine pancreatic functions in primary diabetes. Relationships between visualization and the onset age, sex, morbid period, presence or absence of retinitis, good or poor control of blood glucose control and the therapeutic modality of diabetes were examined. Abnormality was detected in 34 cases (50.7%), being frequent among male patients in their 50s. The more serious the diabetes, i.e., with a longer morbid period, poorer blood glucose control and worse retinitis, the higher was the frequency of abnormality in pancreatic visualization. The frequency of abnormality was high in association with insulin treatment, oral tablets and single dietary treatment in that order. The more severe the hypoinsulinism, the higher was the frequency of abnormality. This technique can be used as a screening means for exocrine pancreatic function tests on diabetics. (Chiba, N.)

Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer

Science.gov (United States)

Hart, Phil A; Bellin, Melena D; Andersen, Dana K; Bradley, David; Cruz-Monserrate, Zobeida; Forsmark, Christopher E; Goodarzi, Mark O; Habtezion, Aida; Korc, Murray; Kudva, Yogish C; Pandol, Stephen J; Yadav, Dhiraj; Chari, Suresh T

2017-01-01

Diabetes mellitus is a group of diseases defined by persistent hyperglycaemia. Type 2 diabetes, the most prevalent form, is characterised initially by impaired insulin sensitivity and subsequently by an inadequate compensatory insulin response. Diabetes can also develop as a direct consequence of other diseases, including diseases of the exocrine pancreas. Historically, diabetes due to diseases of the exocrine pancreas was described as pancreatogenic or pancreatogenous diabetes mellitus, but recent literature refers to it as type 3c diabetes. It is important to note that type 3c diabetes is not a single entity; it occurs because of a variety of exocrine pancreatic diseases with varying mechanisms of hyperglycaemia. The most commonly identified causes of type 3c diabetes are chronic pancreatitis, pancreatic ductal adenocarcinoma, haemochromatosis, cystic fibrosis, and previous pancreatic surgery. In this Review, we discuss the epidemiology, pathogenesis, and clinical relevance of type 3c diabetes secondary to chronic pancreatitis and pancreatic ductal adenocarcinoma, and highlight several important knowledge gaps. PMID:28404095

Pancreatite aguda leve: avaliação pela ultra-sonografia. estudo prospectivo Mild acute pancreatitis: ultrasound evaluation: a prospective study

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Márcio Martins Machado

2002-07-01

Full Text Available Resumo Neste estudo foram avaliados, por meio da ultra-sonografia, 21 pacientes com pancreatite aguda leve. Foram analisadas a presença ou ausência de hipoecogenicidade do pâncreas e a presença ou ausência de líquido peripancreático. Em 19 pacientes (90,5% foi identificada hipoecogenicidade pancreática, e em três (15,8% destes pacientes foi identificada a presença de pequena quantidade de líquido na pequena cavidade dos epíploons. Em dois pacientes (9,5% não se identificou qualquer alteração pancreática. Com relação à possível etiologia da pancreatite aguda, em 15 pacientes (71,5% pôde-se demonstrar a presença de colecistopatia calculosa, em quatro pacientes (19,0% havia história de alcoolismo crônico e não foram identificados cálculos na vesícula biliar, e em dois pacientes (9,5% não foi identificada qualquer causa aparente. Os autores concluem que a ultra-sonografia pode identificar alteração na maioria dos pacientes com pancreatite aguda leve e permite, ainda, o acompanhamento daqueles com pequenas coleções líquidas peripancreáticas.We analyzed the ultrasonographic findings of 21 patients with mild acute pancreatitis. The presence or absence of pancreatic hypoechogenicity and peripancreatic fluid collection was assessed. Pancreatic hypoechogenicity was identified in 19 patients (90.5% whereas small sac fluid collection was identified in 3 (15.8% of these patients. No abnormality was seen in 2 patients (9.5%. Regarding the etiology of acute pancreatitis, cholelithiasis was identified in 15 patients (71.5%, alcohol abuse was identified in 4 patients (19.0%, and in 2 patients (9.5% no probable etiology could be found. The authors conclude that ultrasonography may identify abnormalities in the majority of patients with mild acute pancreatitis and can be used to assess patients with peripancreatic fluid collections.

Interleucina-18 (IL-18 y otros parámetros inmunológicos como marcadores de gravedad en la pancreatitis aguda Interleukin 18 (IL-18 and other immunological parameters as markers of severity in acute pancreatitis

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M. A. Martín

2008-12-01

Full Text Available Objetivo: se trata de comparar prospectivamente el comportamiento durante la primera semana del ingreso de los niveles de interleucina-18 (IL-18, y otros parámetros inmunológicos entre pacientes con pancreatitis aguda con y sin criterios de gravedad, así como entre pacientes con y sin desarrollo ulterior de seudoquiste. Pacientes y métodos: se compararon en 36 pacientes con pancreatitis aguda los resultados de sTNF-RI, IL-1Ra, IL-6 e IL-18 los días 1, 2, 3 y 7 desde el ingreso entre pancretitis leve, grave y un grupo control (13 pacientes con cólico biliar simple, así como entre pacientes con o sin seudoquiste. Resultados: al comparar pancreatitis leve con grave, IL-18 fue significativamente superior sólo el primer día en las pancreatitis graves y los otros parámetros a partir del segundo día de forma mantenida. También en pacientes que desarrollaron seudoquiste, IL-18 estuvo significativamente elevada el primer día. Conclusiones: IL-18 resultó el marcador más precoz de complicaciones y gravedad de la pancreatitis aguda a nivel sistémico y local (seudoquiste.Objective: our aim was to prospectively compare the behavior of interleukin 18 (IL-18 levels and other immunological parameters during the first week of hospitalization between acute pancreatitis patients with and without severity criteria, as well as between patients with and without late pseudocyst development. Patients and methods: in 36 patients with acute pancreatitis we compared sTNF-RI, IL-1Ra, IL-6, and IL-18 levels at days 1, 2, 3 and 7 after hospitalization between mild pancreatitis, severe pancreatitis, and a "control" group (13 patients with uncomplicated biliary colic, as well as between patients with and without pseudocyst. Results: on comparing mild to severe pancreatitis, IL-18 was significantly higher only the first day in severe pancreatitis, while the other parameters were steadily higher after the second day. In patients developing pseudocyst, IL-18 was

Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer.

Science.gov (United States)

Hart, Phil A; Bellin, Melena D; Andersen, Dana K; Bradley, David; Cruz-Monserrate, Zobeida; Forsmark, Christopher E; Goodarzi, Mark O; Habtezion, Aida; Korc, Murray; Kudva, Yogish C; Pandol, Stephen J; Yadav, Dhiraj; Chari, Suresh T

2016-11-01

Diabetes mellitus is a group of diseases defined by persistent hyperglycaemia. Type 2 diabetes, the most prevalent form, is characterised initially by impaired insulin sensitivity and subsequently by an inadequate compensatory insulin response. Diabetes can also develop as a direct consequence of other diseases, including diseases of the exocrine pancreas. Historically, diabetes due to diseases of the exocrine pancreas was described as pancreatogenic or pancreatogenous diabetes mellitus, but recent literature refers to it as type 3c diabetes. It is important to note that type 3c diabetes is not a single entity; it occurs because of a variety of exocrine pancreatic diseases with varying mechanisms of hyperglycaemia. The most commonly identified causes of type 3c diabetes are chronic pancreatitis, pancreatic ductal adenocarcinoma, haemochromatosis, cystic fibrosis, and previous pancreatic surgery. In this Review, we discuss the epidemiology, pathogenesis, and clinical relevance of type 3c diabetes secondary to chronic pancreatitis and pancreatic ductal adenocarcinoma, and highlight several important knowledge gaps. Copyright © 2016 Elsevier Ltd. All rights reserved.

Bases moleculares de la depleción de glutatión y de la necrosis celular en la pancreatitis aguda. Papel de las proteín quinasas activadas por mitógenos.

OpenAIRE

Pereda Cervera, Javier

2006-01-01

RESUMEN La pancreatitis aguda es el proceso inflamatorio agudo del páncreas con afectación variable de otros tejidos regionales y sistemas orgánicos alejados. Es una enfermedad con una incidencia relativamente elevada en España y en el resto del mundo y con una mortalidad entre el 10 y el 45% de los casos graves de la enfermedad. Los mecanismos moleculares por los que una pancreatitis aguda se desarrolla, así como aquellos que conducen a una pancreatitis grave, aún no están del todo esclar...

Estudio por ecoendoscopia de la vía biliar extrahepática en pacientes con pancreatitis aguda biliar Endoscopic ultrasonographic examination of the common bile duct in patients with acute biliary pancreatitis

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A. Repiso

2008-06-01

Full Text Available Objetivo: el objetivo de nuestro estudio fue valorar la utilidad de la ecoendoscopia en el estudio de la vía biliar extrahepática en los pacientes diagnosticados de pancreatitis aguda biliar y determinar los factores clínicos y analíticos relacionados con el resultado de la técnica. Material y métodos: se incluyeron en el estudio de modo consecutivo 73 pacientes (31 varones, 42 mujeres; media de edad 64 ± 15 años con pancreatitis aguda biliar remitidos a nuestro servicio para la realización de ecoendoscopia biliopancreática. En todos los pacientes se realizó la técnica seguida de CPRE con esfinterotomía y técnica endoscópica para la extracción de cálculos cuando se identificó por ecoendoscopia la existencia de coledocolitiasis. Se compararon las características clínico-evolutivas de estos pacientes con respecto al resultado obtenido con la ecoendoscopia. Resultados: la media de tiempo transcurrido desde el ingreso hasta la realización de la ecoendoscopia fue de 7 ± 6 días. En 18 pacientes (24% se observó en la ecoendoscopia la existencia de coledocolitiasis y en 17 de ellos se realizó esfinterotomía endoscópica. La presencia de coledocolitiasis fue más frecuente en aquellos pacientes con dilatación de la vía biliar extrahepática (55 vs. 14%; p 0,05. Tampoco se observó esta diferencia en el subgrupo de pacientes con pancreatitis aguda severa (45 vs. 55%; p > 0,05. Conclusiones: la ecoendoscopia es una técnica útil en la selección de los pacientes con pancreatitis aguda biliar que se beneficiarán de la realización de una esfinterotomía endoscópica.Objective: the objective of our study was to evaluate the usefulness of endoscopic ultrasonography (EUS for the study of the common bile duct in patients diagnosed with acute biliary pancreatitis, and to establish clinical and laboratory factors related to this technique. Materials and methods: seventy-three consecutive patients with acute biliary pancreatitis were

Diabetes mellitus in Tropical Chronic Pancreatitis Is Not Just a Secondary Type of Diabetes

OpenAIRE

Rossi, L.; Parvin, S.; Hassan, Z.; Hildebrand, P.; Keller, U.; Ali, L.; Beglinger, C.; Azad Khan, A. K.; Whitcomb, David C.; Gyr, N.

2004-01-01

AIMS: In chronic calcific pancreatitis of the tropics, etiology and relationship to developing diabetes mellitus are unknown. Some consider these cases a straightforward secondary type of diabetes, while others suggest selective beta-cell impairment. Testing pancreatic function, we investigated whether selective beta-cell impairment triggers diabetes associated with tropical pancreatitis. METHODS: At a Bangladeshi research institute, 8 chronic tropical pancreatitis and no diabetes mellitus su...

Diagnosis and treatment of diabetes mellitus in chronic pancreatitis

OpenAIRE

Ewald, Nils; Hardt, Philip D

2013-01-01

Diabetes secondary to pancreatic diseases is commonly referred to as pancreatogenic diabetes or type 3c diabetes mellitus. It is a clinically relevant condition with a prevalence of 5%-10% among all diabetic subjects in Western populations. In nearly 80% of all type 3c diabetes mellitus cases, chronic pancreatitis seems to be the underlying disease. The prevalence and clinical importance of diabetes secondary to chronic pancreatitis has certainly been underestimated and underappreciated so fa...

Exocrine pancreatic insufficiency in diabetes mellitus: a complication of diabetic neuropathy or a different type of diabetes?

Science.gov (United States)

Hardt, Philip D; Ewald, Nils

2011-01-01

Pancreatic exocrine insufficiency is a frequently observed phenomenon in type 1 and type 2 diabetes mellitus. Alterations of exocrine pancreatic morphology can also be found frequently in diabetic patients. Several hypotheses try to explain these findings, including lack of insulin as a trophic factor for exocrine tissue, changes in secretion and/or action of other islet hormones, and autoimmunity against common endocrine and exocrine antigens. Another explanation might be that diabetes mellitus could also be a consequence of underlying pancreatic diseases (e.g., chronic pancreatitis). Another pathophysiological concept proposes the functional and morphological alterations as a consequence of diabetic neuropathy. This paper discusses the currently available studies on this subject and tries to provide an overview of the current concepts of exocrine pancreatic insufficiency in diabetes mellitus.

Diagnosis and treatment of diabetes mellitus in chronic pancreatitis.

Science.gov (United States)

Ewald, Nils; Hardt, Philip D

2013-11-14

Diabetes secondary to pancreatic diseases is commonly referred to as pancreatogenic diabetes or type 3c diabetes mellitus. It is a clinically relevant condition with a prevalence of 5%-10% among all diabetic subjects in Western populations. In nearly 80% of all type 3c diabetes mellitus cases, chronic pancreatitis seems to be the underlying disease. The prevalence and clinical importance of diabetes secondary to chronic pancreatitis has certainly been underestimated and underappreciated so far. In contrast to the management of type 1 or type 2 diabetes mellitus, the endocrinopathy in type 3c is very complex. The course of the disease is complicated by additional present comorbidities such as maldigestion and concomitant qualitative malnutrition. General awareness that patients with known and/or clinically overt chronic pancreatitis will develop type 3c diabetes mellitus (up to 90% of all cases) is rather good. However, in a patient first presenting with diabetes mellitus, chronic pancreatitis as a potential causative condition is seldom considered. Thus many patients are misdiagnosed. The failure to correctly diagnose type 3 diabetes mellitus leads to a failure to implement an appropriate medical therapy. In patients with type 3c diabetes mellitus treating exocrine pancreatic insufficiency, preventing or treating a lack of fat-soluble vitamins (especially vitamin D) and restoring impaired fat hydrolysis and incretin secretion are key-features of medical therapy.

Exocrine Pancreatic Insufficiency in Diabetes Mellitus: A Complication of Diabetic Neuropathy or a Different Type of Diabetes?

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Philip D. Hardt

2011-01-01

Full Text Available Pancreatic exocrine insufficiency is a frequently observed phenomenon in type 1 and type 2 diabetes mellitus. Alterations of exocrine pancreatic morphology can also be found frequently in diabetic patients. Several hypotheses try to explain these findings, including lack of insulin as a trophic factor for exocrine tissue, changes in secretion and/or action of other islet hormones, and autoimmunity against common endocrine and exocrine antigens. Another explanation might be that diabetes mellitus could also be a consequence of underlying pancreatic diseases (e.g., chronic pancreatitis. Another pathophysiological concept proposes the functional and morphological alterations as a consequence of diabetic neuropathy. This paper discusses the currently available studies on this subject and tries to provide an overview of the current concepts of exocrine pancreatic insufficiency in diabetes mellitus.

Glucose counterregulation in diabetes secondary to chronic pancreatitis

DEFF Research Database (Denmark)

Larsen, S; Hilsted, J; Philipsen, E K

1990-01-01

Glucose counterregulation and hormonal responses after insulin-induced hypoglycemia were investigated in six patients with diabetes mellitus secondary to chronic pancreatitis, in seven with insulin-dependent (type I) diabetes mellitus, and in seven healthy subjects. Glucose counterregulation...... was identical in type I patients and in the patients with chronic pancreatitis, whereas both groups had impaired glucose recovery compared with the healthy subjects. The patients with chronic pancreatitis had no glucagon response to hypoglycemia, whereas epinephrine increased significantly. In an additional...... experiment, glucose recovery did not occur after hypoglycemia during concomitant beta-adrenoceptor blockade in these patients. In conclusion, glucose counterregulation is preserved but slightly impaired in patients with diabetes secondary to chronic pancreatitis, and the combination of total glucagon...

Avaliação da reprodutibilidade da tomografia computadorizada no estadiamento da pancreatite aguda Reproducibility in the assessment of acute pancreatitis with computed tomography

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Edison de Oliveira Freire Filho

2007-12-01

Full Text Available OBJETIVO: Medir a reprodutibilidade da tomografia computadorizada sem e com contraste na avaliação da gravidade da pancreatite aguda. MATERIAIS E MÉTODOS: Cinqüenta e um exames de tomografia computadorizada abdominal sem e com contraste de pacientes com pancreatite aguda foram analisados por dois radiologistas (observadores 1 e 2. Calculamos o índice morfológico pela tomografia computadorizada sem e com contraste, separadamente, e o índice de gravidade da tomografia computadorizada para pancreatite aguda. Medimos a reprodutibilidade intra- e interobservador da tomografia computadorizada através do índice kappa (kapa. RESULTADOS: Para a concordância interobservador obtivemos kapa de 0,666, 0,705, 0,648, 0,547 e 0,631 para índice morfológico sem e com contraste, presença de necrose pancreática, extensão da necrose pancreática e índice de gravidade da tomografia computadorizada, respectivamente. Para a concordância intra-observador dos observadores 1 e 2 obtivemos, respectivamente, kapa de 0,796 e 0,732 para o índice morfológico sem contraste; 0,725 e 0,802 para o índice morfológico com contraste; 0,674 e 0,849 para a presença de necrose pancreática; 0,606 e 0,770 para a extensão da necrose pancreática; e 0,801 e 0,687 para o índice de gravidade da tomografia computadorizada. CONCLUSÃO: O estadiamento da pancreatite aguda pela tomografia computadorizada por meio do índice morfológico e do índice de gravidade da tomografia computadorizada é um método bastante reprodutível. O não-uso do contraste não afeta a reprodutibilidade da tomografia computadorizada para o cálculo do índice morfológico.OBJECTIVE: To evaluate the reproducibility of unenhanced and contrast-enhanced computed tomography in the assessment of patients with acute pancreatitis. MATERIALS AND METHODS: Fifty-one unenhanced and contrast-enhanced abdominal computed tomography studies of patients with acute pancreatitis were blindly reviewed by two

Hereditary chronic pancreatitis in a patient with type 1 diabetes mellitus

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Varalakshmi Muthukrishnan

2018-01-01

Full Text Available In this case report, we present a young patient with type 1 diabetes who had hereditary chronic pancreatitis. We evaluated him for the cause of pancreatitis, but it was inconclusive and finally the genetic testing was done for him, which revealed heterozygous missense mutation in exon 3 of the PRSS1 gene (protease serine 1 gene on chromosome 7. Hence, we were able to make the diagnosis of hereditary chronic pancreatitis. Chronic pancreatitis secondary to any cause can lead to permanent diabetes, which is typically difficult to control. However, in this case, the episodes of recurrent pancreatitis were present after the onset of type 1 diabetes as compared to the usual presentation of diabetes after the advancement of chronic pancreatitis.

Gallstones, a cholecystectomy, chronic pancreatitis, and the risk of subsequent pancreatic cancer in diabetic patients: a population-based cohort study.

Science.gov (United States)

Lai, Hsueh-Chou; Tsai, I-Ju; Chen, Pei-Chun; Muo, Chih-Hsin; Chou, Jen-Wei; Peng, Cheng-Yuan; Lai, Shih-Wei; Sung, Fung-Chang; Lyu, Shu-Yu; Morisky, Donald E

2013-06-01

The causal association between diabetes and pancreatic cancer remains unclear in Asian populations. This study examined whether gallstones, a cholecystectomy, chronic pancreatitis and the treatment of antidiabetic agents affect the risk of subsequent pancreatic cancer for patients with diabetes in a Taiwanese population. Using claims data from the universal health insurance program in Taiwan, 449,685 newly diagnosed diabetic cases among insured people from 2000 to 2003 were identified as the case group. The comparison group, matched for gender, age, and the index year of the diabetes cohort, consisted of 325,729 persons without diabetes. Pancreatic cancer incidence was measured in both groups until the end of 2008. Other risk factors associated with this cancer were also measured. The incidence of pancreatic cancer in the diabetic cohort was 2-fold greater than that in the comparison group (1.46 vs. 0.71 per 10,000 person-years) with an adjusted hazard ratio (HR) of 1.75 [95 % confidence interval (CI) 1.45-2.10]. The risk slightly increased for diabetic patients with gallstones, cholecystitis, and a cholecystectomy (HR 1.92, 95% CI 1.18-3.11), but greatly increased for those with comorbidity of chronic pancreatitis (HR 22.9, 95% CI 12.6-41.4). Pancreatic cancer risk also increased significantly for those patients who used more insulin for treating diabetes (OR 2.20, 95% CI 1.40-3.45). Our data suggest that the risk of pancreatic cancer is moderately increased in patients with diabetes, especially those using insulin therapy. The risk is greatly increased for diabetic patients with chronic pancreatitis.

Targeting pancreatic expressed PAX genes for the treatment of diabetes mellitus and pancreatic neuroendocrine tumors.

Science.gov (United States)

Martin-Montalvo, Alejandro; Lorenzo, Petra I; López-Noriega, Livia; Gauthier, Benoit R

2017-01-01

Four members of the PAX family, PAX2, PAX4, PAX6 and PAX8 are known to be expressed in the pancreas. Accumulated evidences indicate that several pancreatic expressed PAX genes play a significant role in pancreatic development/functionality and alterations in these genes are involved in the pathogenesis of pancreatic diseases. Areas covered: In this review, we summarize the ongoing research related to pancreatic PAX genes in diabetes mellitus and pancreatic neuroendocrine tumors. We dissect the current knowledge at different levels; from mechanistic studies in cell lines performed to understand the molecular processes controlled by pancreatic PAX genes, to in vivo studies using rodent models that over-express or lack specific PAX genes. Finally, we describe human studies associating variants on pancreatic-expressed PAX genes with pancreatic diseases. Expert opinion: Based on the current literature, we propose that future interventions to treat pancreatic neuroendocrine tumors and diabetes mellitus could be developed via the modulation of PAX4 and/or PAX6 regulated pathways.

Stem cell-based approach in diabetes and pancreatic cancer management

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Yi-Zhou Jiang

2017-01-01

Full Text Available Stem cell-mediated therapy is a promising strategy for treating pancreatic diseases such as Type-1 diabetes (T1D and pancreatic cancers. Although islet transplantation has been reported to be an effective diabetes therapy, its worldwide application is extremely limited due to the shortage of donor islets and immune rejection problems. Stem cell-based approach for islet neogenesis in vivo could provide a promising alternative source of islets for treating diabetes. On the other hand, targeting the cancer stem cells could be very effective for the treatment of pancreatic cancers. In this review, we focused on the present progress in the field of adult pancreatic stem cells, stem cell-mediated strategies for treating T1D, and pancreatic cancer stem cells, while discussing of the possible challenges involved in them.

Corelation among clinical, biochemical and tomographic criteria in order to evaluate the severity in acute pancreatitis Correlación entre criterios clínicos, bioquímicos y tomográficos para evaluar la gravedad de la pancreatitis aguda

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L. A. Lujano-Nicolás

2010-06-01

-two point nine per cent of the patients had less than 3 Ranson criteria of which 57.6% got D or E degree. Fifty-seven per cent of the patients with hematocrit value lower than 44% got D and E Balthazar degree, and 64.2% of the patients with hematocrit above 44% got D and E degree. The Pearson correlation (PC for APACHE-II and Ranson p = 0.013 of 0.476 PC for APACHE-II and Balthazar p = 0.367 of 0.476 and Spearman´s correlation p = 0.460 PC for APACHE-II and hematocrit p = 1.32 of 0.476. Conclusions: there does not exist a good correlation between the seriousness scale of Ranson and APACHE-II with the tomographic Balthazar degrees, therefore it is more likely to find very ill patients with an A or B Balthazar and on the other hand patients with acute low pancreatitis with a D or E Balthazar.Antecedentes: la pancreatitis aguda es un proceso inflamatorio que puede involucrar tejido peripancreático y órganos distantes. En 10 a 20% de los pacientes la enfermedad es severa, según criterios de Atlanta. En la actualidad existen diferentes escalas clínicas y bioquímicas de severidad como la de Ranson, APACHE-II (Acute Physiology and Chronic Health Evaluation y hematocrito, las cuales tienen discrepancias al compararlas con escalas tomográficas como la de Balthazar. Existen pocos estudios que correlacionen estos parámetros. Objetivo: evaluar el grado de severidad de la pancreatitis aguda según criterios de Ranson, APACHE-II y hematocrito sérico al ingreso y correlacionar estas escalas con las complicaciones locales pancreáticas según la clasificación de Balthazar. Pacientes y método: estudio retrospectivo, observacional y analítico. Se incluyeron pacientes mayores de 18 años de cualquier género, con diagnóstico de pancreatitis aguda de cualquier etiología, a los que se les realizó tomografía abdominal 72 horas posterior al inicio del cuadro clínico para estadificar el daño pancreático. El diagnóstico de pancreatitis aguda se estableció con 2 de 3 de los

Defects in α-Cell Function in Patients With Diabetes Due to Chronic Pancreatitis Compared With Patients With Type 2 Diabetes and Healthy Individuals.

Science.gov (United States)

Mumme, Lena; Breuer, Thomas G K; Rohrer, Stephan; Schenker, Nina; Menge, Björn A; Holst, Jens J; Nauck, Michael A; Meier, Juris J

2017-10-01

Diabetes frequently develops in patients with chronic pancreatitis. We examined the alterations in the glucagon response to hypoglycemia and to oral glucose administration in patients with diabetes due to chronic pancreatitis. Ten patients with diabetes secondary to chronic pancreatitis were compared with 13 patients with type 2 diabetes and 10 healthy control subjects. A stepwise hypoglycemic clamp and an oral glucose tolerance test (OGTT) were performed. Glucose levels during the OGTT were higher in patients with diabetes and chronic pancreatitis and lower in control subjects ( P chronic pancreatitis and with type 2 diabetes ( P chronic pancreatitis. α-Cell responses to oral glucose ingestion and to hypoglycemia are disturbed in patients with diabetes and chronic pancreatitis and in patients with type 2 diabetes. The similarities between these defects suggest a common etiology. © 2017 by the American Diabetes Association.

INSUFICIENCIA RENAL AGUDA CON UREMIA NORMAL EN PACIENTE MONO-RENO SECUNDARIA A PIELONEFRITIS AGUDA

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Musso CG

2006-03-01

Full Text Available RESUMEN:La insuficiencia renal aguda es un sindrome que característicamente cursa con niveles plasmáticos elevados de urea y creatinina. Sin embargo, hay situaciones clínicas en las cuales este sindrome puede cursar con un incremento de la creatininemia sin presentar elevación de la uremia.En este reporte presentamos un caso clínico de una insuficiencia renal aguda con uremia normal secundaria a una pielonefritis aguda en un paciente con riñón único. El paciente presentaba una elevada excreción fraccional de urea lo cual podía explicar su uremia normal pese a estar cursando una caída del filtrado gomerular. Dicha excreción de urea elevada fue interpretada como secundaria a una diabetes insipida nefrogénica y una alteración en el recirculado intra-renal de la urea ambos producto de la pielonefritis aguda. Concluimos que la pielonefritis aguda en un paciente mono-reno puede presentarse con un patrón de insuficiencia renal aguda con uremia normal. SUMMARYAcute renal failure is a syndrome that usually runs with an increase in creatinine and urea plasma levels. However, there are clinical situations in which this syndrome may run with an increase in plasma creatinine keeping normal the urea one.In this report we present a case of acute renal failure with normal plasma urea level secondary to an acute pyelonephritis in a single kidney patient. The patient had an increased fractional excretion of urea which could explain the normal plasma urea levels found despite of his reduced glomerular filtration. This increased urea excretion state was interpreted as a consequence of the nephrogenic diabetes insipidus and alteration of the intra-renal urea reciclying process that the acute pyelonephritis induced. In conclusion: Acute pyelonephritis in a single kidney patient can appear as a pattern of acute renal failure with normal plasma urea levels.

INSUFICIENCIA RENAL AGUDA CON UREMIA NORMAL EN PACIENTE MONO-RENO SECUNDARIA A PIELONEFRITIS AGUDA

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Musso CG

2007-04-01

Full Text Available RESUMENLa insuficiencia renal aguda es un sindrome que característicamente cursa con niveles plasmáticos elevados de urea y creatinina. Sin embargo, hay situaciones clínicas en las cuales este sindrome puede cursar con un incremento de la creatininemia sin presentar elevación de la uremia. En este reporte presentamos un caso clínico de una insuficiencia renal aguda con uremia normal secundaria a una pielonefritis aguda en un paciente con riñón único. El paciente presentaba una elevada excreción fraccional de urea lo cual podía explicar su uremia normal pese a estar cursando una caída del filtrado gomerular. Dicha excreción de urea elevada fue interpretada como secundaria a una diabetes insipida nefrogénica y una alteración en el recirculado intra-renal de la urea ambos producto de la pielonefritis aguda. Concluimos que la pielonefritis aguda en un paciente mono-reno puede presentarse con un patrón de insuficiencia renal aguda con uremia normal.SUMMARYAcute renal failure is a syndrome that usually runs with an increase in creatinine and urea plasma levels. However, there are clinical situations in which this syndrome may run with an increase in plasma creatinine keeping normal the urea one. In this report we present a case of acute renal failure with normal plasma urea level secondary to an acute pyelonephritis in a single kidney patient. The patient had an increased fractional excretion of urea which could explain the normal plasma urea levels found despite of his reduced glomerular filtration. This increased urea excretion state was interpreted as a consequence of the nephrogenic diabetes insipidus and alteration of the intra-renal urea reciclying process that the acute pyelonephritis induced. In conclusion: Acute pyelonephritis in a single kidney patient can appear as a pattern of acute renal failure with normal plasma urea levels.

Exocrine pancreatic insufficiency in diabetic patients: prevalence, mechanisms, and treatment.

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Piciucchi, Matteo; Capurso, Gabriele; Archibugi, Livia; Delle Fave, Martina Maria; Capasso, Marina; Delle Fave, Gianfranco

2015-01-01

Pancreas is a doubled-entity organ, with both an exocrine and an endocrine component, reciprocally interacting in a composed system whose function is relevant for digestion, absorption, and homeostasis of nutrients. Thus, it is not surprising that disorders of the exocrine pancreas also affect the endocrine system and vice versa. It is well-known that patients with chronic pancreatitis develop a peculiar form of diabetes (type III), caused by destruction and fibrotic injury of islet cells. However, less is known on the influence of diabetes on pancreatic exocrine function. Pancreatic exocrine insufficiency (PEI) has been reported to be common in diabetics, with a prevalence widely ranging, in different studies, in both type I (25-74%) and type II (28-54%) diabetes. A long disease duration, high insulin requirement, and poor glycemic control seem to be risk factors for PEI occurrence. The impact of pancreatic exocrine replacement therapy on glycemic, insulin, and incretins profiles has not been fully elucidated. The present paper is aimed at reviewing published studies investigating the prevalence of PEI in diabetic patients and factors associated with its occurrence.

Malformación arteriovenosa pancreática como causa de pancreatitis aguda tratada por vía endovascular

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Kohan, Gustavo; Provenzano, Matías; Rosado, Martín; Farfan, Grisel; Sánchez, Nicolás; Fastman, Denise

2017-01-01

La malformación arterio-venosa (MAV) en el páncreas es una anomalía anatómica poco frecuente que puede ser causa de pancreatitis aguda. Presentamos el caso de un paciente de 46 años cuyo diagnóstico se sospechó por los hallazgos de la tomografía computarizada con contraste endovenoso y por resonancia magnética y se confirmó mediante una arteriografía del tronco celíaco y de la arteria mesentérica superior. El tratamiento recibido fue por vía endovascular, aunque la otra opción válida para el ...

Pancreatitis, genes y autotrasplante de islotes: actualizaciones y nuevos horizontes

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Rivera Rivera, Edgardo D

2017-01-01

La pancreatitis es una inflamación del páncreas que puede progresar de una presentación aguda, a una presentación aguda recurrente y eventualmente a pancreatitis crónica, caracterizada por cambios morfológicos y formación de cicatriz los cuales son irreversibles. La entidad conocida como pancreatitis hereditaria ha sido reconocida en la literatura por años y ciertamente el hallazgo del gen PRSS1 en 1996 marcó el inicio de una era de descubrimientos genéticos asociados a dicha enfermedad. Desd...

Exocrine Pancreatic Insufficiency in Diabetic Patients: Prevalence, Mechanisms, and Treatment

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Matteo Piciucchi

2015-01-01

Full Text Available Pancreas is a doubled-entity organ, with both an exocrine and an endocrine component, reciprocally interacting in a composed system whose function is relevant for digestion, absorption, and homeostasis of nutrients. Thus, it is not surprising that disorders of the exocrine pancreas also affect the endocrine system and vice versa. It is well-known that patients with chronic pancreatitis develop a peculiar form of diabetes (type III, caused by destruction and fibrotic injury of islet cells. However, less is known on the influence of diabetes on pancreatic exocrine function. Pancreatic exocrine insufficiency (PEI has been reported to be common in diabetics, with a prevalence widely ranging, in different studies, in both type I (25–74% and type II (28–54% diabetes. A long disease duration, high insulin requirement, and poor glycemic control seem to be risk factors for PEI occurrence. The impact of pancreatic exocrine replacement therapy on glycemic, insulin, and incretins profiles has not been fully elucidated. The present paper is aimed at reviewing published studies investigating the prevalence of PEI in diabetic patients and factors associated with its occurrence.

Detection, Evaluation and Treatment of Diabetes Mellitus in Chronic Pancreatitis: Recommendations from PancreasFest 2012

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Rickels, Michael R.; Bellin, Melena; Toledo, Frederico G.S.; Robertson, R. Paul; Andersen, Dana K.; Chari, Suresh T.; Brand, Randall; Frulloni, Luca; Anderson, Michelle A.; Whitcomb, David C.

2013-01-01

Description Diabetes and glucose intolerance are common complications of chronic pancreatitis, yet clinical guidance on their detection, classification, and management is lacking. Methods A working group reviewed the medical problems, diagnostic methods, and treatment options for chronic pancreatitis-associated diabetes for a consensus meeting at PancreasFest 2012. Results Guidance Statement 1.1 Diabetes mellitus is common in chronic pancreatitis. While any patient with chronic pancreatitis should be monitored for development of diabetes, those with long-standing duration of disease, prior partial pancreatectomy, and early onset of calcific disease may be at higher risk. Those patients developing diabetes mellitus are likely to have co-existing pancreatic exocrine insufficiency. Guidance Statement 1.2 Diabetes occurring secondary to chronic pancreatitis should be recognized as pancreatogenic diabetes (type 3c diabetes). Guidance Statement 2.1 The initial evaluation should include fasting glucose and HbA1c. These tests should be repeated annually. Impairment in either fasting glucose or HbA1c requires further evaluation. Guidance Statement 2.2 Impairment in either fasting glucose or HbA1c should be further evaluated by a standard 75 gram oral glucose tolerance test. Guidance Statement 2.3 An absent pancreatic polypeptide response to mixed-nutrient ingestion is a specific indicator of type 3c diabetes. Guidance Statement 2.4 Assessment of pancreatic endocrine reserve, and importantly that of functional beta-cell mass, should be performed as part of the evaluation and follow-up for total pancreatectomy with islet autotransplantation (TPIAT). Guidance Statement 3 Patients with pancreatic diabetes shall be treated with specifically tailored medical nutrition and pharmacologic therapies. Conclusions Physicians should evaluate and treat glucose intolerance in patients with pancreatitis. PMID:23890130

Defects in α-Cell Function in Patients With Diabetes Due to Chronic Pancreatitis Compared With Patients With Type 2 Diabetes and Healthy Individuals

DEFF Research Database (Denmark)

Mumme, Lena; Breuer, Thomas G K; Rohrer, Stephan

2017-01-01

.0002) but not in patients with chronic pancreatitis. CONCLUSIONS: α-Cell responses to oral glucose ingestion and to hypoglycemia are disturbed in patients with diabetes and chronic pancreatitis and in patients with type 2 diabetes. The similarities between these defects suggest a common etiology.......OBJECTIVE: Diabetes frequently develops in patients with chronic pancreatitis. We examined the alterations in the glucagon response to hypoglycemia and to oral glucose administration in patients with diabetes due to chronic pancreatitis. RESEARCH DESIGN AND METHODS: Ten patients with diabetes...... secondary to chronic pancreatitis were compared with 13 patients with type 2 diabetes and 10 healthy control subjects. A stepwise hypoglycemic clamp and an oral glucose tolerance test (OGTT) were performed. RESULTS: Glucose levels during the OGTT were higher in patients with diabetes and chronic...

Colangiopancreatografía magnética: valor diagnóstico para detectar coledocolitiasis en pacientes con pancreatitis aguda leve

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Geanny Mogollón Reyes

Full Text Available Introducción: la pancreatitis aguda (PA es una enfermedad clínica común que puede ser desde leve hasta fatal. En el 40 % de los casos es de origen biliar, y es causada por una obstrucción de la ampolla de Váter por barro biliar o por cálculos. En el diagnóstico de la pancreatitis aguda de origen biliar (PAB se emplean métodos invasivos como la colangiopancreatografía endoscópica retrógrada (CPRE, la cual se asocia a morbilidad y mortalidad, y métodos no invasivos como la colangiopancreatografía magnética (CRM, que emerge como modalidad diagnóstica en los centros de tercer y cuarto nivel de complejidad. Métodos: se evaluaron las características diagnósticas de la CRM a través de los registros históricos de pacientes que ingresaron a un hospital universitario de nivel IV a los que se les realizó CRM y CPRE. Esta última fue considerada el método de referencia para la evaluación. Resultados: Para la CRM se determinó una sensibilidad del 97 % y una especificidad del 44 % para la detección de coledocolitiasis, con un valor predictivo positivo de 0,35 y un valor predictivo negativo de 0,99. Algunos de estos resultados son inferiores a los documentados en la bibliografía mundial. Conclusiones: la CRM permite obtener imágenes precisas de la vía biliar, en un ambiente seguro y sin riesgos para el paciente. Esta técnica tiene una capacidad de detección de coledocolitiasis que oscila entre el 78 y el 97 %, resultado que concuerda con lo descrito en otros estudios.

Diabetes mellitus and exocrine pancreatic insufficiency (review of literature

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L.T. Daminova

2018-02-01

Full Text Available Currently, an increasing importance is given to the study of the problem of exocrine pancreatic insufficiency, which is observed in a significant number of patients with diabetes mellitus (DM type 1 and 2 and can potentially affect the compensation of DM. The mechanism of reducing the external secretion of the pancreas in DM is associated with an imbalance of inhibitory and stimulating pancreatic secretion of hormones, with fibrosis of the gland as a result of diabetic angiopathy. In type 2 DM, the mechanisms that result from the metabolic syndrome are involved in the pathogenesis of exocrine pancreatic insufficiency. Enzyme replacement the­rapy should be considered as one of the promising methods of treating DM patients.

Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes

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Jinzi Wu

2017-09-01

Full Text Available It is well established that NADH/NAD+ redox balance is heavily perturbed in diabetes, and the NADH/NAD+ redox imbalance is a major source of oxidative stress in diabetic tissues. In mitochondria, complex I is the only site for NADH oxidation and NAD+ regeneration and is also a major site for production of mitochondrial reactive oxygen species (ROS. Yet how complex I responds to the NADH/NAD+ redox imbalance and any potential consequences of such response in diabetic pancreas have not been investigated. We report here that pancreatic mitochondrial complex I showed aberrant hyperactivity in either type 1 or type 2 diabetes. Further studies focusing on streptozotocin (STZ-induced diabetes indicate that complex I hyperactivity could be attenuated by metformin. Moreover, complex I hyperactivity was accompanied by increased activities of complexes II to IV, but not complex V, suggesting that overflow of NADH via complex I in diabetes could be diverted to ROS production. Indeed in diabetic pancreas, ROS production and oxidative stress increased and mitochondrial ATP production decreased, which can be attributed to impaired pancreatic mitochondrial membrane potential that is responsible for increased cell death. Additionally, cellular defense systems such as glucose 6-phosphate dehydrogenase, sirtuin 3, and NQO1 were found to be compromised in diabetic pancreas. Our findings point to the direction that complex I aberrant hyperactivity in pancreas could be a major source of oxidative stress and β cell failure in diabetes. Therefore, inhibiting pancreatic complex I hyperactivity and attenuating its ROS production by various means in diabetes might serve as a promising approach for anti-diabetic therapies.

Gestational diabetes as a risk factor for pancreatic cancer: a prospective cohort study

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Calderon R

2007-08-01

Full Text Available Abstract Background Diabetes is known to be associated with cancer of the pancreas, though there is some debate as to whether it is a cause or a consequence of the disease. We investigated the incidence of pancreatic cancer in a cohort of 37926 Israeli women followed for 28–40 years for whom information on diabetes had been collected at the time they gave birth, in 1964–1976, in Jerusalem. There were 54 cases of pancreatic cancer ascertained from the Israel Cancer Registry during follow-up. Methods We used Cox proportional hazards models to adjust for age at baseline and explore effects of other risk factors, including ethnic groups, preeclampsia, birth order and birth weight of offspring. Results We observed no cases of pancreatic cancer in the women with insulin dependent diabetes; however, there were five cases in the women with gestational diabetes. The interval between the record of diabetes in pregnancy and the diagnosis of pancreatic cancer ranged from 14–35 years. Women with a history of gestational diabetes showed a relative risk of pancreatic cancer of 7.1 (95% confidence interval, 2.8–18.0. Conclusion We conclude that gestational diabetes is strongly related to the risk of cancer of the pancreas in women in this population, and that gestational diabetes can precede cancer diagnosis by many years.

Pancreatic adenocarcinoma, chronic pancreatitis, and MODY-8 diabetes: is bile salt-dependent lipase (or carboxyl ester lipase) at the crossroads of pancreatic pathologies?

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Lombardo, Dominique; Silvy, Françoise; Crenon, Isabelle; Martinez, Emmanuelle; Collignon, Aurélie; Beraud, Evelyne; Mas, Eric

2018-02-23

Pancreatic adenocarcinomas and diabetes mellitus are responsible for the deaths of around two million people each year worldwide. Patients with chronic pancreatitis do not die directly of this disease, except where the pathology is hereditary. Much current literature supports the involvement of bile salt-dependent lipase (BSDL), also known as carboxyl ester lipase (CEL), in the pathophysiology of these pancreatic diseases. The purpose of this review is to shed light on connections between chronic pancreatitis, diabetes, and pancreatic adenocarcinomas by gaining an insight into BSDL and its variants. This enzyme is normally secreted by the exocrine pancreas, and is diverted within the intestinal lumen to participate in the hydrolysis of dietary lipids. However, BSDL is also expressed by other cells and tissues, where it participates in lipid homeostasis. Variants of BSDL resulting from germline and/or somatic mutations (nucleotide insertion/deletion or nonallelic homologous recombination) are expressed in the pancreas of patients with pancreatic pathologies such as chronic pancreatitis, MODY-8, and pancreatic adenocarcinomas. We discuss the possible link between the expression of BSDL variants and these dramatic pancreatic pathologies, putting forward the suggestion that BSDL and its variants are implicated in the cell lipid metabolism/reprogramming that leads to the dyslipidemia observed in chronic pancreatitis, MODY-8, and pancreatic adenocarcinomas. We also propose potential strategies for translation to therapeutic applications.

Diabetes insipidus como manifestação inicial de leucemia mieloide aguda em paciente com monossomia do cromossomo 7

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Amanda Dias Lima Morais

2017-04-01

Full Text Available O diabetes insipidus (DI central é uma síndrome caracterizada pela incapacidade de concentração urinária devido à deficiência do hormônio antidiurético. O envolvimento do sistema nervoso central é frequente nas leucemias, mas a ocorrência de DI é rara e confere pior prognóstico. A patogênese do DI na leucemia não é totalmente conhecida, mas a infiltração do eixo hipotálamo-hipofisário por células leucêmicas parece ser um fator responsável. O presente relato descreve o caso de um paciente que apresentou DI como primeira manifestação de leucemia mieloide aguda e que evoluiu com dificuldades de ajustes do sódio sérico, da poliúria e da reposição volêmica, necessitando de permanência prolongada em unidade de cuidados intensivos. Palavras-chave: diabetes insipidus; leucemia mieloide aguda; monossomia; cromossomo 7.

Diabetes Mellitus Secondary to Acute Pancreatitis in a Child with Wolf-Hirschhorn Syndrome

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Asma Deeb

2017-01-01

Full Text Available Wolf-Hirschhorn Syndrome (WHS is a rare genetic disease caused by deletion in the short arm of chromosome 4. It is characterized by typical fascial features and a varying degree of intellectual disabilities and multiple systemic involvement. Epidemiological studies confirmed the association of acute pancreatitis with the development of diabetes. However, this association has not been reported in WHS. We report an 18-year-old girl with WHS who presented acutely with nonketotic Hyperglycemic Hyperosmolar Status (HHS in association with severe acute pancreatitis. Her presentation was preceded by febrile illness with preauricular abscess. She was treated with fluids and insulin infusion and remained on insulin 18 months after presentation. Her parents are cousins and the mother was diagnosed with type 2 diabetes. She had negative autoantibodies and no signs of insulin resistance and her monogenic diabetes genetic testing was negative. Microarray study using WHS probe confirmed deletion of 4p chromosome. Acute pancreatitis is uncommon in children and development of diabetes following pancreatitis has not been reported in WHS. HHS is considerably less frequent than diabetes ketoacidosis in children. We highlight the complex presentation with HHS and acute pancreatitis leading to diabetes that required long term of insulin treatment.

Distribution of Pancreatic Polypeptide-secreting Endocrine Cells in Nondiabetic and Diabetic Cases.

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Śliwińska-Mossoń, Mariola; Milnerowicz, Halina

2017-07-01

The aim of the study was to demonstrate the effects of cigarette smoking and ongoing inflammation in chronic pancreatitis on the functioning of pancreatic polypeptide (PP)-secreting cells and to determine the relationship between the occurrence of an increased number of PP cells in the pancreas, the change in their location, and the intensity of their inflammatory changes in the course of pancreatitis and diabetes. Samples of tissues from healthy persons and from patients were verified histopathologically, and then PP was localized by immunohistochemical staining using the monoclonal anti-human PP antibody. The histopathologic evaluation of the hormone expression intensity in tissue sections was carried out using the semiquantitative method and was calculated with digital image analysis. The present study showed a very strong PP expression in the pancreatic tissue (especially in the head of the pancreas) derived from smoking patients with diabetes. The increase in the percentage of cells in the PP islets, between the acinar cells in smoking patients with diabetes and a statistically significant increase in the expression of PP, indicates a pancreatic endocrine dysfunction and suggests that cigarette smoking has a negative impact on the organ's efficiency. Because of its properties, the PP appears to be a useful marker of the endocrine insufficiency of the pancreas and a specific prognostic parameter of developing diabetes due to chronic pancreatitis.

Pancreatic exocrine insufficiency, diabetes mellitus and serum nutritional markers after acute pancreatitis.

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Vujasinovic, Miroslav; Tepes, Bojan; Makuc, Jana; Rudolf, Sasa; Zaletel, Jelka; Vidmar, Tjasa; Seruga, Maja; Birsa, Bostjan

2014-12-28

To investigate impairment and clinical significance of exocrine and endocrine pancreatic function in patients after acute pancreatitis (AP). Patients with AP were invited to participate in the study. Severity of AP was determined by the Atlanta classification and definitions revised in 2012. Pancreatic exocrine insufficiency (PEI) was diagnosed by the concentration of fecal elastase-1. An additional work-up, including laboratory testing of serum nutritional markers for determination of malnutrition, was offered to all patients with low levels of fecal elastase-1 FE. Hemoglobin A1c or oral glucose tolerance tests were also performed in patients without prior diabetes mellitus, and type 3c diabetes mellitus (T3cDM) was diagnosed according to American Diabetes Association criteria. One hundred patients were included in the study: 75% (75/100) of patients had one attack of AP and 25% (25/100) had two or more attacks. The most common etiology was alcohol. Mild, moderately severe and severe AP were present in 67, 15 and 18% of patients, respectively. The mean time from attack of AP to inclusion in the study was 2.7 years. PEI was diagnosed in 21% (21/100) of patients and T3cDM in 14% (14/100) of patients. In all patients with PEI, at least one serologic nutritional marker was below the lower limit of normal. T3cDM was more frequently present in patients with severe AP (P = 0.031), but was also present in some patients with mild and moderately severe AP. PEI was present in all degrees of severity of AP. There were no statistically significantly differences according to gender, etiology and number of AP attacks. As exocrine and endocrine pancreatic insufficiency can develop after AP, routine follow-up of patients is necessary, for which serum nutritional panel measurements can be useful.

Severe hypertriglyceridemia in diabetic ketoacidosis accompanied by acute pancreatitis: case report.

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Hahn, Suk Jae; Park, Jung-hyun; Lee, Jong Ho; Lee, Jun Kyu; Kim, Kyoung-Ah

2010-09-01

We report a case of diabetic ketoacidosis (DKA) and hypertriglyceridemia (severely elevated to 15,240 mg/dL) complicated by acute pancreatitis, which was treated successfully with insulin therapy and conservative management. A 20-yr-old woman with a history of type 1 diabetes came to the emergency department 7 months after discontinuing insulin therapy. DKA, severe hypertriglyceridemia and acute pancreatitis were diagnosed, with DKA suspected of contributing to the development of the other conditions. In Korea, two cases of DKA-induced hypertriglyceridemia and 13 cases of hypertriglyceridemia-induced acute pancreatitis have been previously reported separately.

[Delayed complications after pancreatic surgery: Pancreatic insufficiency, malabsorption syndrome, pancreoprivic diabetes mellitus and pseudocysts].

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Nitsche, U; Siveke, J; Friess, H; Kleeff, J

2015-06-01

Benign and malignant pathologies of the pancreas can result in a relevant chronic disease burden. This is aggravated by morbidities resulting from surgical resections as well as from progression of the underlying condition. The aim was to summarize the current evidence regarding epidemiology, pathophysiology, diagnosis and treatment of endocrine and exocrine pancreatic insufficiency, as well as of pancreatic pseudocysts. A selective literature search was performed and a summary of the currently available data on the surgical sequelae after pancreatic resection is given. Reduction of healthy pancreatic parenchyma down to 10-15 % leads to exocrine insufficiency with malabsorption and gastrointestinal complaints. Orally substituted pancreatic enzymes are the therapy of choice. Loss of pancreatic islets and/or islet function leads to endocrine insufficiency and pancreoprivic diabetes mellitus. Inflammatory, traumatic and iatrogenic injuries of the pancreas can lead to pancreatic pseudocysts, which require endoscopic, interventional or surgical drainage if symptomatic. Finally, pancreatic surgery harbors the long-term risk of gastrointestinal anastomotic ulcers, bile duct stenosis, portal vein thrombosis and chronic pain syndrome. As the evidence is limited, an interdisciplinary and individually tailored approach for delayed pancreatic morbidity is recommended.

Altered synthesis of some secretory proteins in pancreatic lobules isolated from streptozotocin-induced diabetic rats

International Nuclear Information System (INIS)

Duan, R.D.; Erlanson-Albertsson, C.

1990-01-01

The in vitro incorporation of [35S]cysteine into lipase, colipase, amylase, procarboxypeptidase A and B, and the serine proteases and total proteins was studied in pancreatic lobules isolated from normal and diabetic rats with or without insulin treatment. The incorporation of [35S]cysteine into total proteins was 65% greater in pancreatic lobules from diabetic animals than from normal rats. The increased incorporation was partly reversed by insulin treatment (2 U/100 g/day for 5 days) of diabetic rats. The relative rates of biosynthesis for amylase and the procarboxypeptidases in diabetic pancreatic lobules were decreased by 75 and 25%, respectively, after 1 h of incubation, while those for lipase, colipase, and the serine proteases were increased by 90, 85, and 35%, respectively. The absolute rates of synthesis for these enzymes changed in the same direction as the relative rates in diabetic lobules, except that for the procarboxypeptidases, which did not change. The changed rates of biosynthesis for the pancreatic enzymes were reversed by insulin treatment of the diabetic rats. Kinetic studies showed that the incorporation of [35S]cysteine into amylase, lipase, and colipase was linear until up to 2 h of incubation in normal pancreatic lobules, while in the diabetic lobules the incorporation into lipase and colipase was accelerated, reaching a plateau level already after 1 h of incubation. It is concluded that the biosynthesis of pancreatic secretory proteins in diabetic rats is greatly changed both in terms of quantity and kinetics

Severe Hypertriglyceridemia in Diabetic Ketoacidosis Accompanied by Acute Pancreatitis: Case Report

OpenAIRE

Hahn, Suk Jae; Park, Jung-hyun; Lee, Jong Ho; Lee, Jun Kyu; Kim, Kyoung-Ah

2010-01-01

We report a case of diabetic ketoacidosis (DKA) and hypertriglyceridemia (severely elevated to 15,240 mg/dL) complicated by acute pancreatitis, which was treated successfully with insulin therapy and conservative management. A 20-yr-old woman with a history of type 1 diabetes came to the emergency department 7 months after discontinuing insulin therapy. DKA, severe hypertriglyceridemia and acute pancreatitis were diagnosed, with DKA suspected of contributing to the development of the other co...

Pancreatitis Aguda en Pediatría

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Jaime Forero Gómez

1992-03-01

Full Text Available

Pancreatitis es el término utilizado para describir una inflamación del páncreas, cuya evolución clínica puede variar de síntomas crónicos leves durante años a deterioro rápido, progresivo y mortal en un lapso de pocas horas a días.(l

A diferencia de lo informado en la población adulta, la frecuencia de este padecimiento en edades Pediátricas no se conoce con precisión. Excluyendo a la pancreatitis causada por traumatismo abdominal, se presenta con una frecuencia cinco veces mayor en mujeres.(2

Por la localización del páncreas en la cavidad abdominal, es difícil efectuar una valoración clínica adecuada. Cuando el órgano se inflama, el proceso se manifiesta de diferentes maneras; en múltiples ocasiones en forma totalmente atípica, lo que origina que con frecuencia se diagnostique sólo en estudios post-mortem (2,3.

Frey y Redo confirman el diagnóstico por autopsia en 77% de sus casos. En lo concerniente a pancreatitis secundaria por medicamentos, Buntay y colaboradores (2 consideran la posibilidad de que no se diagnostique en vida en e133% de los casos; estos mismos autores, cuando se trata de pancreatitis por traumatismo abdominal, afirman que no se diagnostica en 25% de los casos. Consideramos conveniente, tomando en cuenta los factores anteriores, realizar una revisión del tema con el propósito de actualizar conocimientos y llamar la atención del Médico en general acerca de la importancia de este diagnóstico en los casos de dolor abdominal y de etiología desconocida, pues el diagnóstico oportuno ofrece un pronóstico con menor riesgo de complicaciones y muerte...

Nutrição na pancreatite aguda : monografia : Nutrition in acute pancreatitis

OpenAIRE

Oliveira, Joana da Silva

2009-01-01

Resumo da tese:A pancreatite aguda (PA) é uma doença inflamatória aguda do pâncreas de etiologia multifactorial e pode ter atingimento local (PA ligeira a moderada) ou sistémico (PA grave). A magnitude da lesão pancreática, a presença e extensão da necrose e de infecção determinam o grau de gravidade. Prever a gravidade é fundamental para direccionar antecipadamente a terapêutica médica e nutricional. Na sua maioria, os episódios de PA são ligeiros a moderados, de resolução espontânea, enquan...

Influencing factors for acute pancreatitis in patients with type 2 diabetes complicated by hypertriglyceridemia

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BAI Yunlei

2017-12-01

Full Text Available ObjectiveTo investigate the association between hypertriglyceridemia and acute pancreatitis in patients with type 2 diabetes, in order to guide the prevention and treatment of acute pancreatitis in patients with diabetes. MethodsA total of 46 patients with type 2 diabetes complicated by acute pancreatitis who were admitted to The First Hospital of Yulin from January 2013 to December 2016 were enrolled as study group, and 52 patients with type 2 diabetes alone who were admitted to our hospital within the same period of time were enrolled as control group. Related data were recorded, including age, sex, course of diabetes, body height and weight, abdominal circumference, smoking, drinking, gallstones, hypertension, blood glucose, and blood lipids ［total cholesterol (TC, triglyceride (TG, high-density lipoprotein cholesterol (HDL-C, and low-density lipoprotein cholesterol (LDL-C］. The incidence rates of complications associated with diabetes were analyzed. The chi-square test was used for comparison of categorical data (general status, blood lipids, and diabetic complications between two groups; and the t-test was used for comparison of such data between two groups. A logistic regression analysis was used for multivariate analysis. ResultsThere were no significant differences between the two groups in age, sex composition, body height and weight, abdominal circumference, smoking and drinking habits, hypertension, gallstones, and course of diabetes (all P＞005. The study group had significantly higher levels of TC, TG, and LDL-C than the control group (t=5.122, 4.127, and 3.524, P＜0.01, ＜0.01, and =0.012, while the control group had a significantly higher level of HDL-C than the study group (t=2.231, P=0.037. The study group had a significantly higher incidence rate of diabetic microangiopathy (diabetic retinopathy and chronic diabetic nephropathy than the control group (χ2=92.126, P＜0.01. The multivariate analysis showed that

Vitamin D and pancreas: The role of sunshine vitamin in the pathogenesis of diabetes mellitus and pancreatic cancer.

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Altieri, Barbara; Grant, William B; Della Casa, Silvia; Orio, Francesco; Pontecorvi, Alfredo; Colao, Annamaria; Sarno, Gerardo; Muscogiuri, Giovanna

2017-11-02

Increasing evidence suggests that vitamin D exerts multiple effects beyond bone and calcium metabolism. Vitamin D seems to play a role in pancreatic disease, including type 1 and type 2 diabetes mellitus as well as pancreatic cancer. Vitamin D's immune-modulatory action suggests that it could help prevent type 1 diabetes. In type 2 diabetes, vitamin D may influence β-cell function, insulin sensitivity, and systematic inflammation-all characteristic pathways of that disease. Data from observational studies correlated vitamin D deficiency with risk of type 1 and type 2 diabetes. Prospective and ecological studies of pancreatic cancer incidence generally support a beneficial effect of higher 25-hydroxyvitamin D concentration as well as inverse correlations between UVB dose or exposure and incidence and/or mortality rate of pancreatic cancer. This review discusses the literature regarding vitamin D's role in risk of diabetes and pancreatic cancer. The results to date generally satisfy Hill's criteria for causality regarding vitamin D and incidence of these pancreatic diseases. However, large randomized, blinded, prospective studies are required to more fully evaluate the potential therapeutic role of vitamin D in preventing pancreatic diseases.

Fatores preditivos de coledocolitíase em doentes com pancreatite aguda biliar Predictors of choledocholithiasis in patients sustaining acute biliary pancreatitis

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José Gustavo Parreira

2004-12-01

Full Text Available OBJETIVO: Avaliar o papel da fosfatase alcalina (FA, gama glutamiltransferase (gamaGT e ultra-sonografia (US como fatores preditivos de coledocolitíase em doentes com pancreatite aguda biliar (PAB. MÉTODOS: Os dados foram coletados prospectivamente durante um período de 31 meses. Quarenta doentes foram incluídos, sendo 30 mulheres, com média etária de 49 + 16 anos. Foram registrados os dados de todos os doentes com pancreatite aguda biliar. Aqueles doentes ictéricos e com a forma grave da doença foram excluídos. As dosagens de FA e GGT, assim como a US, eram realizadas na admissão e 48 horas antes da cirurgia. Todos os pacientes foram submetidos à colangiografia intra-operatória (CIO ou à colangiografia retrógrada endoscópica (CPRE pré-operatória, que era definida baseada na probabilidade de coledocolitíase. Com o intuito de identificar os indicadores de coledocolitíase, as variáveis foram comparadas entre os pacientes com ou sem coledocolitíase. Os testes t de Student, Qui-quadrado e Fisher foram empregados para a análise estatística, considerando-se pBACKGROUND: To assess the role of alkaline phosphatase (AP, gamil-glutamyltransferase (gammaGT and abdominal ultrasound (US as predictors of choledocholithiasis in patients sustaining acute biliary pancreatitis. METHODS: Data was prospectively collected during a period of 31 months. Forty patients were included, 30 were female and the mean age was 49 + 16. All patients sustaining acute biliary pancreatitis were enrolled. Patients with clinical jaundice and severe pancreatitis were excluded. Serum content of AP and gGT as well as US were assessed at admission and 48 hours before cholecistectomy. All patients underwent intra-operative cholangiography (IOC or pre-operative endoscopic retrograde cholangiography (ERCP, which was indicated based on the odds of choledocholithiasis. In order to identify the predictors of choledocholithiasis, variables were compared between patients

Treated of type 1 diabetes mellitus in non-obese diabetic mice by transplantation of allogeneic bone marrow and pancreatic tissue

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Yasumizu, R.; Sugiura, K.; Iwai, H.

1987-01-01

Non-obese diabetic (NOD) mice provide a model for type 1 diabetes mellitus. We previously showed that allogeneic bone marrow transplantation (ABMT) can prevent and treat insulitis and overt diabetes in NOD mice. However, ABMT alone could not be used to treat overt diabetes in NOD mice whose islets had been completely destroyed. To provide insulin-producing cells, pancreatic tissue from newborn mice was grafted under the renal capsules in combination with ABMT. The aims of concomitant ABMT are as follows. (i) It induces immunological tolerance to the donor-type major histocompatibility complex determinants and permits the host to accept subsequent pancreatic allografts from the bone marrow donor. (ii) ABMT replaces abnormal stem cells with normal stem cells. After transplantation of bone marrow plus newborn pancreas, NOD mice showed reduction of the glycosuria and a normal response in the glucose-tolerance test. Immunohistological study revealed the presence of clustered insulin-containing beta cells in the grafted pancreatic transplants. ABMT may become a viable treatment of established type 1 diabetes mellitus in humans

Management of a Dog with Poorly Regulated Diabetes Mellitus, Chronic Pancreatitis, and Suspected Atopy with Cyclosporine

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Jörg M. Steiner

2012-01-01

Full Text Available A 3-year-and-9-months old male neutered Bichon Frise was presented for a second opinion for diabetes mellitus, weight loss, pruritus, and loss of hair. During further work-up, the dog was diagnosed with uncontrolled diabetes mellitus and concurrent diagnoses of pancreatitis and atopy were also suspected. Multiple adjustments of insulin therapy did not improve control of diabetes mellitus. Also, a variety of different treatments failed to improve pruritus. The dog was seen by a veterinary dermatologist who further suspected atopy and started treatment with cyclosporine. Pruritus improved and coincidentally serum Spec cPL and fructosamine concentrations normalized after therapy, suggesting the possibility that cyclosporine may have controlled pancreatic inflammation and improved control of diabetes mellitus. This case report would suggest that further research into autoimmunity in dogs with chronic pancreatitis is warranted. Also, a controlled study is needed and in progress before the use of cyclosporine in dogs with chronic pancreatitis or a subgroup thereof can be advocated.

Features of medical tactics and its perioperative medications in acute pancreatitis of biliary etiology in diabetic patients

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S.I. Savoliuk

2017-03-01

Full Text Available The aim of the study was clinical and laboratory evaluation of the effectiveness of traditional and optimized therapeutic and diagnostic technologies in acute pancreatitis of biliary etiology in diabetic patients with diabetes mellitus. Materials and methods. The article analyzes the results of treatment of 122 diabetic patients with acute biliary pancreatitis. Laboratory analysis was conducted within the monitoring cytopathic hypoxia markers, depending on the morphological forms of acute pancreatitis and effectiveness of optimized and traditional standard therapy. Results. The results indicate that acute pancreatitis of biliary etiology in diabetic patients was accompanied by a consistent pattern of imbalance in the cytopathic hypoxia system, which is determined by the severity of the pancreatic morphological changes. Interstitial form was accompanied by high levels of carbonyl group by 30.7 %, 38.75 % for adenosine deaminase and decreased level of arginine to 18.05 %; localized pancreatic necrosis was characterized by increased endothelial dysfunction markers (nitrates and nitrites to 18.35 %, homocysteine 52 %; diffuse pancreatic necrosis was characterized by increased markers of stimulated catabolism of purine nucleotides (xanthine and hypoxanthine to 85.2 %; subtotal-total pancreatic necrosis — increased levels of relative enzymes (xanthine oxidase and xanthine dehydrogenase to 44.39 %. Pattern dynamics violations of cytopathic hypoxia markers allows use them as the predictors of functional liver failure and multiple organ failure in diabetic patients with necrotic forms of acute biliary pancreatitis. Conclusions. Standard treatment methods do not allow effectively correct cytopathic hypoxia, endotoxemia and hepatic failure. Proposed optimized complex of conservative therapy allow effectively and timely correction them, namely in the interstitial form on day 4, localized pancreatic necrosis on day 7, diffuse pancreatic necrosis on day 10

Early onset of organ failure is the best predictor of mortality in acute pancreatitis El fracaso orgánico precoz como mejor factor predictivo de mortalidad en la pancreatitis aguda

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I. Poves Prim

2004-10-01

Full Text Available Background: APACHE II is a multifactorial scoring system for predicting severity in acute pancreatitis (AP. Organ failure (OF has been correlated with mortality in AP. Objectives: to evaluate the usefulness of APACHE II as an early predictor of severity in AP, its correlation with OF, and the relevance of an early establishment of OF during the course of AP. Patients and methods: from January 1999 to November 2001, 447 consecutive cases of AP were studied. APACHE II scores and Atlanta criteria were used for defining severity and OF. Results: twenty-five percent of patients had severe acute pancreatitis (SAP. APACHE II at 24 h after admission showed a sensitivity, specificity, and positive and negative predictive value of 52, 77, 46, and 84%, respectively, for predicting severity. Mortality for SAP was 20.5%. Seventy percent of patients who developed OF did so within the first 24 hours of admission, and their mortality was 52%. Mortality was statistically significant (p Introducción: el APACHE II se ha utilizado como factor predictivo de gravedad en la pancratitis aguda (PA. La instauración de fracaso orgánico (FO en la PA se correlaciona con una mayor mortalidad. Objetivos: evaluar la utilidad del APACHE II como factor predictivo precoz de gravedad en la PA, su correlación con el FO y la relevancia del establecimiento precoz del FO en la PA. Pacientes y métodos: desde enero de 1999 hasta noviembre de 2001 se estudiaron 447 pacientes ingresados consecutivamente por PA. Se utilizó el sistema APACHE II y los criterios de Atlanta para evaluar la gravedad. Resultados: el 25% de los pacientes presentaron una pancreatitis aguda grave (PAG. El APACHE II a las 24 horas del ingreso mostró una sensibilidad, especificidad, valor predictivo positivo y negativo del 52, 77, 46 y 84%, respectivamente, como marcador de gravedad. La mortalidad global de la PAG fue del 20,5%. El 70% de los pacientes que presentaron FO lo hicieron en las primeras 24 horas

Proposed cut-off value of CA19-9 for detecting pancreatic cancer in patients with diabetes: a case-control study.

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Murakami, Mariko; Nagai, Yoshio; Tenjin, Ayumi; Tanaka, Yasushi

2018-04-11

Pancreatic cancer is a highly lethal malignancy. CA19-9 is a well-known marker for diagnosis of pancreatic cancer, but the serum CA19-9 level is reported to be elevated in patients with poorly controlled diabetes. This study evaluated the sensitivity, specificity, and cut-off value of serum CA19-9 for detection of pancreatic cancer in patients with diabetes. A case-control study of 236 patients was performed. The case group was selected from diabetic patients with pancreatic cancer, while one control was selected for each case from among diabetic patients without pancreatic cancer during the same period. The case group (n = 118) and the control group (n = 118) were matched for age, sex, and pancreatic cancer risk factors. Receiver operating characteristic (ROC) curves were plotted to determine the serum CA19-9 level that predicted pancreatic cancer. Then the sensitivity and specificity of CA19-9 were calculated for the threshold value. There were no significant differences of age, sex, BMI, smoking, alcohol intake, and HbA1c between the case and control groups. According to ROC analysis, a serum CA19-9 level of 75 U/mL had the maximum sensitivity and specificity for separating diabetic patients with or without pancreatic cancer. Using this cut-off value, the sensitivity and specificity of CA19-9 for pancreatic cancer was 69.5% and 98.2%, respectively, while the area under the ROC curve was 0.875 [95%CI: 0.826-0.924]. We propose that a serum CA19-9 level of 75 U/mL should be used as the cut-off value when screening patients with diabetes for pancreatic cancer.

Pancreatic Aquaporin-7: A Novel Target for Anti-diabetic Drugs?

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Méndez-Giménez, Leire; Ezquerro, Silvia; da Silva, Inês V; Soveral, Graça; Frühbeck, Gema; Rodríguez, Amaia

2018-01-01

Aquaporins comprise a family of 13 members of water channels (AQP0-12) that facilitate a rapid transport of water across cell membranes. In some cases, these pores are also permeated by small solutes, particularly glycerol, urea or nitric oxide, among other solutes. Several aquaporins have been identified in the pancreas, an exocrine and endocrine organ that plays an essential role in the onset of insulin resistance and type 2 diabetes. The exocrine pancreas, which accounts for 90% of the total pancreas, secretes daily large volumes of a near-isotonic fluid containing digestive enzymes into the duodenum. AQP1, AQP5, and AQP8 contribute to fluid secretion especially from ductal cells, whereas AQP12 allows the proper maturation and exocytosis of secretory granules in acinar cells of the exocrine pancreas. The endocrine pancreas (10% of the total pancreatic cells) is composed by the islets of Langerhans, which are distributed in α, β, δ, ε, and pancreatic polypeptide (PP) cells that secrete glucagon, insulin, somatostatin, ghrelin and PP, respectively. AQP7, an aquaglyceroporin permeated by water and glycerol, is expressed in pancreatic β-cells and murine studies have confirmed its participation in insulin secretion, triacylglycerol synthesis and proliferation of these endocrine cells. In this regard, transgenic AQP7-knockout mice develop adult-onset obesity, hyperinsulinemia, increased intracellular triacylglycerol content and reduced β-cell mass in Langerhans islets. Moreover, we have recently reported that AQP7 upregulation in β-cells after bariatric surgery, an effective weight loss surgical procedure, contributes, in part, to the improvement of pancreatic steatosis and insulin secretion through the increase of intracytoplasmic glycerol in obese rats. Human studies remain scarce and controversial, with some rare cases of loss-of function mutations of the AQP7 gene being associated with the onset of type 2 diabetes. The present Review is focused on the role

Pancreatic aquaporin-7: a novel target for anti-diabetic drugs?

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Méndez-Giménez, Leire; Ezquerro, Silvia; da Silva, Inês V.; Soveral, Graça; Frühbeck, Gema; Rodríguez, Amaia

2018-04-01

Aquaporins comprise a family of 13 members of water channels (AQP0-12) that facilitate a rapid transport of water across cell membranes. In some cases, these pores are also permeated by small solutes, particularly glycerol, urea or nitric oxide, among other solutes. Several aquaporins have been identified in the pancreas, an exocrine and endocrine organ that plays an essential role in the onset of insulin resistance and type 2 diabetes. The exocrine pancreas, which accounts for 90% of the total pancreas, secretes daily large volumes of a near-isotonic fluid containing digestive enzymes into the duodenum. AQP1, AQP5 and AQP8 contribute to fluid secretion especially from ductal cells, whereas AQP12 allows the proper maturation and exocytosis of secretory granules in acinar cells of the exocrine pancreas. The endocrine pancreas (10% of the total pancreatic cells) is composed by the islets of Langerhans, which are distributed in ,, ,  and pancreatic polypeptide (PP) cells that secrete glucagon, insulin, somatostatin, ghrelin and PP, respectively. AQP7, an aquaglyceroporin permeated by water and glycerol, is expressed in pancreatic -cells and murine studies have confirmed its participation in insulin secretion, triacylglycerol synthesis and proliferation of these endocrine cells. In this regard, transgenic AQP7-knockout mice develop adult-onset obesity, hyperinsulinemia, increased intracellular triacylglycerol content and reduced -cell mass in Langerhans islets. Moreover, we have recently reported that AQP7 upregulation in β-cells after bariatric surgery, an effective weight loss surgical procedure, contributes, in part, to the improvement of pancreatic steatosis and insulin secretion by increasing intracellular glycerol in obese rats. Human studies remain scarce and controversial, with some rare cases of loss-of function variants of the AQP7 gene being associated with the onset of type 2 diabetes. The present Review is focused on the role of

Pancreatic Aquaporin-7: A Novel Target for Anti-diabetic Drugs?

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Leire Méndez-Giménez

2018-04-01

Full Text Available Aquaporins comprise a family of 13 members of water channels (AQP0-12 that facilitate a rapid transport of water across cell membranes. In some cases, these pores are also permeated by small solutes, particularly glycerol, urea or nitric oxide, among other solutes. Several aquaporins have been identified in the pancreas, an exocrine and endocrine organ that plays an essential role in the onset of insulin resistance and type 2 diabetes. The exocrine pancreas, which accounts for 90% of the total pancreas, secretes daily large volumes of a near-isotonic fluid containing digestive enzymes into the duodenum. AQP1, AQP5, and AQP8 contribute to fluid secretion especially from ductal cells, whereas AQP12 allows the proper maturation and exocytosis of secretory granules in acinar cells of the exocrine pancreas. The endocrine pancreas (10% of the total pancreatic cells is composed by the islets of Langerhans, which are distributed in α, β, δ, ε, and pancreatic polypeptide (PP cells that secrete glucagon, insulin, somatostatin, ghrelin and PP, respectively. AQP7, an aquaglyceroporin permeated by water and glycerol, is expressed in pancreatic β-cells and murine studies have confirmed its participation in insulin secretion, triacylglycerol synthesis and proliferation of these endocrine cells. In this regard, transgenic AQP7-knockout mice develop adult-onset obesity, hyperinsulinemia, increased intracellular triacylglycerol content and reduced β-cell mass in Langerhans islets. Moreover, we have recently reported that AQP7 upregulation in β-cells after bariatric surgery, an effective weight loss surgical procedure, contributes, in part, to the improvement of pancreatic steatosis and insulin secretion through the increase of intracytoplasmic glycerol in obese rats. Human studies remain scarce and controversial, with some rare cases of loss-of function mutations of the AQP7 gene being associated with the onset of type 2 diabetes. The present Review is

Acute Pancreatitis and Diabetic Ketoacidosis following L-Asparaginase/Prednisone Therapy in Acute Lymphoblastic Leukemia

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Dania Lizet Quintanilla-Flores

2014-01-01

Full Text Available Acute pancreatitis and diabetic ketoacidosis are unusual adverse events following chemotherapy based on L-asparaginase and prednisone as support treatment for acute lymphoblastic leukemia. We present the case of a 16-year-old Hispanic male patient, in remission induction therapy for acute lymphoblastic leukemia on treatment with mitoxantrone, vincristine, prednisone, and L-asparaginase. He was hospitalized complaining of abdominal pain, nausea, and vomiting. Hyperglycemia, acidosis, ketonuria, low bicarbonate levels, hyperamylasemia, and hyperlipasemia were documented, and the diagnosis of diabetic ketoacidosis was made. Because of uncertainty of the additional diagnosis of acute pancreatitis as the cause of abdominal pain, a contrast-enhanced computed tomography was performed resulting in a Balthazar C pancreatitis classification.

Human embryonic stem cell-derived pancreatic endoderm alleviates diabetic pathology and improves reproductive outcome in C57BL/KsJ-Lep(db/+) gestational diabetes mellitus mice.

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Xing, Baoheng; Wang, Lili; Li, Qin; Cao, Yalei; Dong, Xiujuan; Liang, Jun; Wu, Xiaohua

2015-07-01

Gestational diabetes mellitus is a condition commonly encountered during mid to late pregnancy with pathologic manifestations including hyperglycemia, hyperinsulinemia, insulin resistance, and fetal maldevelopment. The cause of gestational diabetes mellitus can be attributed to both genetic and environmental factors, hence complicating its diagnosis and treatment. Pancreatic progenitors derived from human embryonic stem cells were shown to be able to effectively treat diabetes in mice. In this study, we have developed a system of treating diabetes using human embryonic stem cell-derived pancreatic endoderm in a mouse model of gestational diabetes mellitus. Human embryonic stem cells were differentiated in vitro into pancreatic endoderm, which were then transplanted into db/+ mice suffering from gestational diabetes mellitus. The transplant greatly improved glucose metabolism and reproductive outcome of the females compared with the control groups. Our findings support the feasibility of using differentiated human embryonic stem cells for treating gestational diabetes mellitus patients. Copyright © 2015 Elsevier Inc. All rights reserved.

Application of molecular imaging combined with genetic screening in diagnosing MELAS, diabetes and recurrent pancreatitis.

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Zhiping, W; Quwen, L; Hai, Z; Jian, Z; Peiyi, G

2016-01-01

We report molecular imaging combined with gene diagnosis in a family with 7 members who carried an A3243G mutation in mitochondrial tRNA and p.Thr 137 Met in cationic trypsinogen (PRSS1) gene presented with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS), diabetes, and recurrent pancreatitis. DNA sequencing was used to detect and validate mitochondrial DNA and PRSS1. We also verified that mitochondrial heterozygous mutations and c.410 C>T mutation causing p.Thr 137 Met could be detected in oral epithelial cells or in urine sediment cells. In addition, molecular imaging was carried out in the affected family members. In this pedigree, MELAS syndrome accompanied by pancreatitis was an important clinical feature, followed by diabetes. Heteroplasmy of the mtDNA A3243G and c.410 C>T mutation of PRSS1 was found in all tissue samples of these patients, but no mutations were found in 520 normal control and normal individuals of the family. However, based on molecular imaging observations, patients with relatively higher lactate/pyruvate levels had more typical and more severe symptoms, particularly those of pancreatic disease (diabetes or pancreatitis). MELAS syndrome may be associated with pancreatitis. For the diagnosis, it is more reasonable to perform molecular imaging combined with gene diagnosis.

Diabetes due to recurrent pancreatitis secondary to hypercalcemia due to primary hyperparathyroidism

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Sumit Kumar Chakrabarti

2013-01-01

Full Text Available Acute pancreatitis due to hypercalcemia associated with hyperparathyroidism (HPT is not very common. We herein report a case of a 21-year-old woman, who presented with acute pancreatitis. She had a past history of recurrent nephrolithiasis. Subsequent evaluation revealed hypercalcemia (serum calcium: 12.6 mg/dL; low phosphate (2.9 mg/dL with elevated parathyroid hormone (PTH, 156.7 pg/mL and HbA1c (6.9%. Diagnosis of primary HPT (PHPT was made. Recurrent pancreatitis due to hypercalcemia may have resulted in diabetes mellitus.

The Proteomic Analysis of Pancreatic Exocrine Insufficiency Protein Marker in Type 2 Diabetes Mellitus Patients

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Srihardyastutie, Arie; Soeatmadji, DW; Fatchiyah; Aulanni'am

2018-01-01

Type 2 Diabetes Mellitus (T2D) is the vast majority case of diabetes. Patient with T2D is at higher risk for developing acute or chronic pancreatitis. Prolonged hyperglycemia results in damages to tissue, which also causes dysfunctions of some organ systems, including enzyme or hormone secretions. Commonly, dysfunction or insufficiency of pancreatic exocrine is evaluated by increasing activity of serum pancreatic enzyme, such as amylase and lipase. Although incidence of pancreatitis was found in Indonesian T2D, the pathogenic mechanism still unclear. The aim of this study was to characterize the marker protein that indicated the correlation of pancreatic exocrine insufficiency with progression of T2D. Proteomic analysis using LC-MS/MS was used in identification and characterization of protein marker which indicates insufficiency pancreatic exocrine. First step, protein profile was analyzed by SDS-PAGE methods using serum sample of T2D compared with normal or healthy control, as negative control, and pancreatitis patients, as positive control. Protein with 18 kDa was found as a candidate protein marker which indicated the pancreatic exocrine insufficiency in T2D. The further identification of that protein using LC-MS/MS showed 4 peptide fragments. In silico analysis of the peptide fragment indicated the correlation of pancreatic exocrine insufficiency with progression of T2D was METTL10 - methyltransferase like protein-10.

[Identifying the severe acute pancreatitis].

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Acevedo Tizón, Anais; Targarona Modena, Javier; Málaga Rodríguez, Germán; Barreda Cevasco, Luis

2011-01-01

To compare patients with acute necrotizing pancreatitis without any additional complications during their hospital stay (Group A) versus patients with Acute Necrotizing Pancreatitis with additional complications during their hospital stay (Group B). Data obtained from a pre-existing base from hospitalized patients with diagnosis of acute necrotizing pancreatitis in the specialized unit of "Unidad de Pancreatitis Aguda Grave del Hospital Nacional Edgardo Rebagliati Martins" between 2000 and 2010. Data included patients with diagnosis of acute necrotizing pancreatitis, of ages 18 and over. Data from 215 patients with acute necrotizing pancreatitis was included. Patients from Group A represented 32% (68) and from Group B 68% (147). Group A had a average of 39 hospitalized days and Group B had an average of 56 days (p=0.01). From Group A 22% had more than 50% of necrosis while 43% of Group B had this extension of necrosis (p pancreatitis, based on the presence of necrosis, behave likewise. It is an extended necrosis, described as more than 50% of pancreatic necrosis, and not the presence itself which will determine additional complications during the course of disease and a greater mortality.

Transplantation of bone marrow derived cells promotes pancreatic islet repair in diabetic mice

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Gao Xiaodong; Song Lujun; Shen Kuntang; Wang Hongshan; Niu Weixin; Qin Xinyu

2008-01-01

The transplantation of bone marrow (BM) derived cells to initiate pancreatic regeneration is an attractive but as-yet unrealized strategy. Presently, BM derived cells from green fluorescent protein transgenic mice were transplanted into diabetic mice. Repair of diabetic islets was evidenced by reduction of hyperglycemia, increase in number of islets, and altered pancreatic histology. Cells in the pancreata of recipient mice co-expressed BrdU and insulin. Double staining revealed β cells were in the process of proliferation. BrdU + insulin - PDX-1 + cells, Ngn3 + cells and insulin + glucagon + cells, which showed stem cells, were also found during β-cell regeneration. The majority of transplanted cells were mobilized to the islet and ductal regions. In recipient pancreas, transplanted cells simultaneously expressed CD34 but did not express insulin, PDX-1, Ngn3, Nkx2.2, Nkx6.1, Pax4, Pax6, and CD45. It is concluded that BM derived cells especially CD34 + cells can promote repair of pancreatic islets. Moreover, both proliferation of β cells and differentiation of pancreatic stem cells contribute to the regeneration of β cells

Pancreatic biopsies in type 1 diabetes: revisiting the myth of Pandora's box.

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Atkinson, Mark A

2014-04-01

Over a century ago, inquisitive physicians made remarkable discoveries regarding pancreatic pathology in individuals with diabetes, including those who were likely afflicted with the type 1 (autoimmune) form of the disease. Those studies of post-mortem tissues noted unique anatomical changes in islet architecture as well as the presence of unusual cellular infiltrates. In the time since, investigations of pancreatic pathology have, with near uniformity, been restricted to analysis of organs obtained post-mortem. While clearly beneficial for addressing questions of the disorder's pathogenesis, concern exists regarding potential artefacts that might occur through analysis of tissues that have been recovered hours, often many hours, following death. Beyond this, studies of tissues obtained long after the diagnosis of type 1 diabetes may not disclose important physiological events occurring at onset or even earlier in the natural history of disease, before symptomatic hyperglycaemia. To this end, Krogvold and colleagues (in this issue of Diabetologia, doi: 10.1007/s00125-013-3155-y) undertook a potentially high-reward strategy involving pancreatic biopsy in living adults with recent-onset type 1 diabetes. Procedures were performed under informed consent, undertaken based on recent improvements in laparoscopic techniques, and carried out by individuals with considerable surgical experience. These efforts were terminated for ethical reasons following the occurrence of serious complications (including post-operative bleeding and pancreatic leakage). The experience lends itself to analogy with the Greek myth of Pandora's box where curiosity, in terms of a desire to see what resided inside a closed container, unleashed a series of ills on humans once the container was opened. In considering the moral of that myth, one must question whether the secrets of the pancreas in those living with type 1 diabetes should, for now, remain a mystery as the process of manipulating that

Broccoli (Brassica oleracea) Reduces Oxidative Damage to Pancreatic Tissue and Combats Hyperglycaemia in Diabetic Rats.

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Suresh, Sithara; Waly, Mostafa Ibrahim; Rahman, Mohammad Shafiur; Guizani, Nejib; Al-Kindi, Mohamed Abdullah Badar; Al-Issaei, Halima Khalfan Ahmed; Al-Maskari, Sultan Nasser Mohd; Al-Ruqaishi, Bader Rashid Said; Al-Salami, Ahmed

2017-12-01

Oxidative stress plays a pivotal role in the development of diabetes and hyperglycaemia. The protective effects of natural extracts against diabetes are mainly dependent on their antioxidant and hypoglycaemic properties. Broccoli ( Brassica oleracea ) exerts beneficial health effects in several diseases including diabetes; however, the mechanism has not been elucidated yet. The present study was carried out to evaluate the potential hypoglycaemic and antioxidant properties of aqueous broccoli extracts (BEs) in diabetic rats. Streptozotocin (STZ) drug was used as a diabetogenic agent in a single intraperitoneal injection dose of 50 mg/kg body weight. The blood glucose level for each rat was measured twice a week. After 8 weeks, all animals were fasted overnight and sacrificed; pancreatic tissues were homogenized and used for measuring oxidative DNA damage, biochemical assessment of glutathione (GSH), and total antioxidant capacity (TAC) as well as histopathological examination for pancreatic tissues was examined. Diabetic rats showed significantly higher levels of DNA damage, GSH depletion, and impaired TAC levels in comparison to non-diabetics ( P <0.05). The treatment of diabetic rats with BE significantly reduced DNA damage and conserved GSH and TAC values ( P <0.01). BE attenuated pancreatic histopathological changes in diabetic rats. The results of this study indicated that BE reduced the STZ mediated hyperglycaemia and the STZ-induced oxidative injury to pancreas tissue. The used in vivo model confirmed the efficacy of BE as an anti-diabetic herbal medicine and provided insights into the capacity of BE to be used for phytoremediation purposes for human type 2 diabetes.

A COMPREHENSIVE ANALYSIS DIABETES OF RISK FACTORS IN PATIENTS WITH CHRONIC PANCREATITIS

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M. A. Kunitsyna

2012-01-01

Full Text Available Aim – to perform comprehensive analysis of the risk factors of diabetes mellitus (DM in patients with chronic pancreatitis (CP. Materials and methods. All examined patients with chronic pancreatitis (CP were divided into 2 groups. The first group – 38 patients with the progression of the diabetes in the first 3 years of the CP, the second – 44 people with no diabetes after 10 years of disease. Formation of CP etiologic groups based on the mandatory presence of one of two factors: alcohol abuse, the presence of disease of biliary system. The combination of two etiological factors wasl exclusion criteria. Results and conclusion. Among the examined patients biliary form of CP occurred in 52 patients, alcohol – in 30 patients. It was found that in the first three years of CP risk of diabetes is not associated with family history, obesity, number of exacerbations, but in the form of alcoholic CP DM formed almost two times more often than in the biliary. When combined with CP in patients with diabetes were significantly more common strain of the main flow and structural changes in the tail of the pancreas.

Pancreatic fibrosis correlates with exocrine pancreatic insufficiency after pancreatoduodenectomy.

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Tran, T C K; van 't Hof, G; Kazemier, G; Hop, W C; Pek, C; van Toorenenbergen, A W; van Dekken, H; van Eijck, C H J

2008-01-01

Obstruction of the pancreatic duct can lead to pancreatic fibrosis. We investigated the correlation between the extent of pancreatic fibrosis and the postoperative exocrine and endocrine pancreatic function. Fifty-five patients who were treated for pancreatic and periampullary carcinoma and 19 patients with chronic pancreatitis were evaluated. Exocrine pancreatic function was evaluated by fecal elastase-1 test, while endocrine pancreatic function was assessed by plasma glucose level. The extent of fibrosis, duct dilation and endocrine tissue loss was examined histopathologically. A strong correlation was found between pancreatic fibrosis and elastase-1 level less than 100 microg/g (p pancreatic insufficiency. A strong correlation was found between pancreatic fibrosis and endocrine tissue loss (p pancreatic fibrosis nor endocrine tissue loss were correlated with the development of postoperative diabetes mellitus. Duct dilation alone was neither correlated with exocrine nor with endocrine function loss. The majority of patients develop severe exocrine pancreatic insufficiency after pancreatoduodenectomy. The extent of exocrine pancreatic insufficiency is strongly correlated with preoperative fibrosis. The loss of endocrine tissue does not correlate with postoperative diabetes mellitus. Preoperative dilation of the pancreatic duct per se does not predict exocrine or endocrine pancreatic insufficiency postoperatively. Copyright 2008 S. Karger AG, Basel.

Attenuation of endocrine-exocrine pancreatic communication in type 2 diabetes: pancreatic extracellular matrix ultrastructural abnormalities.

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Hayden, Melvin R; Patel, Kamlesh; Habibi, Javad; Gupta, Deepa; Tekwani, Seema S; Whaley-Connell, Adam; Sowers, James R

2008-01-01

Ultrastructural observations reveal a continuous interstitial matrix connection between the endocrine and exocrine pancreas, which is lost due to fibrosis in rodent models and humans with type 2 diabetes mellitus (T2DM). Widening of the islet-exocrine interface appears to result in loss of desmosomes and adherens junctions between islet and acinar cells and is associated with hypercellularity consisting of pericytes and inflammatory cells in T2DM pancreatic tissue. Organized fibrillar collagen was closely associated with pericytes, which are known to differentiate into myofibroblasts-pancreatic stellate cells. Of importance, some pericyte cellular processes traverse both the connecting islet-exocrine interface and the endoacinar interstitium of the exocrine pancreas. Loss of cellular paracrine communication and extracellular matrix remodeling fibrosis in young animal models and humans may result in a dysfunctional insulino-acinar-ductal-incretin gut hormone axis, resulting in pancreatic insufficiency and glucagon-like peptide deficiency, which are known to exist in prediabetes and overt T2DM in humans.

Teripang Pasir Meningkatkan Kandungan Antioksidan Superoksida Dismutase pada Pankreas Tikus Diabetes (SEA CUCUMBER INCREASED ANTIOXIDANT SUPEROXIDE DISMUTASE IN THE PANCREATIC TISSUE OF DIABETIC RATS

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Tutik Wresdiyati

2015-05-01

Full Text Available High level of blood glucose is an indicator for diabetes mellitus (DM condition. The condition iscaused by low level of insulin secretion or impairement of insulin receptor. The number of DM patientincreases every year. The World Health Organization reported that the number of DM patient in Indonesiawas the 4th highest in the world, after following China, India, and the United States of America, respectively.This study was conducted to analyze the effect of sea cucumber (Holothuria scabra J on the profile ofantioxidant copper, zinc-superoxide dismutase (Cu, Zn-SOD in the pancreatic tissues of diabetic rats. Atotal of 25 male white rats (Sprague Dawley were used in this study. They were divided into five groups;(1 negative control (KN, (2 positive control, diabetic rats (KP, (3 diabetic rats treated with hydrolyzatedprotein of sea cucumber (HDL, (4 diabetic rats treated with concentrated protein of sea cucumber (KST,and (5 diabetic rats treated with isolated protein of sea cucumber (ISL, respectively. Diabetic conditionwas obtained by alloxan injection 110 mg/kg bw. The treatments were done for 28 days. At the end oftreatment period, the rats were sacrificed and pancreatic tissues were collected and fixed in Bouin solution and then processed to paraffin embedding standard method. The tissues were then stained withimmunohistochemical staining techniques using monoclonal antibody of Cu, Zn-SOD. The results showedthat treatment of HDL, KST, and ISL of sea cucumber (Holothuria scabra J increased the content ofantioxidant Cu, Zn-SOD either in Langerhans islets and acinar cells of pancreatic tissues-diabetic rats.The HDL of sea cucumber treatment gave the best effect in increasing the antioxidant content of Cu, Zn-SOD in pancreatic tissue of diabetic rats.

Is Type-2 Diabetes a Glycogen Storage Disease of Pancreatic β-Cells?

Science.gov (United States)

Ashcroft, Frances M; Rohm, Maria; Clark, Anne; Brereton, Melissa F

2018-01-01

Elevated plasma glucose leads to pancreatic β-cell dysfunction and death in type 2 diabetes. Glycogen accumulation, due to impaired metabolism, contributes to this ‘glucotoxicity’ via dysregulated biochemical pathways promoting β-cell dysfunction. Here, we review emerging data, and re-examine published findings, on the role of glycogen in β-cells in normoglycaemia and in diabetes. PMID:28683284

Influence of SPK with Enteric Drainage on the Pancreatic Exocrine Function in Diabetic Patients with Uremia

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Guanghui Pei

2017-01-01

Full Text Available Objective. This study aimed to determine the use of fecal elastase in evaluating the effect of simultaneous pancreas–kidney transplantation with enteric drainage on the pancreatic exocrine function of diabetic patients with uremia. Methods. A total of 19 patients with simultaneous pancreas–kidney transplantation (SPK with enteric drainage, 31 diabetic patients with uremia (chronic renal failure (CRF, 22 diabetic patients with uremia who underwent renal transplantation (RT, and 20 normal individuals (CON were included in the study. Pancreatic exocrine insufficiency was determined using fecal elastase. Results. The fecal pancreatic elastase level in SPK patients with enteric drainage was 479 μg/g, which was significantly higher than 229 μg/g in CRF patients and 197 μg/g in RT patients. Using 200 μg/g as the established threshold, a reduced fecal pancreatic elastase level was found in 14/31 of CRF patients, 12/22 of RT patients, 1/19 of SPK patients with enteric drainage, and 1/20 of CON patients. The correlation analysis revealed a significant association between fecal elastase and glycosylated hemoglobin. Conclusions. The present study indicated that SPK with enteric drainage improves pancreatic endocrine and exocrine functions. Fecal elastase may be a clinically relevant means to determine the therapeutic effects.

Mucopolysaccharidosis type VI in a juvenile miniature schnauzer dog with concurrent hypertriglyceridemia, necrotizing pancreatitis, and diabetic ketoacidosis.

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Pérez, Mayrim L; Kridel, Heather A; Gallagher, Alex; Sheppard, Barbara J; Reese, Shona; Kondo, Hirotaka; Alleman, Rick; Giger, Urs

2015-03-01

A 7-month-old, neutered male miniature schnauzer dog with a history of cryptorchidism and umbilical hernia was referred for diabetic ketoacidosis. Clinical evaluation revealed stunted growth, skeletal abnormalities, hypertriglyceridemia, diabetic ketoacidosis, and acute necrotizing pancreatitis. Further testing was diagnostic for mucopolysaccharidosis type VI causing the stunted growth and skeletal deformities, but no connection between mucopolysaccharidosis type VI, hypertriglyceridemia, and pancreatic diseases was found.

Population-Level Incidence and Predictors of Surgically Induced Diabetes and Exocrine Insufficiency after Partial Pancreatic Resection.

Science.gov (United States)

Elliott, Irmina A; Epelboym, Irene; Winner, Megan; Allendorf, John D; Haigh, Philip I

2017-01-01

Endocrine and exocrine insufficiency after partial pancreatectomy affect quality of life, cardiovascular health, and nutritional status. However, their incidence and predictors are unknown. To identify the incidence and predictors of new-onset diabetes and exocrine insufficiency after partial pancreatectomy. We retrospectively reviewed 1165 cases of partial pancreatectomy, performed from 1998 to 2010, from a large population-based database. Incidence of new onset diabetes and exocrine insufficiency RESULTS: Of 1165 patients undergoing partial pancreatectomy, 41.8% had preexisting diabetes. In the remaining 678 patients, at a median 3.6 months, diabetes developed in 274 (40.4%) and pancreatic insufficiency developed in 235 (34.7%) patients. Independent predictors of new-onset diabetes were higher Charlson Comorbidity Index (CCI; hazard ratio [HR] = 1.62 for CCI of 1, p = 0.02; HR = 1.95 for CCI ≥ 2, p pancreatitis (HR = 1.51, p = 0.03). There was no difference in diabetes after Whipple procedure vs distal pancreatic resections, or malignant vs benign pathologic findings. Independent predictors of exocrine insufficiency were female sex (HR = 1.32, p = 0.002) and higher CCI (HR = 1.85 for CCI of 1, p insufficiency (HR = 0.35, p endocrine and exocrine insufficiency were 40% and 35%, respectively. These data are critical for informing patients' and physicians' expectations.

Urtica Dioica Distillate Regenerates Pancreatic Beta Cells in Streptozotocin-Induced Diabetic Rats

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Gohari, Ali; Noorafshan, Ali; Akmali, Masoumeh; Zamani-Garmsiri, Fahimeh; Seghatoleslam, Atefeh

2018-01-01

Background Urtica dioica is known as an anti-hyperglycemic plant. Urtica dioica distillate (UD) is a traditional Iranian drink, locally known as “aragh gazaneh”. In spite of its widespread consumption in Iran, according to traditional Iranian medicine, there is no scientific report on the usefulness of UD for diabetic patients. This survey was designed to evaluate its protective effects for the recovery from diabetes by determining the serum insulin, blood glucose, volume of pancreatic islets, and the number and volume of β-cells in diabetic rats. Methods A total of 48 Sprague-Dawley male rats (200-250 g) were randomly distributed into 6 groups (n=8), including non-diabetic plus distilled water (DW), non-diabetic plus UD, diabetic plus DW, diabetic plus UD, diabetic plus insulin, and diabetic plus glibenclamide. DW, UD, and glibenclamide were administered via intragastric gavage and insulin was injected subcutaneously. After four weeks of experiments, blood samples were collected for serum insulin and blood glucose assay. Pancreas was also evaluated using stereological method. The SPSS software was used for statistical analysis. Kruskal-Wallis, repeated measurements, and Mann-Whitney U test were applied for comparisons between the groups. Results The treatment of diabetic rats with UD reduced the blood glucose dramatically (P<0.001) and increased serum insulin levels significantly (P=0.03) in comparison to the diabetic plus DW rats. Treatment with UD did not affect the mean β-cell volumes in the diabetic rats when compared to the diabetic plus DW rats, but the islet volumes and β-cell numbers were significantly recovered. Conclusion UD treatment in diabetic rats improves hyperglycemia by partially restoring plasma insulin levels. The data suggest that UD prevents islet atrophy and/or regenerate pancreatic β-cells. PMID:29749986

Diabetic Hyperglycemia: Link to Impaired Glucose Transport in Pancreatic β Cells

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Unger, Roger H.

1991-03-01

Glucose uptake into pancreatic β cells by means of the glucose transporter GLUT-2, which has a high Michaelis constant, is essential for the normal insulin secretory response to hyperglycemia. In both autoimmune and nonautoimmune diabetes, this glucose transport is reduced as a consequence of down-regulation of the normal β-cell transporter. In autoimmune diabetes, circulating immunoglobulins can further impair this glucose transport by inhibiting functionally intact transporters. Insights into mechanisms of the unresponsiveness of β cells to hyperglycemia may improve the management and prevention of diabetes.

Pancreatic Cancer

Science.gov (United States)

... hormones that help control blood sugar levels. Pancreatic cancer usually begins in the cells that produce the juices. Some risk factors for developing pancreatic cancer include Smoking Long-term diabetes Chronic pancreatitis Certain ...

Hypertriglyceridemia-induced acute pancreatitis with diabetic ketoacidosis: A rare presentation of type 1 diabetes mellitus

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Prabhat Kumar

2017-01-01

Full Text Available Diabetic ketoacidosis (DKA is a frequently encountered complication of diabetes mellitus. DKA is an insulin deficit state and results in moderate to severe hypertriglyceridemia (HTG. HTG is the third leading cause of acute pancreatitis (AP and often goes unnoticed. The triad of DKA, HTG, and AP is rarely seen, and literature on the same is sparse. We report a case of AP which was due to DKA-induced secondary HTG in an adult with previously undiagnosed type 1 diabetes. His HbA1c was significantly raised, and C-peptide level was low, confirming chronic hyperglycemia. He was treated successfully with insulin infusion, intravenous crystalloid, and analgesics.

Uptake in the pancreatic islets of nicotimamide, nicotinic acid and tryptophan and their ability to prevent streptozotocin diabetes in mice

Energy Technology Data Exchange (ETDEWEB)

Tjaelve, H; Wilander, E [Uppsala Univ. (Sweden)

1976-01-01

The uptake of the nicotinamide adenine dinucleotide (NAD)-precursors nicotinamide, nicotinic acid and tryptophan in the pancreatic islets of mice was studied by use of autoradio-graphical methods. The ability of these substances to prevent streptozotocin diabetes was studied in the same species. It was found that only nicotinamide was strongly accumulated in the pancreatic islets and nicotinamide was also the only NAD-precursor which protected against the streptozotocin diabetes. Apparently there is a relationship between the ability of the NAD-precursors to be taken up in the pancreatic islets and their ability to prevent streptozotocin diabetes.

Type 2 diabetes mellitus is associated with increased risk of pancreatic cancer: A veteran administration registry study

OpenAIRE

Makhoul, Issam; Yacoub, Abdulraheem; Siegel, Eric

2016-01-01

Background: The etiology of pancreatic cancer remains elusive. Several studies have suggested a role for diabetes mellitus, but the magnitude of its contribution remains controversial. Objectives: Utilizing a large administrative database, this retrospective cohort study was designed to investigate the relationship between type 2 diabetes mellitus and pancreatic cancer. Patients and design: Using the Veterans Integrated Services Network 16 database, 322,614 subjects were enrolled in the study...

Curcumin enhances recovery of pancreatic islets from cellular stress induced inflammation and apoptosis in diabetic rats

International Nuclear Information System (INIS)

Rashid, Kahkashan; Sil, Parames C.

2015-01-01

The phytochemical, curcumin, has been reported to play many beneficial roles. However, under diabetic conditions, the detail mechanism of its beneficial action in the glucose homeostasis regulatory organ, pancreas, is poorly understood. The present study has been designed and carried out to explore the role of curcumin in the pancreatic tissue of STZ induced and cellular stress mediated diabetes in eight weeks old male Wistar rats. Diabetes was induced with a single intraperitoneal dose of STZ (65 mg/kg body weight). Post to diabetes induction, animals were treated with curcumin at a dose of 100 mg/kg body weight for eight weeks. Underlying molecular and cellular mechanism was determined using various biochemical assays, DNA fragmentation, FACS, histology, immunoblotting and ELISA. Treatment with curcumin reduced blood glucose level, increased plasma insulin and mitigated oxidative stress related markers. In vivo and in vitro experimental results revealed increased levels of proinflammatory cytokines (TNF-α, IL1-β and IFN-γ), reduced level of cellular defense proteins (Nrf-2 and HO-1) and glucose transporter (GLUT-2) along with enhanced levels of signaling molecules of ER stress dependent and independent apoptosis (cleaved Caspase-12/9/8/3) in STZ administered group. Treatment with curcumin ameliorated all the adverse changes and helps the organ back to its normal physiology. Results suggest that curcumin protects pancreatic beta-cells by attenuating inflammatory responses, and inhibiting ER/mitochondrial dependent and independent pathways of apoptosis and crosstalk between them. This uniqueness and absence of any detectable adverse effect proposes the possibility of using this molecule as an effective protector in the cellular stress mediated diabetes mellitus. - Highlights: • STZ induced cellular stress plays a vital role in pancreatic dysfunction. • Cellular stress causes inflammation, pancreatic islet cell death and diabetes. • Deregulation of Nrf-2

Curcumin enhances recovery of pancreatic islets from cellular stress induced inflammation and apoptosis in diabetic rats

Energy Technology Data Exchange (ETDEWEB)

Rashid, Kahkashan; Sil, Parames C., E-mail: parames@jcbose.ac.in

2015-02-01

The phytochemical, curcumin, has been reported to play many beneficial roles. However, under diabetic conditions, the detail mechanism of its beneficial action in the glucose homeostasis regulatory organ, pancreas, is poorly understood. The present study has been designed and carried out to explore the role of curcumin in the pancreatic tissue of STZ induced and cellular stress mediated diabetes in eight weeks old male Wistar rats. Diabetes was induced with a single intraperitoneal dose of STZ (65 mg/kg body weight). Post to diabetes induction, animals were treated with curcumin at a dose of 100 mg/kg body weight for eight weeks. Underlying molecular and cellular mechanism was determined using various biochemical assays, DNA fragmentation, FACS, histology, immunoblotting and ELISA. Treatment with curcumin reduced blood glucose level, increased plasma insulin and mitigated oxidative stress related markers. In vivo and in vitro experimental results revealed increased levels of proinflammatory cytokines (TNF-α, IL1-β and IFN-γ), reduced level of cellular defense proteins (Nrf-2 and HO-1) and glucose transporter (GLUT-2) along with enhanced levels of signaling molecules of ER stress dependent and independent apoptosis (cleaved Caspase-12/9/8/3) in STZ administered group. Treatment with curcumin ameliorated all the adverse changes and helps the organ back to its normal physiology. Results suggest that curcumin protects pancreatic beta-cells by attenuating inflammatory responses, and inhibiting ER/mitochondrial dependent and independent pathways of apoptosis and crosstalk between them. This uniqueness and absence of any detectable adverse effect proposes the possibility of using this molecule as an effective protector in the cellular stress mediated diabetes mellitus. - Highlights: • STZ induced cellular stress plays a vital role in pancreatic dysfunction. • Cellular stress causes inflammation, pancreatic islet cell death and diabetes. • Deregulation of Nrf-2

Comparison of Fasting Human Pancreatic Polypeptide Levels Among Patients With Pancreatic Ductal Adenocarcinoma, Chronic Pancreatitis, and Type 2 Diabetes Mellitus.

Science.gov (United States)

Nagpal, Sajan Jiv Singh; Bamlet, William R; Kudva, Yogish C; Chari, Suresh T

2018-05-17

Human pancreatic polypeptide (HPP) is a hormone secreted by the ventral pancreas. While postprandial HPP levels have been studied in chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC), there are limited data on fasting HPP in these diseases. Fasting serum HPP was measured in the following groups of patients: CP with diabetes mellitus (DM) (n = 16), CP without DM (n = 34), PDAC with new-onset DM (n = 50), PDAC without DM (n = 49), new-onset type 2 DM (n = 50), and controls without DM (n = 49). Sixty-six had type 3c DM (CP with DM, n = 16; PDAC with new-onset DM, n = 50). Median fasting HPP levels (in picograms per milliliter) were similar among all groups. Median (interquartile range) HPP levels in new-onset type 2 DM (n = 50; 288.3 [80.1-1072.1]) were similar to those in type 3c DM (n = 66; 242.3 [64.9-890.9]) (P = 0.71). In PDAC (n = 99), HPP values were similar in pancreatic head (n = 75) versus body/tail (n = 24) tumors (245.3 [64.3-1091.3] vs 334.7 [136.1-841.5]; P = 0.95), regardless of DM. Fasting HPP levels are similar in CP, PDAC, and controls regardless of glycemic status.

Diabetes Mellitus en el servicio de urgencias: manejo de las complicaciones agudas en adultos

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Eder A. Hernández-Ruiz

2008-01-01

Full Text Available La Diabetes Mellitus (DM es una enfermedad de alta prevalencia, reconocida como un problema de salud pública, debido a sus altas tasas de morbilidad y mortalidad asociadas. Diferentes estudios han documentado que la falta de adherencia al tratamiento, constituye uno de los principales factores desencadenantes para las descompensaciones agudas en el paciente diabético. Dentro del espectro de dichas alteraciones se encuentran las crisis hiperglicémicas agudas, las cuales se han dicotomizado en dos entidades clínicas: la Cetoacidosis Diabética (CAD y el Estado Hiperglicémico Hiperosmolar (EHH, que constituyen complicaciones metabólicas potencialmente fatales en el corto plazo y de las cuales pueden encontrarse cuadros superpuestos. Se han establecido criterios diagnósticos específicos buscando realizar un diagnóstico diferencial acertado, que permita un tratamiento idóneo; sin embargo, las tasas de morbilidad y mortalidad siguen siendo considerables. Por su parte, la Hipoglicemia también constituye una emergencia médica que, de no ser tratada oportunamente, puede ocasionar daño neurológico permanente e incluso la muerte. De lo anterior se deduce la importancia de que existan guías claras de manejo de estas alteraciones en todos los centros y servicios donde se preste atención médica de urgencias. Se siguen realizando investigaciones en busca de nuevas estrategias diagnósticas y terapéuticas que permitan un manejo más integral de la DM y sus complicaciones, en aras de mejorar la calidad de vida de los pacientes.

Is Type 2 Diabetes a Glycogen Storage Disease of Pancreatic β Cells?

Science.gov (United States)

Ashcroft, Frances M; Rohm, Maria; Clark, Anne; Brereton, Melissa F

2017-07-05

Elevated plasma glucose leads to pancreatic β cell dysfunction and death in type 2 diabetes. Glycogen accumulation, due to impaired metabolism, contributes to this "glucotoxicity" via dysregulated biochemical pathways promoting β cell dysfunction. Here, we review emerging data, and re-examine published findings, on the role of glycogen in β cells in normoglycemia and in diabetes. Copyright © 2017 Elsevier Inc. All rights reserved.

Amylase, Lipase, and Acute Pancreatitis in People With Type 2 Diabetes Treated With Liraglutide: Results From the LEADER Randomized Trial.

Science.gov (United States)

Steinberg, William M; Buse, John B; Ghorbani, Marie Louise Muus; Ørsted, David D; Nauck, Michael A

2017-07-01

To evaluate serum amylase and lipase levels and the rate of acute pancreatitis in patients with type 2 diabetes and high cardiovascular risk randomized to liraglutide or placebo and observed for 3.5-5.0 years. A total of 9,340 patients with type 2 diabetes were randomized to either liraglutide or placebo (median observation time 3.84 years). Fasting serum lipase and amylase were monitored. Acute pancreatitis was adjudicated in a blinded manner. Compared with the placebo group, liraglutide-treated patients had increases in serum lipase and amylase of 28.0% and 7.0%, respectively. Levels were increased at 6 months and then remained stable. During the study, 18 (0.4% [1.1 events/1,000 patient-years of observation] [PYO]) liraglutide-treated and 23 (0.5% [1.7 events/1,000 PYO]) placebo patients had acute pancreatitis confirmed by adjudication. Most acute pancreatitis cases occurred ≥12 months after randomization. Liraglutide-treated patients with prior history of pancreatitis ( n = 147) were not more likely to develop acute pancreatitis than similar patients in the placebo group ( n = 120). Elevations of amylase and lipase levels did not predict future risk of acute pancreatitis (positive predictive value pancreatitis among liraglutide-treated patients (regardless of previous history of pancreatitis) compared with the placebo group. Liraglutide was associated with increases in serum lipase and amylase, which were not predictive of an event of subsequent acute pancreatitis. © 2017 by the American Diabetes Association.

Insulin Resistance and Impaired Pancreatic β-Cell Function in Adult Offspring of Women With Diabetes in Pregnancy

DEFF Research Database (Denmark)

Kelstrup, Louise; Damm, Peter; Mathiesen, Elisabeth R

2013-01-01

Context:Offspring of women with diabetes during pregnancy have increased risk of glucose intolerance in adulthood, but the underlying mechanisms are unknown.Objective:We aimed to investigate effects of intrauterine hyperglycemia on insulin secretion and - action in adult offspring of mothers...... a standard oral glucose tolerance test (120 minutes, 75 gram glucose). Pancreatic beta-cell function taking the prevailing insulin sensitivity into account was estimated by disposition indices.Results:Both groups of offspring exposed during pregnancy to either maternal gestational diabetes or type 1 diabetes.......005).Conclusion:Reduced insulin sensitivity as well as impaired pancreatic beta cell function may contribute to the increased risk of glucose intolerance among adult offspring born to women with diabetes during pregnancy....

[Effect of jiaotai pill on pancreatic fat accumulation and islet cell apoptosis in rats with type 2 diabetes].

Science.gov (United States)

Zou, Xin; Liu, De-Liang; Lu, Fu-Er; Dong, Hui; Xu, Li-Jun; Luo, Yun-Huan; Wang, Kai-Fu

2014-06-01

In this study, the rat type 2 diabetes mellitus (T2DM) model was established through tail vein injection with low dose of streptozotocin (STZ) and high fat diet for 8 weeks, and then treated with Jiaotai Pill. The oral glucose tolerance test (OGTT), fasting serum insulin (FINS), free fatty acid(FFA) levels and blood lipid were assayed. HOMA-IR was calculated. Pancreatic pathology was performed. And pancreatic triglyceride (TG) content was examined by the lipid extraction method. Pancreatic islet cell apoptosis were detected by terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL). According to the results, the model group showed abnormal OGTT, increased FINS, HOMA-IR, FFA, lipid disorder, obvious fat accumulation and significantly increased TG content in pancreatic tissues, and enhanced pancreatic islet cell apoptosis. Compared with the model group, the Jiaotai Pill group displayed improved OGTT, reduced FINS, HOMA-IR, FFA, recovered lipid disorder, decreased fat accumulation and significantly declined TG content in pancreatic tissues, and lowered pancreatic islet cell apoptosis. In summary, Jiaotai pill could effectively treat type 2 diabetes in rats. Its mechanism may be related to the reduction in pancreatic fat accumulation and islet cell apoptosis.

Silver nanoparticle based surface enhanced Raman scattering spectroscopy of diabetic and normal rat pancreatic tissue under near-infrared laser excitation

International Nuclear Information System (INIS)

Huang, H; Shi, H; Chen, W; Yu, Y; Lin, D; Xu, Q; Feng, S; Lin, J; Huang, Z; Li, Y; Chen, R

2013-01-01

This paper presents the use of high spatial resolution silver nanoparticle based near-infrared surface enhanced Raman scattering (SERS) from rat pancreatic tissue to obtain biochrmical information about the tissue. A high quality SERS signal from a mixture of pancreatic tissues and silver nanoparticles can be obtained within 10 s using a Renishaw micro-Raman system. Prominent SERS bands of pancreatic tissue were assigned to known molecular vibrations, such as the vibrations of DNA bases, RNA bases, proteins and lipids. Different tissue structures of diabetic and normal rat pancreatic tissues have characteristic features in SERS spectra. This exploratory study demonstrated great potential for using SERS imaging to distinguish diabetic and normal pancreatic tissues on frozen sections without using dye labeling of functionalized binding sites. (letter)

Impaired pancreatic polypeptide response to a meal in type 1 diabetic patients

DEFF Research Database (Denmark)

Rasmussen, M H; Carstensen, H; List, S

1993-01-01

The pancreatic polypeptide (PP) response to a mixed meal was investigated in seven insulin-dependent diabetics without measurable signs of diabetic autonomic neuropathy, and in seven healthy subjects. Since acute changes in metabolic regulation might influence the meal-induced PP response...... is independent of short-term changes in metabolic control. Since the response was attenuated in the insulin-dependent diabetic patients, who had no otherwise measurable signs of neuropathy, the PP response to a meal could be a sensitive indicator of dysfunction of the reflex arc controlling PP secretion...

Fatal hypertriglyceridaemia, acute pancreatitis and diabetic ketoacidosis possibly induced by quetiapine

DEFF Research Database (Denmark)

Madsen, Kristian Roerbaek

2014-01-01

A 27-year-old man treated with quetiapine for anxiety disorder developed hypertriglyceridaemia-induced acute pancreatitis and diabetic ketoacidosis. He was otherwise physically healthy with no family history of hyperlipidaemia. Despite aggressive intensive therapy he died of multiorgan failure wi...... and possibly plasmapheresis in case of extreme hypertriglyceridaemia....

Immunohistochemical detection of vimentin in pancreatic islet β- and α-cells of macrosomic infants of diabetic and nondiabetic mothers.

Science.gov (United States)

Krivova, Yuliya S; Proshchina, Alexandra E; Barabanov, Valeriy M; Barinova, Irina V; Saveliev, Sergey V

2018-02-01

Expression of the intermediate filament protein vimentin has been recently observed in the pancreatic islet β- and α-cells of humans with type 2 diabetes mellitus. It was suggested that the presence of vimentin in endocrine cells may indicate islet tissue renewal, or potentially represent the dedifferentiation of endocrine cells, which could contribute to the onset of type 2 diabetes or islet cell dysfunction. To analyze the expression of vimentin in pancreatic β- and α-cells of macrosomic infants of diabetic and nondiabetic mothers. Pancreatic samples of five macrosomic infants (gestational age 34-40weeks) from three diabetic and two nondiabetic mothers were compared to six control infants (32-40weeks, weight appropriate for gestational age) from normoglycemic mothers. Pancreatic autopsy samples were examined by double immunofluorescent labeling with antibodies against vimentin and either insulin or glucagon. Alterations in the endocrine pancreas were measured using morphometric methods, then data were statistically analyzed. In the pancreatic islets of macrosomic infants from diabetic and nondiabetic mothers, we observed vimentin-positive cells, some of which simultaneously contained insulin or glucagon. We also quantitatively showed that the presence of such cells was associated with hypertrophy and hyperplasia of the islets, and with an increase in β- and α-cell density. We speculate that the appearance of vimentin-positive islet cells may reflect induction of differentiation in response to the increased insulin demand, and vimentin may serve as an early marker of endocrine pancreas disorders. Copyright © 2017 Elsevier B.V. All rights reserved.

Treatment and prevention of hepatic failure in acute biliary pancreatitis in patients with diabetes mellitus

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S.I. Savoliuk

2017-10-01

Full Text Available Background. The purpose of the study was to evaluate the effectiveness of traditional and optimized programs for integrated treatment and prevention of clinical and laboratory manifestations of hepatic dysfunction in acute biliary pancreatitis in patients with diabetes mellitus by observing the dynamics of markers of cytopathic hypoxia, erythron system and iron metabolism. Materials and methods. The work is based on the analysis of the results of the comprehensive treatment of 122 patients with acute biliary pancreatitis against the background of diabetes mellitus. Laboratory analysis was performed to monitor markers of cytopathic hypoxia, erythron system and iron metabolism depending on the morphological form of acute pancreatitis and the effectiveness of optimized and traditional treatment. Results. The interstitial form of acute biliary pancreatitis in diabetes mellitus is characterized by significant changes in the dynamics of carbonyl groups, the content of arginine and adenosine deamination on the background of physiological fluctuations of the remaining markers of cytopathic hypoxia, and the signs of a distinct functional iron deficiency state in the form of microcytosis and hypochromia were detected. The emergence of pancreatic parenchyma necrosis of different planes, depending on the morphological form of acute biliary pancreatitis, is accompanied by reliable evidence of an absolute iron deficiency state of varying intensity and negative dynamics of indicators of endothelial dysfunction with a separate form. In patients with widespread necrotizing acute biliary pancreatitis, the pathological changes in the systemic metabolism are associated with the catabolism of purine nucleotides — the growth of xanthine and hypoxanthine levels. The stage of decompensation of systemic disorders of homeostasis is observed in patients with subtotal-total forms, when additional increase in the concentrations of enzymes responsible for utilization of

Is antibiotic prophylaxis beneficial in acute pancreatitis? - First update

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Gabriel Rada

2015-04-01

Full Text Available Resumen Este resumen Epistemonikos (Living FRISBEE: Living FRIendly Summary of the Body of Evidence using Epistemonikos es una actualización del resumen publicado en Agosto de 2014, basado en dos nuevas revisiones sistemáticas aparecidas en Enero y Febrero de 2015. Existe controversia sobre los efectos del uso de antibióticos profilácticos en pacientes con pancreatitis aguda. Utilizando la base de datos Epistemonikos, la cual es mantenida mediante búsquedas en 30 bases de datos, identificamos 18 revisiones sistemáticas que en conjunto incluyen 19 estudios aleatorizados. Los combinamos mediante un metanálisis y generamos tablas de resumen de resultados utilizando el método GRADE. Concluimos que el uso de antibióticos profilácticos podría disminuir la mortalidad y el tiempo de hospitalización en pacientes con pancreatitis aguda, pero la certeza de la evidencia es baja. La probabilidad que la aparición de nueva evidencia cambie lo que sabemos es alta.

Treating Diet-Induced Diabetes and Obesity with Human Embryonic Stem Cell-Derived Pancreatic Progenitor Cells and Antidiabetic Drugs

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Jennifer E. Bruin

2015-04-01

Full Text Available Human embryonic stem cell (hESC-derived pancreatic progenitor cells effectively reverse hyperglycemia in rodent models of type 1 diabetes, but their capacity to treat type 2 diabetes has not been reported. An immunodeficient model of type 2 diabetes was generated by high-fat diet (HFD feeding in SCID-beige mice. Exposure to HFDs did not impact the maturation of macroencapsulated pancreatic progenitor cells into glucose-responsive insulin-secreting cells following transplantation, and the cell therapy improved glucose tolerance in HFD-fed transplant recipients after 24 weeks. However, since diet-induced hyperglycemia and obesity were not fully ameliorated by transplantation alone, a second cohort of HFD-fed mice was treated with pancreatic progenitor cells combined with one of three antidiabetic drugs. All combination therapies rapidly improved body weight and co-treatment with either sitagliptin or metformin improved hyperglycemia after only 12 weeks. Therefore, a stem cell-based therapy may be effective for treating type 2 diabetes, particularly in combination with antidiabetic drugs.

Garlic and Resveratrol attenuate diabetic complications, loss of β-cells, pancreatic and hepatic oxidative stress in streptozotocin-induced diabetic rats

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Gagandeep Kaur

2016-10-01

Full Text Available Abstract:The study was aimed at finding the effect of garlic and resveratrol on loss of β-cells and diabetic complication in streptozotocin (STZ-induced Type-I diabetic rats. Rats were injected with single dose STZ (50mg/kg, i.p. for induction of type 1 diabetes (Dia and compared with control group. Rats from third (Dia+Gar, fourth (Dia+Resv and fifth (Dia+Met groups were fed raw garlic homogenate (250 mg/kg/day, resveratrol (25 mg/kg/day and metformin (500 mg/kg/day orally, respectively for a period of 4 weeks. Diabetic group had decreased serum insulin and hydrogen sulfide levels along with increased blood glucose and glycated hemoglobin, triglyceride, uric acid and nitric oxide levels. Significant (p<0.05 increase in pancreatic and hepatic TBARS, conjugated dienes, nitric oxide, and AGE level and significant (p<0.05 decrease in SOD, catalase, H2S, GSH level were observed in diabetic group. Administration of garlic, resveratrol and metformin significantly (p<0.05 normalized most of the altered metabolic and oxidative stress parameters as well as histopathological changes. Administration of garlic, resveratrol and 9metformin in diabetic rat decreases pancreatic β-cell damage and hepatic injury. Our data concluded that administration of garlic showed more promising effect in terms of reducing oxidative stress and pathological changes when compared to resveratrol and metformin groups.

Higher mortality of patients on haemodialysis with pancreatic diabetes compared to type 2-diabetes

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Bodlaj Gert

2012-03-01

Full Text Available Abstract In rare cases (1-8% diabetic patients with end-stage renal disease (ESRD suffer from diabetic nephropathy (dNP due to pancreatic diabetes mellitus (PDM. Aim of this study was to investigate differences in the outcome of patients with PDM and those with type 2 diabetes. In a retrospective study we evaluated 96 diabetic patients, who started hemodialysis (HD in our dialysis centre (1997-2005. In 12 patients PMD was diagnosed, and 84 patients had type 2 diabetes. In both groups we compared vascular risk factors and prevalence of vascular diseases at the start of dialysis. We also evaluated incidence of malnutrition, and 5-year survival in both patient groups. The vascular risk factors were similar in both patient groups, also the prevalence of vascular diseases at the initiation of HD was similar in both groups. In the patients with PDM the mean BMI (kg/m2 was lower (22 + 3 versus 25 + 3, and also their serum albumin was lower (2.7 + 0.3 versus 3.4 + 0.3 g/dl, p Conclusions in HD-treated patients with type 2 diabetes or PDM the prevalence of vascular diseases was not significantly different. The lower survival of PDM patients can be related to poor nutrition status.

Hypertriglyceridemia, an important and independent risk factor for acute pancreatitis in patients with type 2 diabetes mellitus

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Albai O

2017-04-01

Full Text Available Oana Albai,1 Deiana Roman,2 Mirela Frandes2 1Second Department of Internal Medicine, 2Department of Functional Sciences, “Victor Babes” University of Medicine and Pharmacy, Timisoara, Romania Purpose: Acute pancreatitis (AP is a frequent inflammatory disease of the pancreas with multiple causes, among which high triglyceride (TG level is the most common. The main purpose of this study has been to research the prevalence of AP in patients with diabetes mellitus (DM and to underline the importance of hypertriglyceridemia (HTG as a risk factor in triggering AP. The possible link between AP and glycemic control has been studied also, alongside some cardiovascular risk factors and long-term diabetes complications.Patients and methods: The patient cohort comprised 1,586 patients with DM, admitted to the Internal Medicine Clinic of Diabetes, Nutrition and Metabolic Disease within the Emergency Hospital in Timisoara between January and August 2016. Following a series of clinical and biological investigations, these patients were diagnosed with AP. The patients’ antidiabetic treatment and chronic diabetes-related complications have also been recorded.Results: The prevalence of pancreatitis in this group of patients was 3.7%. The presence of pancreatitis was associated with a higher HbA1c (8.5% vs 7.7%; P<0.001, fasting glycemia (167.5 vs 95 mg/dL; P<0.001, postprandial glycemia (244.5 vs 118 mg/dL; P<0.001, total cholesterol (256.5 vs 189.5 mg/dL; P<0.001, low-density lipoprotein cholesterol (LDLc (208.7 vs 112.8 mg/dL; P<0.001, and TGs (495 vs 161 mg/dL; P<0.001. HDL cholesterol (HDLc was found to be a significant protective factor against the risk of pancreatitis. On the contrary, high LDLc values were a significant risk factor for pancreatitis along with high non-HDLc and high TG values, respectively.Conclusion: The development of AP events in patients with DM is associated with unsatisfactory glycemic control, HTG, hypertension, and the

Histomorphological and morphometric studies of the pancreatic islet cells of diabetic rats treated with aqueous extracts of Momordica charantia (karela fruits

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Mohammad Aftab Hossain

2014-09-01

Full Text Available Objective: To investigate the effect of aqueous extract of Momordica charantia (karela (M. charantia fruits on blood glucose level, pancreatic weight changes and histopathology of pancreatic changes in the streptozotocin (STZ induced diabetic rats. Methods: Thirty-six albino rats were used in the experiment; diabetes mellitus was induced in 30 adult albino rats, using intraperitoneal injection of 55 mg/kg STZ. Six non diabetic rats remained as control (T1 . The diabetic rats were randomly assigned into five equal groups: diabetic control (T2 without any treatment, groups T3, T4, T5 and T6 were treated with aqueous extract of karela fruits daily at a doses of 250, 500 and 750 mg/kg and glibenclamide (5 mg/kg up to 90 d, respectively. At Day 90, all rats were sacrificed, the pancreases of the rats were excised and processed. Results: The results of this study indicate that aqueous extract of M. charantia fruits was able to reduce blood glucose level significantly compared with the diabetic control group (P<0.01. Histopathologically, STZ resulted severe necrotic changes in pancreatic islets. Tissues sections of pancreas in the treated groups showed regeneration of β cells and increased size of pancreatic islets. Conclusions: The present study suggests that oral feeding of M. charantia fruit juice has a significant anti-hyperglycemic effect and may have a role in the regeneration of the β cells in STZ diabetic rats.

Incidence of and risk factors for developing pancreatic cancer in patients with chronic pancreatitis.

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Kudo, Yujin; Kamisawa, Terumi; Anjiki, Hajime; Takuma, Kensuke; Egawa, Naoto

2011-01-01

Pancreatic cancer sometimes occurs during the course of chronic pancreatitis. This study aimed to identify risk factors for developing pancreatic cancer associated with chronic pancreatitis. The incidence of pancreatic cancer developing in 218 patients with chronic pancreatitis and clinical features of the chronic pancreatitis patients who developed pancreatic cancer were studied. Nine patients developed pancreatic cancer. Average period from the diagnosis of chronic pancreatitis to the diagnosis of pancreatic cancer was 9.6 years. All pancreatic cancers were diagnosed at an advanced stage. Only 2 patients had been followed-up periodically. There were no significant differences between chronic pancreatitis patients who developed pancreatic cancer and those who did not in male/female ratio (3.5 vs. 8), average age on diagnosis (65.0 vs. 56.5), alcoholic/non-alcoholic chronic pancreatitis (1.6 vs. 2.6), smoking habits (62.5% vs. 70.7%), diabetes mellitus (77.8% vs. 54.4%), and continued alcohol drinking (37.5% vs. 53.1%). Over the period examined, 4% of chronic pancreatitis patients developed pancreatic cancer. Sex ratio, onset age, etiology, smoking habits, diabetes mellitus, and continued alcohol drinking were not significant risk factors for developing pancreatic cancer in chronic pancreatitis patients. Periodic follow-up due to the possibility of pancreatic cancer is necessary in chronic pancreatitis patients.

Relationship between the exocrine and endocrine pancreas after acute pancreatitis.

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Das, Stephanie L M; Kennedy, James I C; Murphy, Rinki; Phillips, Anthony R J; Windsor, John A; Petrov, Maxim S

2014-12-07

To determine the prevalence and time course of pancreatic exocrine insufficiency in individuals with newly diagnosed prediabetes or diabetes mellitus after acute pancreatitis. Relevant literature cited in three major biomedical journal databases (EMBASE, MEDLINE, and Scopus) was reviewed independently by two authors. There were no language constraints but the search was limited to human studies. Studies included were cohort studies of adult patients who were discharged after an attack of acute pancreatitis. Patients were excluded if they were under 18 years of age or had a previous diagnosis of prediabetes or diabetes mellitus, pancreatic exocrine insufficiency, or chronic pancreatitis. The main outcome measure was the prevalence of concomitant pancreatic exocrine insufficiency in patients who were diagnosed with prediabetes and diabetes mellitus after an attack of acute pancreatitis. Subgroup analysis was conducted for patients who were diagnosed with prediabetes only and those who were diagnosed with diabetes mellitus only. Subgroup analysis looking at the time course of concomitant pancreatic exocrine and endocrine insufficiency was also conducted. Pooled prevalence and corresponding 95% confidence intervals were calculated for all outcome measures and P-values pancreatitis was 43% (95%CI: 30%-56%). The pooled prevalence of pancreatic exocrine insufficiency in individuals after acute pancreatitis was 29% (95%CI: 19%-39%). The prevalence of concomitant pancreatic exocrine insufficiency in individuals with newly diagnosed prediabetes or diabetes was 40% (95%CI: 25%-55%). The prevalence of concomitant pancreatic exocrine insufficiency among individuals with prediabetes alone and diabetes mellitus alone was 41% (95%CI: 12%-75%) and 39% (95%CI: 28%-51%), respectively. Further analysis showed that the prevalence of concomitant pancreatic exocrine insufficiency in individuals with prediabetes or diabetes decreases over time after an attack of acute pancreatitis

Pancreatic Function, Type 2 Diabetes, and Metabolism in Aging

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Zhenwei Gong

2012-01-01

Full Text Available Aging is a risk factor for impaired glucose tolerance and diabetes. Of the reported 25.8 million Americans estimated to have diabetes, 26.9% are over the age of 65. In certain ethnic groups, the proportion is even higher; almost 1 in 3 older Hispanics and African Americans and 3 out of 4 Pima Indian elders have diabetes. As per the NHANES III (Third National Health and Nutrition Examination survey, the percentage of physician-diagnosed diabetes increased from 3.9% in middle-aged adults (40–49 years to 13.2% in elderly adults (≥75 years. The higher incidence of diabetes is especially alarming considering that diabetes in itself increases the risk for multiple other age-related diseases such as cancer, stroke, cardiovascular diseases, Parkinson’s disease, and Alzheimer’s disease (AD. In this review, we summarize the current evidence on how aging affects pancreatic β cell function, β cell mass, insulin secretion and insulin sensitivity. We also review the effects of aging on the relationship between insulin sensitivity and insulin secretion. Understanding the mechanisms that lead to impaired glucose homeostasis and T2D in the elderly will lead to development of novel treatments that will prevent or delay diabetes, substantially improve quality of life and ultimately increase overall life span.

Exocrine pancreatic insufficiency in type 1 and type 2 diabetes mellitus: do we need to treat it? A systematic review.

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Zsóri, Gábor; Illés, Dóra; Terzin, Viktória; Ivány, Emese; Czakó, László

2018-05-17

The exocrine and endocrine pancreata are very closely linked both anatomically and physiologically. Abdominal symptoms such as nausea, bloating, diarrhea, steatorrhea, and weight loss can often occur in diabetic patients. Impairments of the exocrine pancreatic function seem to be a frequent complication of diabetes mellitus; however, they are largely overlooked. The aim of this paper is to provide an overview of the current concepts of exocrine pancreatic insufficiency (PEI) in diabetes mellitus. The prevalence and symptoms of PEI in diabetes mellitus, the pathomechanism, and difficulties of diagnosis and therapy of PEI are summarized in this systematic review. Copyright © 2018 IAP and EPC. Published by Elsevier B.V. All rights reserved.

Chronic pancreatitis with secondary diabetes mellitus treated by use of insulin in an adult California sea lion.

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Meegan, Jenny M; Sidor, Inga F; Steiner, Jörg M; Sarran, Delphine; Dunn, J Lawrence

2008-06-01

A 21-year-old neutered male captive California sea lion developed chronic polyuria; polydipsia; polyphagia; accelerated development of existing cataracts; and frequent episodes of gastrointestinal upset including anorexia, signs of abdominal discomfort, diarrhea, and vomiting. Chronic hypercholesterolemia, hypertriglyceridemia, hyperglycemia, and glucosuria were identified. During episodes of gastrointestinal abnormalities, transient hyperbilirubinemia and increased serum J-glutamyltransferase activities developed. Clinical findings strongly suggested chronic pancreatitis with secondary diabetes mellitus and intermittent cholestasis. Multiple diagnostic tests, including abdominal ultrasonography, serial hematologic and serum biochemical analyses, fecal examinations, urinalyses and bacteriologic culture of urine, measurement of serum fructosamine and insulin concentrations, and evaluation of thyroid and adrenal function, did not reveal any specific parasitic, endocrine, hepatic, or neoplastic etiologies. For 1.5 years, the sea lion received once-daily administration of glargine insulin, gastrointestinal protectants, and a strict high-protein, low-fat diet. Daily monitoring of glucose regulation was achieved by training the sea lion to submit to blood and urine sampling. Glucose regulation ranged from fair to good, and clinical signs of diabetes mellitus lessened. Episodes of gastrointestinal upset still occurred, although the frequency and severity decreased. Ultimately, a severe episode developed, associated with diabetic ketoacidosis and sepsis, and the sea lion died. Severe fibrosing pancreatitis with exocrine and endocrine atrophy and abscesses arising from ectatic pancreatic ducts were found. Peripancreatic fibrosis caused stricture of the common bile duct, resulting in gallbladder distension without cholecystitis. Diabetes mellitus can occur secondary to chronic pancreatitis in California sea lions and insulin therapy should be considered.

Increased Levels of YKL-40 and Interleukin 6 in Patients With Chronic Pancreatitis and Secondary Diabetes

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Hansen, Morten; Nielsen, Anders Rinnov; Vilsbøll, Tina

2012-01-01

Circulating levels of YKL-40 and interleukin 6 (IL-6) are elevated in patients with type 2 diabetes. We aimed to evaluate YKL-40 levels in patients with chronic pancreatitis (CP) with and without secondary diabetes mellitus (DM) to investigate whether elevated plasma YKL-40 could play a primary...

Absence of diabetes and pancreatic exocrine dysfunction in a transgenic model of carboxyl-ester lipase-MODY (maturity-onset diabetes of the young.

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Helge Ræder

Full Text Available CEL-MODY is a monogenic form of diabetes with exocrine pancreatic insufficiency caused by mutations in CARBOXYL-ESTER LIPASE (CEL. The pathogenic processes underlying CEL-MODY are poorly understood, and the global knockout mouse model of the CEL gene (CELKO did not recapitulate the disease. We therefore aimed to create and phenotype a mouse model specifically over-expressing mutated CEL in the pancreas.We established a monotransgenic floxed (flanking LOX sequences mouse line carrying the human CEL mutation c.1686delT and crossed it with an elastase-Cre mouse to derive a bitransgenic mouse line with pancreas-specific over-expression of CEL carrying this disease-associated mutation (TgCEL. Following confirmation of murine pancreatic expression of the human transgene by real-time quantitative PCR, we phenotyped the mouse model fed a normal chow and compared it with mice fed a 60% high fat diet (HFD as well as the effects of short-term and long-term cerulein exposure.Pancreatic exocrine function was normal in TgCEL mice on normal chow as assessed by serum lipid and lipid-soluble vitamin levels, fecal elastase and fecal fat absorption, and the normoglycemic mice exhibited normal pancreatic morphology. On 60% HFD, the mice gained weight to the same extent as controls, had normal pancreatic exocrine function and comparable glucose tolerance even after resuming normal diet and follow up up to 22 months of age. The cerulein-exposed TgCEL mice gained weight and remained glucose tolerant, and there were no detectable mutation-specific differences in serum amylase, islet hormones or the extent of pancreatic tissue inflammation.In this murine model of human CEL-MODY diabetes, we did not detect mutation-specific endocrine or exocrine pancreatic phenotypes, in response to altered diets or exposure to cerulein.

Absence of diabetes and pancreatic exocrine dysfunction in a transgenic model of carboxyl-ester lipase-MODY (maturity-onset diabetes of the young).

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Ræder, Helge; Vesterhus, Mette; El Ouaamari, Abdelfattah; Paulo, Joao A; McAllister, Fiona E; Liew, Chong Wee; Hu, Jiang; Kawamori, Dan; Molven, Anders; Gygi, Steven P; Njølstad, Pål R; Kahn, C Ronald; Kulkarni, Rohit N

2013-01-01

CEL-MODY is a monogenic form of diabetes with exocrine pancreatic insufficiency caused by mutations in CARBOXYL-ESTER LIPASE (CEL). The pathogenic processes underlying CEL-MODY are poorly understood, and the global knockout mouse model of the CEL gene (CELKO) did not recapitulate the disease. We therefore aimed to create and phenotype a mouse model specifically over-expressing mutated CEL in the pancreas. We established a monotransgenic floxed (flanking LOX sequences) mouse line carrying the human CEL mutation c.1686delT and crossed it with an elastase-Cre mouse to derive a bitransgenic mouse line with pancreas-specific over-expression of CEL carrying this disease-associated mutation (TgCEL). Following confirmation of murine pancreatic expression of the human transgene by real-time quantitative PCR, we phenotyped the mouse model fed a normal chow and compared it with mice fed a 60% high fat diet (HFD) as well as the effects of short-term and long-term cerulein exposure. Pancreatic exocrine function was normal in TgCEL mice on normal chow as assessed by serum lipid and lipid-soluble vitamin levels, fecal elastase and fecal fat absorption, and the normoglycemic mice exhibited normal pancreatic morphology. On 60% HFD, the mice gained weight to the same extent as controls, had normal pancreatic exocrine function and comparable glucose tolerance even after resuming normal diet and follow up up to 22 months of age. The cerulein-exposed TgCEL mice gained weight and remained glucose tolerant, and there were no detectable mutation-specific differences in serum amylase, islet hormones or the extent of pancreatic tissue inflammation. In this murine model of human CEL-MODY diabetes, we did not detect mutation-specific endocrine or exocrine pancreatic phenotypes, in response to altered diets or exposure to cerulein.

Periodontitis aggravated pancreatic β-cell dysfunction in diabetic mice through interleukin-12 regulation on Klotho.

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Liu, Yihua; Zhang, Qiuli

2016-05-01

Recent studies have shown that periodontitis can contribute to adipose tissue inflammation and subsequent systemic insulin resistance in the obese rat model. However, the related inflammatory mechanism is not yet clear. The present study aims to investigate the effects of periodontitis on the function of pancreatic β-cells with pro-inflammatory cytokines-related immune mechanism in a mouse model. C57BL/6-db/db and inbred C57BL/6 mice were chosen here to establish a mouse model with periodontitis, which was induced by ligatures for 8 weeks. Glucose-stimulated insulin secretion was introduced to evaluate the function of pancreatic islets and β-cells. Serum levels of pro-inflammatory cytokines and Klotho were also measured, and the correlation between immunostimulation and Klotho level was deeply investigated in vitro. Pancreatic β-cell failure, with insulin resistance, was observed in db/db mice, while periodontitis could aggravate β-cell dysfunction-related features. Serum levels of interleukin (IL)-12 and Klotho showed a negatively synergistic change, whereas the expression of Klotho was also inhibited under IL-12 treatment in MIN6 β-cells or isolated islets. Furthermore, IL-12-induced immune stimulation and also decreased insulin secretion were proven to be reversed by Klotho overexpression. Periodontitis aggravated pancreatic β-cell failure in diabetic mice. Further in vitro studies showed IL-12 regulation on Klotho, while Klotho also acted as an inhibitor on IL-12, indicating the potential of Klotho for preserving pancreatic β-cell function in diabetes.

Simplifying the Evaluation of Children With New Onset Diabetes: Utility of Pancreatic Autoantibodies for Diabetes Type Classification and Use of Serum Bicarbonate to Diagnose and Classify Diabetic Ketoacidosis.

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Von Oettingen, Julia Elisabeth

2015-01-01

Objectives: To assess whether routinely measuring pancreatic autoantibodies (PAA) in pediatric new onset diabetes (NODM) is necessary, and to evaluate serum bicarbonate (HCO3) as a substitute for venous pH (vpH) in the diagnosis of diabetic ketoacidosis (DKA). Methods: Retrospective analysis of all patients with NODM admitted to Boston Children's Hospital from 10/1/07-7/1/13. Logistic regression was used to develop a clinical score to classify diabetes type. Linear and logistic regression...

Pancreatitis and systemic lupus erythematosus Pancreatitis y lupus eritematoso sistémico

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J. Lariño Noia

2009-08-01

Full Text Available Gastrointestinal symptoms in patients with SLE are common, specifically abdominal pain. However, the rate of pancreatic diseases is much lower and does not reach 5% according to published series in Europe and the USA. This association between SLE and pancreatic disease is basically at the expense of episodes of acute pancreatitis. An association with chronic pancreatitis is much more uncommon, and only four articles have been published showing this relationship. Three cases of SLE-associated pancreatitis are described, and disease onset, etiological factors, and clinical progression are analyzed. A review of the literature and a brief discussion about pathophysiological mechanisms and the role of corticosteroids are also included.Los síntomas gastrointestinales en los pacientes con lupus eritematoso sistémico (LES son comunes, específicamente el dolor abdominal. Sin embargo la tasa de enfermedades pancreáticas es mucho menor, una tasa que no alcanza ni al 5% según las series publicadas en Europa y EE. UU. Esta asociación entre enfermedades pancreáticas y LES es fundamentalmente a expensas de episodios de pancreatitis aguda. La asociación con pancreatitis crónica es muchísimo más infrecuente, teniendo en cuenta que tan sólo cuatro artículos han sido publicados reflejando esta asociación. Describimos tres casos de asociación entre pancreatitis y LES, analizando el debut de la enfermedad, los factores etiológicos y también la evolución clínica. Hemos realizado, además, una breve discusión de la fisiopatología y del papel de corticosteroides, así como una revisión de la literatura.

In vitro fertilization–induced hypertriglyceridemia with secondary acute pancreatitis and diabetic ketoacidosis

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Claire Michael Issa

2017-01-01

Full Text Available Introduction: In vitro fertilization is becoming more and more popular lately, as such light is to be shed on any possible related complication. One of these complications is the possible hormonal effect on the lipid profile of the patients. Case presentation: We present a case of a 39-year-old woman with no prior or family history of dyslipidemia, who presented with post in vitro fertilization severe hypertriglyceridemia and secondary acute pancreatitis and diabetic ketoacidosis. Discussion of the case is followed by a brief review of the literature related to in vitro fertilization–induced hypertriglyceridemia. Conclusion: This is, up to our knowledge, the sixth reported case of in vitro fertilization–induced hypertriglyceridemia with secondary acute pancreatitis. This is a serious and life-threatening complication. As such, it might be wise at least in high-risk patients (such as patients with diabetes mellitus, polycystic ovaries syndrome, obesity, and family and personal history of dyslipidemia to screen for lipid abnormalities before initiating in vitro fertilization and monitor these levels afterward.

Pancreatic Tissue Transplanted in TheraCyte Encapsulation Devices Is Protected and Prevents Hyperglycemia in a Mouse Model of Immune-Mediated Diabetes.

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Boettler, Tobias; Schneider, Darius; Cheng, Yang; Kadoya, Kuniko; Brandon, Eugene P; Martinson, Laura; von Herrath, Matthias

2016-01-01

Type 1 diabetes (T1D) is characterized by destruction of glucose-responsive insulin-producing pancreatic β-cells and exhibits immune infiltration of pancreatic islets, where CD8 lymphocytes are most prominent. Curative transplantation of pancreatic islets is seriously hampered by the persistence of autoreactive immune cells that require high doses of immunosuppressive drugs. An elegant approach to confer graft protection while obviating the need for immunosuppression is the use of encapsulation devices that allow for the transfer of oxygen and nutrients, yet prevent immune cells from making direct contact with the islet grafts. Here we demonstrate that macroencapsulation devices (TheraCyte) loaded with neonatal pancreatic tissue and transplanted into RIP-LCMV.GP mice prevented disease onset in a model of virus-induced diabetes mellitus. Histological analyses revealed that insulin-producing cells survived within the device in animal models of diabetes. Our results demonstrate that these encapsulation devices can protect from an immune-mediated attack and can contain a sufficient amount of insulin-producing cells to prevent overt hyperglycemia.

Is pancreatic polypeptide response to food ingestion a reliable index of vagal function in type 1 diabetes?

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Damholt, M B; Arlien-Soeborg, P; Hilsted, L

2006-01-01

The diagnosis of autonomic neuropathy in diabetic patients is based on cardiovascular reflex tests. Since cardiac function may be affected by arteriosclerosis and cardiomyopathy in type 1 diabetes mellitus, alternative tests reflecting vagal nerve function, in other organ systems, are needed....... In this study the pancreatic polypeptide (PP) response to a mixed meal was evaluated in healthy subjects and in recently diagnosed type 1 diabetic patients....

Single Cell Dissection of Human Pancreatic Islet Dysfunction in Diabetes

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2017-06-01

of memory T cells , innate cells and the differentiation potential of naive T cells during ME/CFS; and 3) To determine the T cell and innate cell ...apoptosis and the innate immune response in human pancreatic β- cells . Diabetes 64: 3808–3817. Marselli L, Thorne J, Dahiya S, Sgroi DC, Sharma A, Bonner-Weir...interactive nature of CellView aids in cell doublet identification. In the PBMC data, ‘Subcluster-analysis’ reveals a mixture of lymphoid and myeloid

Downregulation of Type II Diabetes Mellitus and Maturity Onset Diabetes of Young Pathways in Human Pancreatic Islets from Hyperglycemic Donors

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Jalal Taneera

2014-01-01

Full Text Available Although several molecular pathways have been linked to type 2 diabetes (T2D pathogenesis, it is uncertain which pathway has the most implication on the disease. Changes in the expression of an entire pathway might be more important for disease pathogenesis than changes in the expression of individual genes. To identify the molecular alterations in T2D, DNA microarrays of human pancreatic islets from donors with hyperglycemia n=20 and normoglycemia n=58 were subjected to Gene Set Enrichment Analysis (GSEA. About 178 KEGG pathways were investigated for gene expression changes between hyperglycemic donors compared to normoglycemic. Pathway enrichment analysis showed that type II diabetes mellitus (T2DM and maturity onset diabetes of the young (MODY pathways are downregulated in hyperglycemic donors, while proteasome and spliceosome pathways are upregulated. The mean centroid of gene expression of T2DM and MODY pathways was shown to be associated positively with insulin secretion and negatively with HbA1c level. To conclude, downregulation of T2DM and MODY pathways is involved in islet function and might be involved in T2D. Also, the study demonstrates that gene expression profiles from pancreatic islets can reveal some of the biological processes related to regulation of glucose hemostats and diabetes pathogenesis.

Paracrine GABA and insulin regulate pancreatic alpha cell proliferation in a mouse model of type 1 diabetes.

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Feng, Allen L; Xiang, Yun-Yan; Gui, Le; Kaltsidis, Gesthika; Feng, Qingping; Lu, Wei-Yang

2017-06-01

This study aimed to elucidate the mechanism of increased proliferation of alpha cells in recent-onset type 1 diabetes. Pancreatic beta cells express GAD and produce γ-aminobutyric acid (GABA), which inhibits alpha cell secretion of glucagon. We explored the roles of GABA in alpha cell proliferation in conditions corresponding to type 1 diabetes in a mouse model and in vitro. Type 1 diabetes was induced by injecting the mice with streptozotocin (STZ). Some of the STZ-injected mice were treated with GABA (10 mg/kg daily) for 12 days. Isolated pancreatic islets were treated with STZ or STZ together with GABA for 2 days. The effects of GABA treatment on STZ-induced alpha cell proliferation in vivo and in vitro were assessed. The effect of muscimol, a GABA receptor agonist, on αTC1-6 cell proliferation was also examined. STZ injection substantially decreased levels of GAD, GABA and insulin in pancreatic beta cells 12 h after injection; this was followed by an upsurge of phosphorylated mechanistic target of rapamycin (p-mTOR) in the alpha cells at day 1, and a significant increase in alpha cell mass at day 3. Treating STZ-injected mice with GABA largely restored the immunodetectable levels of insulin and GAD in the beta cells and significantly decreased the number of aldehyde dehydrogenase 1 family, member A3 (ALDH1a3)-positive cells, alpha cell mass and hyperglucagonaemia. STZ treatment also increased alpha cell proliferation in isolated islets, which was reversed by co-treatment with GABA. Muscimol, together with insulin, significantly lowered the level of cytosolic Ca 2+ and p-mTOR, and decreased the proliferation rate of αTC1-6 cells. GABA signalling critically controls the alpha cell population in pancreatic islets. Low intraislet GABA may contribute to alpha cell hyperplasia in early type 1 diabetes.

Pancreatic nitric oxide and oxygen free radicals in the early stages of streptozotocin-induced diabetes mellitus in the rat

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González E.

2000-01-01

Full Text Available The objective of the present study was to explore the regulatory mechanisms of free radicals during streptozotocin (STZ-induced pancreatic damage, which may involve nitric oxide (NO production as a modulator of cellular oxidative stress. Removal of oxygen species by incubating pancreatic tissues in the presence of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD (1 U/ml produced a decrease in nitrite levels (42% and NO synthase (NOS activity (50% in diabetic but not in control samples. When NO production was blocked by N G-monomethyl-L-arginine (L-NMMA (600 µM, SOD activity increased (15.21 ± 1.23 vs 24.40 ± 2.01 U/mg dry weight. The increase was abolished when the NO donor, spermine nonoate, was added to the incubating medium (13.2 ± 1.32. Lipid peroxidation was lower in diabetic tissues when PEG-SOD was added (0.40 ± 0.02 vs 0.20 ± 0.03 nmol/mg protein, and when L-NMMA blocked NOS activity in the incubating medium (0.28 ± 0.05; spermine nonoate (100 µM abolished the decrease in lipoperoxide level (0.70 ± 0.02. We conclude that removal of oxygen species produces a decrease in pancreatic NO and NOS levels in STZ-treated rats. Moreover, inhibition of NOS activity produces an increase in SOD activity and a decrease in lipoperoxidation in diabetic pancreatic tissues. Oxidative stress and NO pathway are related and seem to modulate each other in acute STZ-induced diabetic pancreas in the rat.

Pancreatic Islet Protein Complexes and Their Dysregulation in Type 2 Diabetes

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Pedersen, Helle Krogh; Gudmundsdottir, Valborg; Brunak, Søren

2017-01-01

Type 2 diabetes (T2D) is a complex disease that involves multiple genes. Numerous risk loci have already been associated with T2D, although many susceptibility genes remain to be identified given heritability estimates. Systems biology approaches hold potential for discovering novel T2D genes...... by considering their biological context, such as tissue-specific protein interaction partners. Pancreatic islets are a key T2D tissue and many of the known genetic risk variants lead to impaired islet function, hence a better understanding of the islet-specific dysregulation in the disease-state is essential...... to unveil the full potential of person-specific profiles. Here we identify 3,692 overlapping pancreatic islet protein complexes (containing 10,805 genes) by integrating islet gene and protein expression data with protein interactions. We found 24 of these complexes to be significantly enriched for genes...

UNDERSTANDING THE INTERNATIONAL CONSENSUS FOR ACUTE PANCREATITIS: CLASSIFICATION OF ATLANTA 2012.

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Souza, Gleim Dias de; Souza, Luciana Rodrigues Queiroz; Cuenca, Ronaldo Máfia; Jerônimo, Bárbara Stephane de Medeiros; Souza, Guilherme Medeiros de; Vilela, Vinícius Martins

2016-01-01

Contrast computed tomography and magnetic resonance imaging are widely used due to its image quality and ability to study pancreatic and peripancreatic morphology. The understanding of the various subtypes of the disease and identification of possible complications requires a familiarity with the terminology, which allows effective communication between the different members of the multidisciplinary team. Demonstrate the terminology and parameters to identify the different classifications and findings of the disease based on the international consensus for acute pancreatitis ( Atlanta Classification 2012). Search and analysis of articles in the "CAPES Portal de Periódicos with headings "acute pancreatitis" and "Atlanta Review". Were selected 23 articles containing radiological descriptions, management or statistical data related to pathology. Additional statistical data were obtained from Datasus and Population Census 2010. The radiological diagnostic criterion adopted was the Radiology American College system. The "acute pancreatitis - 2012 Rating: Review Atlanta classification and definitions for international consensus" tries to eliminate inconsistency and divergence from the determination of uniformity to the radiological findings, especially the terminology related to fluid collections. More broadly as "pancreatic abscess" and "phlegmon" went into disuse and the evolution of the collection of patient fluids can be described as "acute peripancreatic collections", "acute necrotic collections", "pseudocyst" and "necrosis pancreatic walled or isolated". Computed tomography and magnetic resonance represent the best techniques with sequential images available for diagnosis. Standardization of the terminology is critical and should improve the management of patients with multiple professionals care, risk stratification and adequate treatment. A tomografia computadorizada contrastada e a ressonância magnética são exames amplamente utilizados no estudo da

Hereditary chronic pancreatitis

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Mössner Joachim

2007-01-01

Full Text Available Abstract Hereditary chronic pancreatitis (HCP is a very rare form of early onset chronic pancreatitis. With the exception of the young age at diagnosis and a slower progression, the clinical course, morphological features and laboratory findings of HCP do not differ from those of patients with alcoholic chronic pancreatitis. As well, diagnostic criteria and treatment of HCP resemble that of chronic pancreatitis of other causes. The clinical presentation is highly variable and includes chronic abdominal pain, impairment of endocrine and exocrine pancreatic function, nausea and vomiting, maldigestion, diabetes, pseudocysts, bile duct and duodenal obstruction, and rarely pancreatic cancer. Fortunately, most patients have a mild disease. Mutations in the PRSS1 gene, encoding cationic trypsinogen, play a causative role in chronic pancreatitis. It has been shown that the PRSS1 mutations increase autocatalytic conversion of trypsinogen to active trypsin, and thus probably cause premature, intrapancreatic trypsinogen activation disturbing the intrapancreatic balance of proteases and their inhibitors. Other genes, such as the anionic trypsinogen (PRSS2, the serine protease inhibitor, Kazal type 1 (SPINK1 and the cystic fibrosis transmembrane conductance regulator (CFTR have been found to be associated with chronic pancreatitis (idiopathic and hereditary as well. Genetic testing should only be performed in carefully selected patients by direct DNA sequencing and antenatal diagnosis should not be encouraged. Treatment focuses on enzyme and nutritional supplementation, pain management, pancreatic diabetes, and local organ complications, such as pseudocysts, bile duct or duodenal obstruction. The disease course and prognosis of patients with HCP is unpredictable. Pancreatic cancer risk is elevated. Therefore, HCP patients should strongly avoid environmental risk factors for pancreatic cancer.

Fecal pancreatic elastase-1 levels in older individuals without known gastrointestinal diseases or diabetes mellitus

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Idziak Joanna

2011-01-01

Full Text Available Abstract Background Structural changes occur in the pancreas as a part of the natural aging process. With aging, also the incidence of maldigestive symptoms and malnutrition increases, raising the possibility that these might be caused at least in part by inadequate pancreatic enzyme secretion due to degenerative processes and damage of the gland. Fecal elastase-1 is a good marker of pancreatic exocrine secretion. The aim of this study was to investigate the fecal elastase-1 levels among over 60 years old Finnish and Polish healthy individuals without any special diet, known gastrointestinal disease, surgery or diabetes mellitus. Methods A total of 159 patients participated in this cross-sectional study. 106 older individuals (aged 60-92 years were recruited from outpatient clinics and elderly homes. They were divided to three age groups: 60-69 years old (n = 31; 70-79 years old (n = 38 and over 80 years old (n = 37. 53 young subjects (20-28 years old were investigated as controls. Inclusion criteria were age over 60 years, normal status and competence. Exclusion criteria were any special diet, diabetes mellitus, any known gastrointestinal disease or prior gastrointestinal surgery. Fecal elastase-1 concentration was measured from stool samples with an ELISA that uses two monoclonal antibodies against different epitopes of human elastase-1. Results Fecal elastase-1 concentrations correlated negatively with age (Pearson r = -0,3531, P P Conclusion In our study one fifth of healthy older individuals without any gastrointestinal disorder, surgery or diabetes mellitus suffer from pancreatic exocrine insufficiency and might benefit from enzyme supplementation therapy.

Amelioration of pancreatic and renal derangements in streptozotocin-induced diabetic rats by polyphenol extracts of Ginger (Zingiber officinale) rhizome.

Science.gov (United States)

Kazeem, Mutiu Idowu; Akanji, Musbau Adewunmi; Yakubu, Musa Toyin

2015-12-01

Free and bound polyphenol extracts of Zingiber officinale rhizome were investigated for their antidiabetic potential in the pancreatic and renal tissues of diabetic rats at a dose of 500mg/kg body weight. Forty Wistar rats were completely randomized into five groups: A-E consisting of eight animals each. Group A (control) comprises normal healthy animals and were orally administered 1.0mL distilled water on a daily basis for 42 days while group B-E were made up of 50mg/kg streptozotocin (STZ)-induced diabetic rats. Group C and D received 1.0mL 500mg/kg body weight free and bound polyphenol extracts respectively while group E received 1.0mL 0.6mg/kg of glibenclamide. Administration of the extracts to the diabetic rats significantly reduced (pZingiber officinale could ameliorate diabetes-induced pancreatic and renal derangements in rats. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells

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Lingling Jia

2017-10-01

Full Text Available Recent evidence indicates that indigenous Clostridium species induce colonic regulatory T cells (Tregs, and gut lymphocytes are able to migrate to pancreatic islets in an inflammatory environment. Thus, we speculate that supplementation with the well-characterized probiotics Clostridium butyricum CGMCC0313.1 (CB0313.1 may induce pancreatic Tregs and consequently inhibit the diabetes incidence in non-obese diabetic (NOD mice. CB0313.1 was administered daily to female NOD mice from 3 to 45 weeks of age. The control group received an equal volume of sterile water. Fasting glucose was measured twice a week. Pyrosequencing of the gut microbiota and flow cytometry of mesenteric lymph node (MLN, pancreatic lymph node (PLN, pancreatic and splenic immune cells were performed to investigate the effect of CB0313.1 treatment. Early oral administration of CB0313.1 mitigated insulitis, delayed the onset of diabetes, and improved energy metabolic dysfunction. Protection may involve increased Tregs, rebalanced Th1/Th2/Th17 cells and changes to a less proinflammatory immunological milieu in the gut, PLN, and pancreas. An increase of α4β7+ (the gut homing receptor Tregs in the PLN suggests that the mechanism may involve increased migration of gut-primed Tregs to the pancreas. Furthermore, 16S rRNA gene sequencing revealed that CB0313.1 enhanced the Firmicutes/Bacteroidetes ratio, enriched Clostridium-subgroups and butyrate-producing bacteria subgroups. Our results provide the basis for future clinical investigations in preventing type 1 diabetes by oral CB0313.1 administration.

Elevation of serum pancreatic amylase and distortion of pancreatic ...

African Journals Online (AJOL)

Background: Diabetes mellitus has been shown to cause severe impairment in exocrine pancreatic function and cyto-architecture. Ocimum grattissimum has been reported to lower blood glucose levels in experimental diabetic animals. This study, therefore, aims to investigate if treatment with O. grattissimum can alleviate ...

Endocrine pancreatic function changes after acute pancreatitis.

Science.gov (United States)

Wu, Deqing; Xu, Yaping; Zeng, Yue; Wang, Xingpeng

2011-10-01

This study aimed to investigate the impairment of pancreatic endocrine function and the associated risk factors after acute pancreatitis (AP). Fifty-nine patients were subjected to tests of pancreatic function after an attack of pancreatitis. The mean time after the event was 3.5 years. Pancreatic endocrine function was evaluated by fasting blood glucose (FBG), glycosylated hemoglobin, fasting blood insulin, and C-peptide. Homeostasis model assessment was used to evaluate insulin resistance and islet β-cell function. Pancreatic exocrine function was evaluated by fecal elastase 1. Factors that could influence endocrine function were also investigated. Nineteen patients (32%) were found to have elevated FBG, whereas 5 (8%) had abnormal glycosylated hemoglobin levels. The levels of FBG, fasting blood insulin, and C-peptide were higher in patients than in controls (P endocrine insufficiency. Pancreatic exocrine functional impairment was found at the same time. Endocrine functional impairment with insulin resistance was found in patients after AP. Obesity, hyperlipidemia, and diabetes-related symptoms increased the likelihood of developing functional impairment after AP.

β-Cell regeneration through the transdifferentiation of pancreatic cells: Pancreatic progenitor cells in the pancreas.

Science.gov (United States)

Kim, Hyo-Sup; Lee, Moon-Kyu

2016-05-01

Pancreatic progenitor cell research has been in the spotlight, as these cells have the potential to replace pancreatic β-cells for the treatment of type 1 and 2 diabetic patients with the absence or reduction of pancreatic β-cells. During the past few decades, the successful treatment of diabetes through transplantation of the whole pancreas or isolated islets has nearly been achieved. However, novel sources of pancreatic islets or insulin-producing cells are required to provide sufficient amounts of donor tissues. To overcome this limitation, the use of pancreatic progenitor cells is gaining more attention. In particular, pancreatic exocrine cells, such as duct epithelial cells and acinar cells, are attractive candidates for β-cell regeneration because of their differentiation potential and pancreatic lineage characteristics. It has been assumed that β-cell neogenesis from pancreatic progenitor cells could occur in pancreatic ducts in the postnatal stage. Several studies have shown that insulin-producing cells can arise in the duct tissue of the adult pancreas. Acinar cells also might have the potential to differentiate into insulin-producing cells. The present review summarizes recent progress in research on the transdifferentiation of pancreatic exocrine cells into insulin-producing cells, especially duct and acinar cells.

PROSPECTS OF APPLICATION OF TISSUE-ENGINEERED PANCREATIC CONSTRUCTS IN THE TREATMENT OF TYPE 1 DIABETES

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G. N. Skaletskaya

2016-01-01

Full Text Available Allotransplantation of pancreatic islets remains the most effective method of treatment of diabetes mellitus type 1 being capable under combination of favorable conditions (suffi cient number of isolated islets, effective combination of immunosuppressive drugs to reach the recipients’ insulin independence for several years. However, the overwhelming shortage of donor pancreas and limited post-transplantation islet survival do not allow increasing the number of such transplants and their effectiveness. This review presents a critical analysis of the work done by Russian and foreign authors onto creation of tissue-engineered pancreatic constructs that may lead to the resolution of the three main pancreatic islet transplantation issues: 1 lack of donor material; 2 necessity of immunosuppressive therapy; 3 limited survival and functional activity of the islet.

Effects of acute exercise on pancreatic endocrine function in subjects with type 2 diabetes

DEFF Research Database (Denmark)

Knudsen, Sine H; Karstoft, Kristian; Winding, Kamilla

2015-01-01

We determined the effects of exercise on pancreatic endocrine responses to metabolic stimuli in type 2 diabetic (T2D) subjects and examined the influence of the diabetic status. Fourteen subjects underwent a hyperglycaemic clamp with GLP-1 infusion and arginine injection, the morning after a one.......05-P arginine (P = 0.08). The same trends were seen for low HbA1c subjects. Furthermore, exercise increased GLP-1- and arginine-stimulated insulin secretion (P diabetic......-hour walk or no exercise. Subjects were stratified by high and low quantiles of fasting plasma glucose (FPG) and HbA1c as well as current use/non-use of anti-diabetic medication. In the entire cohort, exercise did not alter insulin secretion, while glucagon levels were increased in all clamp phases (P 

Adverse drug reactions associated with the use of liraglutide in patients with type 2 diabetes - focus on pancreatitis and pancreas cancer

DEFF Research Database (Denmark)

Chalmer, Thor; Almdal, Thomas P; Vilsbøll, Tina

2014-01-01

Introduction: The glucagon-like peptide-1 (GLP-1) receptor agonist, liraglutide , is a widely used drug for the treatment of type 2 diabetes. Liraglutide is one of several incretin-based agents that have been suggested to be associated with pancreatitis and pancreas cancer. The suspicion accelera......Introduction: The glucagon-like peptide-1 (GLP-1) receptor agonist, liraglutide , is a widely used drug for the treatment of type 2 diabetes. Liraglutide is one of several incretin-based agents that have been suggested to be associated with pancreatitis and pancreas cancer. The suspicion....... However, a recently published analysis suggests a trend toward a slightly elevated risk of pancreatitis with GLP-1 receptor agonists (including liraglutide), which may become statistical significant as more data become available. Well-established side effects are of gastrointestinal origin, typical mild...

Changes in pancreatic somatostatin content in spontaneously diabetic mice, as determined by radioimmunoassay and immunohistochemical methods

International Nuclear Information System (INIS)

Makino, H.; Matsushima, Y.; Kanatsuka, A.; Yamamoto, M.; Kumagai, A.; Nishimura, M.

1979-01-01

A specific RIA for somatostatin (SRIF) was used to determine the SRIF content of the pancreas and hypothalamus in spontaneously diabetic C57BL/KsJ dbdb and C57BL/6J obob mice. In addition, SRIF- and glucagon-containing cells were examined in the pancreatic islets with an immunohistochemical technique. In dbdb mice, immunoassayable pancreatic SRIF content was increased, as was the number of SRIF- or glucagon-containing cells. In obob mice, immunoassayable pancreatic SRIF content was also increased, but no increase was noted in the number of SRIF- or glucagon-containing cells. The hypothalamic SRIF content of either strain was not different from that of controls. These results regarding pancreatic SRIF content were in accord with some but not all previous reports. These differences may be related to the age of the mice or to the conditions in which they were bred. The pancreatic SRIF increase in both dbdb and obob mice may be attributable to hyperglucagonemia, hyperglycemia, or a decrease in insulin action. Further work is necessary to clearly delineate the mechanism

El problema Patogénico de las Pancreatitis Agudas. Lesiones producidas por la Etionina.

OpenAIRE

Pera Blanco-Morales, Cristóbal

2016-01-01

Cuando en el año 1952 realizamos una extensa revisión del problema de la necrosis aguda del páncreas, conveníamos en que eran tres las razones que justifican el gran interés que el estudio de esta afección conserva en la actualidad: a) Las dudas existentes acerca de su etiología y patogénesis. b) La extraordinaria gravedad del proceso que conduce a la muerte en una elevada proporción de casos. c) La incertidumbre sobre cua...

Reduced insulin exocytosis in human pancreatic β-cells with gene variants linked to type 2 diabetes

DEFF Research Database (Denmark)

Rosengren, Anders H; Braun, Matthias; Mahdi, Taman

2012-01-01

The majority of genetic risk variants for type 2 diabetes (T2D) affect insulin secretion, but the mechanisms through which they influence pancreatic islet function remain largely unknown. We functionally characterized human islets to determine secretory, biophysical, and ultrastructural features ...

Acute Pancreatitis Secondary to Diabetic Ketoacidosis Induced Hypertriglyceridemia in a Young Adult with Undiagnosed Type 2 Diabetes

OpenAIRE

Animesh A Singla; Francis Ting; Apresh Singla

2015-01-01

Context The triad of acute pancreatitis, hypertriglyceridemia and diabetes is a rare occurrence. Case report A previously well 19-year-old male presented to the emergency department with 24-hour history of epigastric pain, associated with polyuria and nausea. Biochemical markers showed the presence of hyperglycemia (blood sugar level 15 mmol/L) and ketonemia (5.3 mmol/L). Further investigation revealed severe hypertriglyceridemia (4009 mg/dL) and elevated lipase (1,714 U/L). Abdominal ultraso...

Endocrine pancreatic insufficiency secondary to chronic herpesvirus pancreatitis in a cockatiel (Nymphicus hollandicus).

Science.gov (United States)

Phalen, David N; Falcon, Michelle; Tomaszewski, Elizabeth K

2007-06-01

A cockatiel (Nymphicus hollandicus) examined because of weight loss, polydipsia, and polyuria was diagnosed with diabetes mellitus based on the presence of glucosuria and marked hyperglycemia. Medical attempts to manage the diabetes mellitus were unsuccessful, and the bird was euthanatized. Histopathologic examination of the pancreas revealed a chronic active pancreatitis with herpesviral inclusions in many of the pancreatic acinar and duct cells. Psittacid herpesvirus-1 (PsHV-1) DNA was amplified from the lesion by polymerase chain reaction. Sequencing of the amplicon showed it to be the genotype 1 variant, which is most commonly associated with Pacheco's disease, an acute rapidly fatal systemic infection. The findings in this case suggest that the PsHV-1 genotype may also cause a localized disease of the pancreas. Infection with this virus should be considered as a differential diagnosis in birds with pancreatitis with or without diabetes mellitus.

Beetle (Ulomoides dermestoides) fat improves diabetes: effect on liver and pancreatic architecture and on PPARγ expression

OpenAIRE

Jasso-Villagomez, E.I.; Garcia-Lorenzana, M.; Almanza-Perez, J.C.; Fortis-Barrera, M.A.; Blancas-Flores, G.; Roman-Ramos, R.; Prado-Barragan, L.A.; Alarcon-Aguilar, F.J.

2018-01-01

Ulomoides dermestoides is a beetle traditionally consumed to treat diabetes. In this study, we performed a composition analysis of U. dermestoides to obtain the principal fractions, which were used to assess the effect on glycemia, liver and pancreatic architecture, and PPARγ and GLUT4 expression. Normal mice and alloxan-induced diabetic mice were administered fractions of chitin, protein or fat, and the acute hypoglycemic effect was evaluated. A subacute study involving daily administration ...

Oxidative stress is enhanced by hypothermia imposed on cerulein-induced pancreatitis in rats Aumento do estresse oxidativo após hipotermia em ratos com pancreatite induzida por ceruleína

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Wellington Andraus

2007-01-01

Full Text Available BACKGROUND: Hypothermia is a frequent event in severe acute pancreatitis (AP and its real effects on the normal pancreas have not been well demonstrated. Moreover, neither have its effects on the outcome of acute pancreatitis been fully investigated. One hypothesis is that oxidative stress may be implicated in lesions caused or treated by hypothermia. AIM OF THE STUDY: To investigate the effect of hypothermia in cerulein-induced acute pancreatitis (CIAP in rats and the role played by oxidative stress in this process. METHODS: Male Wistar rats were divided into hypothermic and normothermic groups. Hypothermia was induced with a cold mattress and rectal temperature was kept at 30ºC for one hour. Acute pancreatitis was induced with 2 doses of cerulein (20 ìg/kg administered at a one-hour interval. Serum amylase, pancreas vascular permeability by Evan's blue method, pancreas wet-to-dry weight ratio and histopathology were analyzed in each group. RESULTS: When compared with normothermic rats, hypothermic animals, with cerulein-induced acute pancreatitis, showed higher levels of pancreatic vascular permeability (p BACKGROUND: Hipotermia é um evento freqüente em episódios de pancreatite aguda, contudo seu efeito real sobre pâncreas normal ainda não esta bem demonstrado. Além do mais, o efeito da hipotermia no decorrer da pancreatite aguda também não está completamente esclarecido. Uma das hipóteses sobre as causas das lesões causadas ou tratadas por hipotermia aventa a implicação de estresse oxidativo. OBJETIVOS: Investigar o efeito da hipotermia em ratos com pancreatite aguda induzida por ceruleína e o papel do estresse oxidativo neste processo. MÉTODOS: Ratos Wistar machos foram divididos em grupos hipotérmicos e normotérmicos. Hipotermia foi induzida com uma bolsa gelada de forma que a temperatura retal permanecesse em 30ºC por uma hora. Pancreatite aguda foi induzida com duas aplicações de ceruleína (20 ìg/kg administradas

Jiang Tang Xiao Ke Granule Play an Anti-diabetic Role in Diabetic Mice Pancreatic Tissue by Regulating the mRNAs and MicroRNAs Associated with PI3K-Akt Signaling Pathway

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Fang-Fang Mo

2017-11-01

Full Text Available Purpose: To investigate the effect of JTXK granule on the expression pattern of miRNA in pancreatic tissue of KKAy diabetic mice, and to explore the molecular mechanism and pathways of JTXK granule in anti-diabetic effect.Methods: We used high fat diet (HFD to induce the KKAy diabetic mice and screened the differentially expressed miRNAs (DEMs between JTXK-treated group (n = 6 and the diabetic group (n = 6 using MicroRNA (miRNA Microarray. C57BL/6J mice were given a normal diet as the control group (n = 6. Subsequently, miRNA target gene prediction, GO and Pathway analysis were used to explore the function of DEMs. Finally, the mechanism of anti-diabetic effects of JTXK granule was tested by in vitro INS-1 pancreatic β-cell experiment.Results: The blood glucose and body weight of JTXK-treated group was significantly lower compared with the model group. Moreover, a total of 45 miRNAs with significant differences were detected in the model group and the JTXK-treated group (P ≤ 0.05, Fold Change > 2. Further, miRNA-mRNA analysis showed that the differential expression of mmu-miR-192-5p, mmu-miR-291a-3p, mmu-miR-320-3p, mmu-miR-139-5p and mmu-miR-378a-3p are closely related to pancreatic histological changes. In addition, pathway analysis showed that the DEMs were closely related to PI3K-Akt Signaling Pathway. Furthermore, the levels of serine/threonine-protein kinase (Akt, phosphorylated Akt (p-Akt and phosphorylated forkhead transcription factor O1 (p-Foxo1 in INS-1-FOXO1 overexpressing model cells were lower than those in normal group, while JTXK granules could increase the expression of Akt, p-Akt and p-Foxo1.Conclusions: The results showed that JTXK granule could play an anti-diabetic role by regulating the mRNA and miRNAs associated with PI3K-Akt pathway in diabetic mice pancreatic tissue.

Obesity adversely affects survival in pancreatic cancer patients.

Science.gov (United States)

McWilliams, Robert R; Matsumoto, Martha E; Burch, Patrick A; Kim, George P; Halfdanarson, Thorvardur R; de Andrade, Mariza; Reid-Lombardo, Kaye; Bamlet, William R

2010-11-01

Higher body-mass index (BMI) has been implicated as a risk factor for developing pancreatic cancer, but its effect on survival has not been thoroughly investigated. The authors assessed the association of BMI with survival in a sample of pancreatic cancer patients and used epidemiologic and clinical information to understand the contribution of diabetes and hyperglycemia. A survival analysis using Cox proportional hazards by usual adult BMI was performed on 1861 unselected patients with pancreatic adenocarcinoma; analyses were adjusted for covariates that included clinical stage, age, and sex. Secondary analyses incorporated self-reported diabetes and fasting blood glucose in the survival model. BMI as a continuous variable was inversely associated with survival from pancreatic adenocarcinoma (hazard ratio [HR], 1.019 for each increased unit of BMI [kg/m2], PFasting blood glucose and diabetes did not affect the results. Higher BMI is associated with decreased survival in pancreatic cancer. Although the mechanism of this association remains undetermined, diabetes and hyperglycemia do not appear to account for the observed association. Copyright © 2010 American Cancer Society.

Stages of Pancreatic Cancer

Science.gov (United States)

... overweight. Having a personal history of diabetes or chronic pancreatitis . Having a family history of pancreatic cancer or ... have not started treatment. Five types of standard treatment are used: Surgery ... Whipple procedure : A surgical procedure in which the head of the pancreas , ...

Notas sobre apendicitis aguda

OpenAIRE

Méndez S., Martín

2011-01-01

Hacer un buen diagnóstico, tener el valor de la responsabilidad operando precozmente los enfermos, en los cuales después de minucioso examen se cree o se tiene certeza de una apendicitis aguda, es uno de los méritos de todo buen cirujano. Sin duda tendrá que luchar contra todo, la familia, el enfermo y los allegados; pero si triunfa y vence logrará éxitos y salvará vidas. Parece fácil diagnosticar unaapendicitis aguda y sin embargo, es necesario decirlo claro, nada hay tan complicado y en oca...

Pancreatic effect of andrographolide isolated from Andrographis paniculata (Burm. f.) Nees.

Science.gov (United States)

Nugroho, Agung Endro; Rais, Ichwan Ridwan; Setiawan, Iwan; Pratiwi, Pramita Yuli; Hadibarata, Tony; Tegar, Maulana; Pramono, Suwidjiyo

2014-01-01

Andrographis paniculata (Burm. f.) Nees is a plant that originates from India and grows widely to Southeast which used for several purposes mainly as treatment of diabetes mellitus so the aim of this study was evaluate andrographolide for its pancreatic effect in neonatal streptozotocin (STZ)-induced diabetic rats, a model of type 2 diabetic rats. Diabetic condition was induced with an intraperitoneal injection of 90 mg kg(-1) streptozotocin in two-day-old rats. After three months, the neonatal STZ-induced diabetic rats were treated with andrographolide or andrographolide-enriched extract of A. paniculata (AEEAP) for 8 consecutive days. Pancreatic effect was evaluated by estimating mainly the preprandial and postprandial blood glucose levels and other parameters such as morphology of pancreatic islet, beta cells density and morphology and immunohistochemically pancreatic insulin. Andrographolide significantly (p < 0.05) decreased the levels of blood glucose and improved diabetic rat islet and beta cells. However, AEEAP exhibited moderate hypoglycaemic effects on the blood glucose levels. Moderate changes in beta cells were observed after AEEAP treatment. They could restore decreasing of pancreatic insulin contents. Based on these results andrographolide and AEEAP exhibited pancreatic actions in neonatal STZ-induced diabetic rats. The activity of andrographolide was more effective than this of AEEAP.

Leucemia congénita aguda

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Nilvia Esther González García

2011-06-01

Full Text Available La leucemia aguda durante el período neonatal es poco frecuente de evolución rápida y pronóstico sombrío. Sus características clínicas y biológicas difieren de las encontradas en niños de mayor edad, y su inicio se caracteriza por afectación cutánea, hepatoesplenomegalia, hiperleucocitosis e infiltración del sistema nervioso central. Se han observado pacientes con formas tanto mieloides como linfoides, pero la leucemia mieloide aguda parece predominar en esta etapa de la vida. Se presenta el caso de un paciente con leucemia congénita clasificada morfológicamente, con aparición de manifestaciones clínicas de enfermedad hematológica desde el nacimiento y diagnóstico de leucemia linfoblástica aguda congénita.

A role of pancreatic stellate cells in islet fibrosis and β-cell dysfunction in type 2 diabetes mellitus

International Nuclear Information System (INIS)

Lee, Esder; Ryu, Gyeong Ryul; Ko, Seung-Hyun; Ahn, Yu-Bae; Song, Ki-Ho

2017-01-01

Objectives: To investigate whether the activation of pancreatic stellate cells (PSCs) leads to pancreatic β-cell dysfunction in type 2 diabetes mellitus (T2DM). Methods: The pancreases of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an animal model of T2DM, and patient with T2DM were analyzed. And the in vitro and in vivo effects of pirfenidone, an antifibrotic agent, on PSC activation, islet fibrosis, and β-cells were studied. Results: The extent of islet fibrosis and the percentage of activated PSCs, positive for α-smooth muscle actin, in the islets were significantly greater in OLETF rats compared with non-diabetic rats. Also, the extent of islet fibrosis in patients with T2DM was slightly greater compared with age- and BMI-matched non-diabetic patients. In rat PSCs cultured with high glucose for 72 h, pirfenidone produced decreases in cell proliferation, release of collagen, and the expression of fibronectin and connective tissue growth factor. Treatment of OLETF rats with pirfenidone for 16 weeks decreased the activation of PSCs and the extent of islet fibrosis, but did not enhance glucose tolerance, pancreatic insulin content, or β-cell mass. Conclusions: Activated PSCs in islets might lead to islet fibrosis in T2DM. However, PSC activation itself might not contribute significantly to progressive β-cell failure in T2DM. - Highlights: • Islet fibrosis developed progressively in OLETF rats, a model of type 2 diabetes. • PSCs in the islets became activated in OLETF rats. • Islet fibrosis was increased in patients with type 2 diabetes. • Pirfenidone attenuated the activation of PSCs and islet fibrosis in OLETF rats. • Pirfenidonet had no effects on glucose tolerance or on β-cells in OLETF rats.

An update on pancreatic pathophysiology (do we have to rewrite pancreatic pathophysiology?).

Science.gov (United States)

Hammer, Heinz F

2014-02-01

This review focuses on seven aspects of physiology and pathophysiology of the exocrine pancreas that have been intensively discussed and studied within the past few years: (1) the role of neurohormonal mechanisms like melatonin, leptin, or ghrelin in the stimulation of pancreatic enzyme secretion; (2) the initiation processes of acute pancreatitis, like fusion of zymogen granules with lysosomes leading to intracellular activation of trypsinogen by the lysosomal enzyme cathepsin B, or autoactivation of trypsinogen; (3) the role of genes in the pathogenesis of acute pancreatitis; (4) the role of alcohol and constituents of alcoholic beverages in the pathogenesis of acute pancreatitis; (5) the role of pancreatic hypertension, neuropathy, and central mechanisms for the pathogenesis of pain in chronic pancreatitis; (6) the relation between exocrine pancreatic function and diabetes mellitus; and (7) pathophysiology, diagnosis and treatment of pancreatic steatorrhea.

Determinants of exocrine pancreatic function as measured by fecal elastase-1 concentrations (FEC in patients with diabetes mellitus

Directory of Open Access Journals (Sweden)

Ewald N

2009-03-01

Full Text Available Abstract Objective Recently it has been shown that there is not only endocrine insufficiency in diabetic patients, but a frequent co-morbidity of both, the endocrine and exocrine pancreas. The present study was performed to further analyse the determinants of exocrine pancreatic function in patients with diabetes mellitus. Methods The records of 1992 patients with diabetes mellitus who had been treated in our hospital during a 2-year period were re-evaluated. Defined parameters were documented in standardized data sheets. Records were further checked for the results of imaging procedures of the pancreas. In 307 patients FEC had been performed and documented. Only these patients were included in further evaluation. Results FEC was inversely correlated with diabetes duration and HbA1c-levels but not with age. C-peptide levels correlated positively with FEC. BMI and FEC were also significantly correlated. There was no correlation between diabetes therapy and exocrine pancreatic function as there was no correlation with any concomitant medication. The presence of diabetes-associated antibodies was not related to FEC. According to the documented data 38 were classified as type-1 diabetes (12.4%, 167 as type-2 (54.4%, and 88 patients met the diagnostic criteria of type-3 (28.7%. Fourteen patients could not be classified because of lacking information (4.6%. Conclusions Exocrine insufficiency might be explained as a complication of diabetes mellitus. However, it is more likely that type-3 diabetes is much more frequent than previously believed. Consequently the evaluation of exocrine function and morphology should be included into the clinical workup of any diabetic patient at least at the time of manifestation.

[Chronic pancreatitis diagnosed after the first attack of acute pancreatitis].

Science.gov (United States)

Bojková, Martina; Dítě, Petr; Uvírová, Magdalena; Dvořáčková, Nina; Kianička, Bohuslav; Kupka, Tomáš; Svoboda, Pavel; Klvaňa, Pavel; Martínek, Arnošt

2016-02-01

One of the diseases involving a potential risk of developing chronic pancreatitis is acute pancreatitis. Of the overall number of 231 individuals followed with a diagnosis of chronic pancreatitis, 56 patients were initially treated for acute pancreatitis (24.2 %). Within an interval of 12- 24 months from the first attack of acute pancreatitis, their condition gradually progressed to reached the picture of chronic pancreatitis. The individuals included in the study abstained (from alcohol) following the first attack of acute pancreatitis and no relapse of acute pancreatitis was proven during the period of their monitoring. The etiology of acute pancreatitis identified alcohol as the predominant cause (55.3 %), biliary etiology was proven in 35.7 %. According to the revised Atlanta classification, severe pancreatitis was established in 69.6 % of the patients, the others met the criterion for intermediate form, those with the light form were not included. Significant risk factors present among the patients were smoking, obesity and 18 %, resp. 25.8 % had pancreatogenous diabetes mellitus identified. 88.1 % of the patients with acute pancreatitis were smokers. The majority of individuals with chronic pancreatitis following an attack of acute pancreatitis were of a productive age from 25 to 50 years. It is not only acute alcoholic pancreatitis which evolves into chronic pancreatitis, we have also identified this transition for pancreatitis of biliary etiology.

The management of acute and chronic pancreatitis.

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Banks, Peter A; Conwell, Darwin L; Toskes, Phillip P

2010-02-01

Pancreatitis, which is most generally described as any inflammation of the pancreas, is a serious condition that manifests in either acute or chronic forms. Chronic pancreatitis results from irreversible scarring of the pancreas, resulting from prolonged inflammation. Six major etiologies for chronic pancreatitis have been identified: toxic/ metabolic, idiopathic, genetic, autoimmune, recurrent and severe acute pancreatitis, and obstruction. The most common symptom associated with chronic pancreatitis is pain localized to the upper-to-middle abdomen, along with food malabsorption, and eventual development of diabetes. Treatment strategies for acute pancreatitis include fasting and short-term intravenous feeding, fluid therapy, and pain management with narcotics for severe pain or nonsteroidal anti-inflammatories for milder cases. Patients with chronic disease and symptoms require further care to address digestive issues and the possible development of diabetes. Dietary restrictions are recommended, along with enzyme replacement and vitamin supplementation. More definitive outcomes may be achieved with surgical or endoscopic methods, depending on the role of the pancreatic ducts in the manifestation of disease.

Pancreatitis aguda recidivante con enteropatía por gluten asociada: Características clínico-analíticas y evolutivas en 34 pacientes Relapsing acute pancreatitis associated with gluten enteropathy: Clinical, laboratory, and evolutive characteristics in thirty-four patients

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L. Rodrigo

2008-12-01

Full Text Available Objetivos: describir la frecuencia y características clínico-analíticas de la pancreatitis aguda (PA recidivante con enteropatía por gluten (EG asociada. Pacientes y métodos: estudiamos de forma prospectiva los casos de pancreatitis agudas ingresados en nuestro Servicio durante el año 2006. Registramos un total de 185 pacientes. A las formas recurrentes que fueron 40 en total (22%, les aplicamos un protocolo clínico-analítico consistente en la determinación de marcadores serológicos, genéticos y biopsias duodenales, para descartar una EG asociada. Resultados: un total de 34 pacientes (18% cumplían criterios clínico-biológicos de EG asociada (grupo 1 y se compararon con el resto de las PA no-EG (n = 161 (grupo 2. La edad media en la EG fue de 54 ± 25 años, ligeramente inferior al grupo 2, (61 ± 14 (NS. Existía un ligero predominio de mujeres (50% en el grupo 1, respecto al grupo 2 (38,5% (NS. Siete pacientes del grupo 1 (20% presentaron una PA grave, frente a 27 (17% en el grupo 2 (NS. La presencia de colelitiasis en el grupo 1, fue de 6 casos (18%, significativamente inferior a la del grupo 2, de 72 casos (45% (p Objectives: to describe the frequency and the clinical and laboratory characteristics of relapsing acute pancreatitis (AP associated with gluten enteropathy (GE. Patients and methods: we prospectively examined all acute pancreatitis cases admitted to our Department in 2006. We recorded a total of 185 patients. With recurring forms, 40 (22% in all, we used a clinical-lab protocol including serologic and genetic markers, and duodenal biopsy to rule out GE. Results: a total of 34 patients (18% met clinical-biological criteria for GE (group 1, and were compared to the remaining non-GE AP cases (n = 161 (group 2. Mean age in the GE group was 54 ± 25 years, slightly younger than group 2 (61 ± 14 (NS. There was a mild predominance of women (50% in group 1 versus group 2 (38.5% (NS. Seven patients in group 1 (20% had severe

[Pancreatic infringement exocrine and endocrine in cystic fibrosis].

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Kessler, L; Abély, M

2016-12-01

The exocrine pancreatic insufficiency affects more than 80% of cystic fibrosis (CF) infants. Pancreatic insufficiency is diagnosed by low levels of fecal elastase. An optimal caloric intake, a pancreatic enzyme treatment are the keys to maintain a good nutritional status. The fat soluble vitamins supplementation will be associated with pancreatic enzymes treatment and will be adapted to plasma levels. Iron and oligo-element deficiency such as zinc is common. The pancreatic enzymes function is not optimal in the proximal bowel: the intraluminal intestinal pH is low because of the absence of bicarbonate release by the pancreas. The use of proton pump inhibitors may improve the functionality of pancreatic enzymes treatment. New therapies such as ivacaftor in patients with a G551D mutation allows a weight gain in particular by restoring intestinal pH similar to controls. Lengthening of the life expectancy of patients with CF is accompanied by the emergence new aspects of the disease, especially diabetes, favored by pancreatic cystic fibrosis resulting in an anatomical destruction of pancreatic islets. Currently, diabetes affects a third of the patients after 20 years, and half after 30 years. Cystic fibrosis-related diabetes is a major factor of morbidity-mortality in all stages of the disease and is characterized by a preclinical phase of glucose intolerance particularly long reaching up to 10 years. Its pathophysiology combines a lack of insulin secretion, an insulin resistance secondary to chronic infection, and a decrease in the production of the GIP and GLP-1. The insulin secretion depending on the channel chlorine (Cystic Fibrosis Transmembrane conductance Regulator [CFTR]) activity at the membrane surface of insulin cell is reduced prior to the occurrence of pancreatic histological lesions. At the stage of diabetes, obtaining a normoglycemia by insulin treatment began very early allows to slow the decline of lung function and nutritional status. Given the silent

Analysis of Transcription Factors Key for Mouse Pancreatic Development Establishes NKX2-2 and MNX1 Mutations as Causes of Neonatal Diabetes in Man

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Flanagan, Sarah E.; De Franco, Elisa; Lango Allen, Hana; Zerah, Michele; Abdul-Rasoul, Majedah M.; Edge, Julie A.; Stewart, Helen; Alamiri, Elham; Hussain, Khalid; Wallis, Sam; de Vries, Liat; Rubio-Cabezas, Oscar; Houghton, Jayne A.L.; Edghill, Emma L.; Patch, Ann-Marie; Ellard, Sian; Hattersley, Andrew T.

2014-01-01

Summary Understanding transcriptional regulation of pancreatic development is required to advance current efforts in developing beta cell replacement therapies for patients with diabetes. Current knowledge of key transcriptional regulators has predominantly come from mouse studies, with rare, naturally occurring mutations establishing their relevance in man. This study used a combination of homozygosity analysis and Sanger sequencing in 37 consanguineous patients with permanent neonatal diabetes to search for homozygous mutations in 29 transcription factor genes important for murine pancreatic development. We identified homozygous mutations in 7 different genes in 11 unrelated patients and show that NKX2-2 and MNX1 are etiological genes for neonatal diabetes, thus confirming their key role in development of the human pancreas. The similar phenotype of the patients with recessive mutations and mice with inactivation of a transcription factor gene support there being common steps critical for pancreatic development and validate the use of rodent models for beta cell development. PMID:24411943

Imaging in pancreatic transplants

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Heller, Matthew T; Bhargava, Puneet

2014-01-01

Pancreatic transplantation, performed alone or in conjunction with kidney transplantation, is an effective treatment for advanced type I diabetes mellitus and select patients with type II diabetes mellitus. Following advancements in surgical technique, postoperative management, and immunosuppression, pancreatic transplantation has significantly improved the length and quality of life for patients suffering from pancreatic dysfunction. While computed tomography (CT) and magnetic resonance imaging (MRI) have more limited utility, ultrasound is the preferred initial imaging modality to evaluate the transplanted pancreas; gray-scale assesses the parenchyma and fluid collections, while Doppler interrogation assesses vascular flow and viability. Ultrasound is also useful to guide percutaneous interventions for the transplanted pancreas. With knowledge of the surgical anatomy and common complications, the abdominal radiologist plays a central role in the perioperative and postoperative evaluation of the transplanted pancreas

Exocrine and endocrine pancreatic function in 21 patients suffering from autoimmune pancreatitis before and after steroid treatment.

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Frulloni, Luca; Scattolini, Chiara; Katsotourchi, Anna Maria; Amodio, Antonio; Gabbrielli, Armando; Zamboni, Giuseppe; Benini, Luigi; Vantini, Italo

2010-01-01

Autoimmune pancreatitis (AIP) responds rapidly and dramatically to steroid therapy. The aim of this study was to evaluate pancreatic exocrine and endocrine function in patients suffering from AIP both before and after steroid therapy. Fecal elastase 1 and diabetes were evaluated before steroid therapy and within 1 month of its suspension in 21 patients (13 males and 8 females, mean age 43 +/- 16.5 years) diagnosed as having AIP between 2006 and 2008. At clinical onset, fecal elastase 1 was 107 +/- 126 microg/g stool. Thirteen patients (62%) showed severe pancreatic insufficiency (insufficiency (100-200 microg/g stool), while 4 (19%) had normal pancreatic function (>200 microg/g stool). Before steroids, diabetes was diagnosed in 5 patients (24%), all of whom had very low levels of fecal elastase 1 (endocrine pancreatic insufficiency at clinical onset. These insufficiencies improve after steroid therapy. Copyright 2010 S. Karger AG, Basel.

General Information about Pancreatic Cancer

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... overweight. Having a personal history of diabetes or chronic pancreatitis . Having a family history of pancreatic cancer or ... have not started treatment. Five types of standard treatment are used: Surgery ... Whipple procedure : A surgical procedure in which the head of the pancreas , ...

Pancreatic islet regeneration: Therapeutic potential, unknowns and controversy

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Ingrid L. Cockburn

2015-07-01

Full Text Available Glucose homeostasis in mammals is primarily maintained by the insulin-secreting β-cells contained within pancreas-resident islets of Langerhans. Gross disruption of this glucose regulation as a result of pancreatic dysfunction frequently results in diabetes, which is currently a major health concern in South Africa, as well as globally. For many years, researchers have realised that the pancreas, and specifically the islets of Langerhans, have a regenerative capacity, as islet mass has frequently been shown to increase following induced pancreatic injury. Given that gross β-cell loss contributes significantly to the pathogenesis of both type 1 and type 2 diabetes, endogenous pancreatic islet regeneration has been investigated extensively as a potential β-cell replacement therapy for diabetes. From the extensive research conducted on pancreatic regeneration, opposing findings and opinions have arisen as to how, and more recently even if, pancreatic regeneration occurs following induced injury. In this review, we outline and discuss the three primary mechanisms by which pancreatic regeneration is proposed to occur: neogenesis, β-cell replication and transdifferentiation. We further explain some of the advanced techniques used in pancreatic regeneration research, and conclude that despite the technologically advanced research tools available to researchers today, the mechanisms governing pancreatic regeneration may remain elusive until more powerful techniques are developed to allow for real-time, live-cell assessment of morphology and gene expression within the pancreas.

Endocrine and exocrine pancreatic insufficiency after acute pancreatitis: long-term follow-up study.

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Tu, Jianfeng; Zhang, Jingzhu; Ke, Lu; Yang, Yue; Yang, Qi; Lu, Guotao; Li, Baiqiang; Tong, Zhihui; Li, Weiqin; Li, Jieshou

2017-10-27

Patients could develop endocrine and exocrine pancreatic insufficiency after acute pancreatitis (AP), but the morbidity, risk factors and outcome remain unclear. The aim of the present study was to evaluate the incidence of endocrine and exocrine pancreatic insufficiency after AP and the risk factors of endocrine pancreatic insufficiency through a long-term follow-up investigation. Follow-up assessment of the endocrine and exocrine function was conducted for the discharged patients with AP episodes. Oral Glucose Tolerance Test (OGTT) and faecal elastase-1(FE-1) test were used as primary parameters. Fasting blood-glucose (FBG), fasting insulin (FINS), glycosylated hemoglobin HBA1c, 2-h postprandial blood glucose (2hPG), Homa beta cell function index (HOMA-β), homeostasis model assessment of insulin resistance (HOMA-IR) and FE-1 were collected. Abdominal contrast-enhanced computed tomography (CECT) was performed to investigate the pancreatic morphology and the other related data during hospitalization was also collected. One hundred thirteen patients were included in this study and 34 of whom (30.1%) developed diabetes mellitus (DM), 33 (29.2%) suffered impaired glucose tolerance (IGT). Moreover, 33 patients (29.2%) developed mild to moderate exocrine pancreatic insufficiency with 100μg/gpancreatic insufficiency with FE-1pancreatic necrosis was significant higher than that in the non-pancreatic necrosis group (X 2  = 13.442,P = 0.001). The multiple logistic regression analysis showed that extent of pancreatic necrosisendocrine pancreatic insufficiency. HOMA-IR (P = 0.002, OR = 6.626), Wall-off necrosis (WON) (P = 0.013, OR = 184.772) were the risk factors. The integrated morbidity of DM and IGT after AP was 59.25%, which was higher than exocrine pancreatic insufficiency. 6.2% and 29.2% of patients developed severe and mild to moderate exocrine pancreatic insufficiency, respectively. The extent of pancreatic necrosis>50%, WON and insulin resistance were

A Case of Chronic Calcific Nonalcoholic Pancreatitis

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Aaron Kangas-Dick

2016-01-01

Full Text Available Tropical Calcific Pancreatitis (TCP is a type of chronic calcific nonalcoholic pancreatitis. Similar to nonalcoholic chronic pancreatitis, it presents in the second and third decades of life; however this type is reported mostly in the developing tropical and subtropical countries. It is associated with the formation of pancreatic calculi and a high probability of developing insulin-dependent diabetes mellitus. Epidemiologic studies have shown that these patients have an increased risk of developing pancreatic carcinoma. The etiology of TCP remains uncertain, with the current consensus suggesting genetics as well as possible toxicity from consuming large amounts of cassava, a tuber. Definite diagnosis of TCP requires younger age of onset, history of malnutrition, and presence of diabetes mellitus along with extensive pancreatic calcification and ductal calculi. When patients meet most but not all of these conditions the term Idiopathic Chronic Pancreatitis (ICP is used. This is a case of a 44-year-old man who presented with most features seen in TCP, and however, was diagnosed with ICP.

Asparaginase-associated pancreatitis in children.

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Raja, Raheel Altaf; Schmiegelow, Kjeld; Frandsen, Thomas Leth

2012-10-01

l-asparaginase has been an element in the treatment for acute lymphoblastic leukaemia (ALL) and non-Hodgkin lymphoma since the late 1960s and remains an essential component of their combination chemotherapy. Among the major toxicities associated with l-asparaginase therapy are pancreatitis, allergic reactions, thrombotic events, hepatotoxicity and hyperlipidaemia. Acute pancreatitis is one of the most common reasons for stopping treatment with l-asparaginase. Short-term complications of asparaginase-associated pancreatitis include development of pseudocysts and pancreatic necrosis. Long-term complications include chronic pancreatitis and diabetes. The pathophysiology of asparaginase-associated pancreatitis remains to be uncovered. Individual clinical and genetic risk factors have been identified, but they are only weak predictors of pancreatitis. This review explores the definition, possible risk factors, treatment and complications of asparaginase-associated pancreatitis. © 2012 Blackwell Publishing Ltd.

B cell depletion reduces T cell activation in pancreatic islets in a murine autoimmune diabetes model.

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Da Rosa, Larissa C; Boldison, Joanne; De Leenheer, Evy; Davies, Joanne; Wen, Li; Wong, F Susan

2018-06-01

Type 1 diabetes is a T cell-mediated autoimmune disease characterised by the destruction of beta cells in the islets of Langerhans, resulting in deficient insulin production. B cell depletion therapy has proved successful in preventing diabetes and restoring euglycaemia in animal models of diabetes, as well as in preserving beta cell function in clinical trials in the short term. We aimed to report a full characterisation of B cell kinetics post B cell depletion, with a focus on pancreatic islets. Transgenic NOD mice with a human CD20 transgene expressed on B cells were injected with an anti-CD20 depleting antibody. B cells were analysed using multivariable flow cytometry. There was a 10 week delay in the onset of diabetes when comparing control and experimental groups, although the final difference in the diabetes incidence, following prolonged observation, was not statistically significant (p = 0.07). The co-stimulatory molecules CD80 and CD86 were reduced on stimulation of B cells during B cell depletion and repopulation. IL-10-producing regulatory B cells were not induced in repopulated B cells in the periphery, post anti-CD20 depletion. However, the early depletion of B cells had a marked effect on T cells in the local islet infiltrate. We demonstrated a lack of T cell activation, specifically with reduced CD44 expression and effector function, including IFN-γ production from both CD4 + and CD8 + T cells. These CD8 + T cells remained altered in the pancreatic islets long after B cell depletion and repopulation. Our findings suggest that B cell depletion can have an impact on T cell regulation, inducing a durable effect that is present long after repopulation. We suggest that this local effect of reducing autoimmune T cell activity contributes to delay in the onset of autoimmune diabetes.

Ataxias agudas en la infancia

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Yaline Betancourt Fursow

2013-09-01

Full Text Available La ataxia cerebelosa aguda infantil (ACAI es la forma más frecuente de complicación neurológica por el virus de la varicela.Descritas dentro del grupo de las cerebelitis agudas. Los objetivos de este estudio fueron: evaluar la presentación clínica, manejo y seguimiento de niños hospitalizados con ACAI en un hospital pediátrico terciario donde la inmunización para varicela no está disponible (parte I y describir los diagnósticos diferenciales de la cerebelitis aguda (parte II. Estudiamos 95 pacientes. Los criterios diagnósticos de ataxia aguda se basaron en: pérdida aguda de la coordinación o dificultad para la marcha con o sin nistagmo asociado y duración menor de 48 horas, en un niño previamente sano. Estos criterios se cumplían en todos los casos valorados, excepto en las ataxias secundarias a ingesta de tóxicos, en los que la duración debía ser menor de 24 horas para su inclusión en el estudio. Se registraron los datos en una historia clínica pediátrica y neurológica. Entre los pacientes inmunosuprimidos la incidencia mayor fue la complicación por varicela. La mayoría de los pacientes fueron varones. El rango de edad fue la preescolar, 5 años . El intervalo entre la presentación del rash y el ingreso fue de 1 a 3 días. El estudio de LCR se practicó en 59.5% de los casos. La TAC y la resonancia magnética cerebral (RM presentaron edema en el 33.3%. El aciclovir endovenoso fue utilizado en 23 pacientes; pero no hubo diferencias significativas en las manifestaciones clínicas y seguimiento entre tratados y no tratados. La ataxia fue la primera manifestación clínica. La estadía hospitalaria fue de 4 días (rango: 2-11 días.

Chronic Pancreatitis

International Nuclear Information System (INIS)

Vavrecka, A.; Bilicky, J.

2011-01-01

Chronic pancreatitis is an ongoing inflammatory process that may over time lead to mal digestion, malabsorption and diabetic syndrome. Identification of risk (etiological) factors based on classifications TIGAR-O or later M-ANNHEIM. These factors (environmental and / or genetic) leads to failure of the stability of the digestive and lysosomal enzymes in the acinar cells, resulting in premature activation of digestive enzymes in the pancreas, and repeated nekroinflamation and fibrosis. The incidence has of the upward trend. Clinically the disease manifests itself in most cases with pain and possibly with nonspecific dyspeptic troubles. Decisive role in the diagnosis playing imaging methods, trans abdominal ultrasonography, computed tomography, magnetic resonance imaging, magnetic cholangiopancretography and foremost endoscopic ultrasonography, which has the highest sensitivity and specificity. Endoscopic retrograde cholangiopancreatography is currently regarded as a method for therapy, not for diagnosis. Less importance is now attached to a functional test. Symptomatic treatment is usually conservative. Abstinence is necessary, easily digestible, but calorie-rich diet with reduced fat. Most patients needed treatment with analgesics. In case of insufficient effect of analgesics is necessary to consider endoscopic therapy or surgery. If the external secretory insufficiency is present are served pancreatic extracts. Diabetic syndrome requires insulin delivery. Generally, chronic pancreatitis is a disease treatable but incurable. Proportion of patients are also dying of pancreatic cancer. (author)

Fumarate Hydratase Deletion in Pancreatic β Cells Leads to Progressive Diabetes

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Julie Adam

2017-09-01

Full Text Available We explored the role of the Krebs cycle enzyme fumarate hydratase (FH in glucose-stimulated insulin secretion (GSIS. Mice lacking Fh1 in pancreatic β cells (Fh1βKO mice appear normal for 6–8 weeks but then develop progressive glucose intolerance and diabetes. Glucose tolerance is rescued by expression of mitochondrial or cytosolic FH but not by deletion of Hif1α or Nrf2. Progressive hyperglycemia in Fh1βKO mice led to dysregulated metabolism in β cells, a decrease in glucose-induced ATP production, electrical activity, cytoplasmic [Ca2+]i elevation, and GSIS. Fh1 loss resulted in elevated intracellular fumarate, promoting succination of critical cysteines in GAPDH, GMPR, and PARK 7/DJ-1 and cytoplasmic acidification. Intracellular fumarate levels were increased in islets exposed to high glucose and in islets from human donors with type 2 diabetes (T2D. The impaired GSIS in islets from diabetic Fh1βKO mice was ameliorated after culture under normoglycemic conditions. These studies highlight the role of FH and dysregulated mitochondrial metabolism in T2D.

Comportamento da síndrome coronariana aguda: resultados de um registro brasileiro

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Leopoldo Soares Piegas

2013-06-01

Full Text Available FUNDAMENTO: O Brasil carece de registros multicêntricos publicados de síndrome coronariana aguda. OBJETIVO: O Registro Brasileiro de Síndrome Coronariana Aguda é um estudo multicêntrico nacional com objetivo de apresentar dados representativos das características clínicas, e manejo e evolução hospitalares dessa síndrome. MÉTODOS: Participaram 23 hospitais de 14 cidades. Foram elegíveis pacientes que se apresentaram com suspeita de síndrome coronariana aguda nas primeiras 24 horas, com quadro clínico sugestivo, associado a alterações eletrocardiográficas compatíveis e/ou marcadores de necrose. O seguimento foi realizado até o óbito ou a alta hospitalar. RESULTADOS: Entre os anos de 2003 e 2008, foram incluídos 2.693 pacientes com diagnóstico de síndrome coronariana aguda, sendo 864 (32,1% mulheres. O diagnóstico final foi de angina instável para 1.141 (42,4% pacientes, com mortalidade de 3,06% deles; de infarto agudo do miocárdio sem supradesnível de ST para 529 (19,6% pacientes, com mortalidade de 6,8% deles; e de infarto agudo do miocárdio com supradesnível de ST para 950 (35,3% pacientes, com mortalidade de 8,1% deles; tiveram diagnóstico não confirmado 73 (2,7% pacientes, com mortalidade de 1,36% deles. A mortalidade global foi de 5,53%. O modelo de regressão logística múltipla identificou o gênero feminino (OR=1,45, o diabetes melito (OR=1,59, o índice de massa corporal (OR=1,27 e a intervenção coronariana percutânea (OR=0,70 como fatores de risco de óbito, para demografia e intervenções. Um modelo para óbito por complicações maiores identificou choque cardiogênico/Edema Agudo de Pulmão (OR=4,57, reinfarto (OR=3,48, acidente vascular cerebral (OR=21,56, sangramento grave (OR=3,33, parada cardiorrespiratória (OR=40,27 e classe funcional de Killip (OR=3,37. CONCLUSÃO: Os dados do Registro Brasileiro de Síndrome Coronariana Aguda não diferem de outros coletados fora do país. Seus achados poder

Effect of ethanolic extract of seeds of Linum usitatissimum (Linn. in hyperglycaemia associated ROS production in PBMNCs and pancreatic tissue of alloxan induced diabetic rats

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Arvindkumar E Ghule

2012-10-01

Full Text Available Objective: To evaluate the effect of ethanolic extract of seeds of Linum usitatissimum (EELU in hyperglycemia associated reactive oxygen species (ROS production in peripheral blood mononuclear cells (PBMNCs and pancreatic antioxidant enzymes in alloxan induced diabetic rat. Methods: Diabetes was induced in male Wistar rats by alloxan (120 mg/kg, i.p. . After acute and subacute treatment serum glucose was determined. Oral glucose tolerance test (OGTT was performed in EELU pretreated animals. ROS production in PBMNCs and pancreatic antioxidant enzymes were measured in alloxan induced diabetic rat. Results: Our results showed that, treatment of EELU (200 and 400 mg/kg significantly reduced serum glucose level in acute and subacute study. The antihyperglycaemic effects of EELU showed onset at 4th h (P<0.001 and peak effect at 6th h (P<0.001. The effect was sustained until 24th h with 400 mg/kg. In subacute study, significant antihyperglycaemic effect was observed from 14th day (P<0.001 onwards. In EELU treated rat the body weight was significantly (P<0.001 increased as compared to diabetic group on 21st day onwards. In OGTT, increased glucose utilization was observed. Treatment of EELU 400 mg/kg showed significant reversal in pancreatic GSH (P<0.01 and SOD (P<0.05 indicating antioxidant nature of EELU. Flow cytometric estimation of total ROS production in PBMNCs in diabetic rats was significantly increased (P<0.001, whereas EELU treatment showed significant (P<0.001 decrease in PBMNCs ROS. Conclusions: It is concluded from the investigation that EELU showed antihyperglycaemic effect mediated through inhibition of ROS level in PBMNCs and preservation of endogenous antioxidant enzymes in pancreatic tissue in alloxan induced diabetic rat.

The effect of the modified puestow procedure on diabetes in patients with tropical chronic pancreatitis--a prospective study.

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Sidhu, S S; Nundy, S; Tandon, R K

2001-01-01

Surgical decompression of the pancreatic duct in patients with chronic pancreatitis relieves pain in 80-90% of subjects, but its effect on exocrine and endocrine pancreatic function is not clear. We sought to further examine such effects. We performed the modified Puestow procedure (lateral pancreaticojejunostomy) in 53 patients with chronic tropical pancreatitis. Pain evaluation was done subjectively and objectively, and the fasting and postprandial blood glucose, insulin requirements, and 72-h fecal fat levels were estimated before and at 3 months and 5 yr after operation. We compared 46 operated patients who completed 5 yr of follow-up with 40 patients who did not undergo operation. Forty-one patients (89%) had complete pain relief. The mean fasting (209 mg/dl) and postprandial (320 mg/dl) blood glucose and insulin requirements (40 U/day) decreased postoperatively (fasting, 162 mg/dl; postprandial blood glucose, 254mg/dl; insulin requirement, 18.2 U/day; p Puestow procedure not only have relief from pain but also improvement of diabetes.

Insuficiencia renal aguda con necrosis tubular aguda secundaria a picadura masiva de abejas

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Gustavo A. Aroca - Martínez

2006-01-01

Full Text Available Leñador de 46 años consulta al servicio de nefrología, de la Clínica Renal de la Costa en Barranquilla, con episodio de insuficiencia renal aguda 48 horas después de haber sufrido múltiples picaduras por abejas africanizadas. Durante su estancia hospitalaria presentó incremento de enzimas musculares (AST LDH, y de pruebas de función renal, motivo por el cual fue dializado en varias ocasiones. Con mejoría total, se decide egresar y manejar ambulatoriamente. Se concluye que el caso se trata de una insuficiencia renal por necrosis tubular aguda por rabdomiolisis debida a la picadura múltiple de abejas africanizadas.

Metabolic pancreatitis: Etiopathogenesis and management

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Sunil Kumar Kota

2013-01-01

Full Text Available Acute pancreatitis is a medical emergency. Alcohol and gallstones are the most common etiologies accounting for 60%-75% cases. Other important causes include postendoscopic retrograde cholangiopancreatography procedure, abdominal trauma, drug toxicity, various infections, autoimmune, ischemia, and hereditary causes. In about 15% of cases the cause remains unknown (idiopathic pancreatitis. Metabolic conditions giving rise to pancreatitis are less common, accounting for 5%-10% cases. The causes include hypertriglyceridemia, hypercalcemia, diabetes mellitus, porphyria, and Wilson′s disease. The episodes of pancreatitis tend to be more severe. In cases of metabolic pancreatitis, over and above the standard routine management of pancreatitis, careful management of the underlying metabolic abnormalities is of paramount importance. If not treated properly, it leads to recurrent life-threatening bouts of acute pancreatitis. We hereby review the pathogenesis and management of various causes of metabolic pancreatitis.

Diabetes and exocrine pancreatic insufficiency in E2F1/E2F2 double-mutant mice.

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Iglesias, Ainhoa; Murga, Matilde; Laresgoiti, Usua; Skoudy, Anouchka; Bernales, Irantzu; Fullaondo, Asier; Moreno, Bernardino; Lloreta, José; Field, Seth J; Real, Francisco X; Zubiaga, Ana M

2004-05-01

E2F transcription factors are thought to be key regulators of cell growth control. Here we use mutant mouse strains to investigate the function of E2F1 and E2F2 in vivo. E2F1/E2F2 compound-mutant mice develop nonautoimmune insulin-deficient diabetes and exocrine pancreatic dysfunction characterized by endocrine and exocrine cell dysplasia, a reduction in the number and size of acini and islets, and their replacement by ductal structures and adipose tissue. Mutant pancreatic cells exhibit increased rates of DNA replication but also of apoptosis, resulting in severe pancreatic atrophy. The expression of genes involved in DNA replication and cell cycle control was upregulated in the E2F1/E2F2 compound-mutant pancreas, suggesting that their expression is repressed by E2F1/E2F2 activities and that the inappropriate cell cycle found in the mutant pancreas is likely the result of the deregulated expression of these genes. Interestingly, the expression of ductal cell and adipocyte differentiation marker genes was also upregulated, whereas expression of pancreatic cell marker genes were downregulated. These results suggest that E2F1/E2F2 activity negatively controls growth of mature pancreatic cells and is necessary for the maintenance of differentiated pancreatic phenotypes in the adult.

Demethylation of induced pluripotent stem cells from type 1 diabetic patients enhances differentiation into functional pancreatic β cells.

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Manzar, Gohar S; Kim, Eun-Mi; Zavazava, Nicholas

2017-08-25

Type 1 diabetes (T1D) can be managed by transplanting either the whole pancreas or isolated pancreatic islets. However, cadaveric pancreas is scarcely available for clinical use, limiting this approach. As such, there is a great need to identify alternative sources of clinically usable pancreatic tissues. Here, we used induced pluripotent stem (iPS) cells derived from patients with T1D to generate glucose-responsive, insulin-producing cells (IPCs) via 3D culture. Initially, T1D iPS cells were resistant to differentiation, but transient demethylation treatment significantly enhanced IPC yield. The cells responded to high-glucose stimulation by secreting insulin in vitro The shape, size, and number of their granules, as observed by transmission electron microscopy, were identical to those found in cadaveric β cells. When the IPCs were transplanted into immunodeficient mice that had developed streptozotocin-induced diabetes, they promoted a dramatic decrease in hyperglycemia, causing the mice to become normoglycemic within 28 days. None of the mice died or developed teratomas. Because the cells are derived from "self," immunosuppression is not required, providing a much safer and reliable treatment option for T1D patients. Moreover, these cells can be used for drug screening, thereby accelerating drug discovery. In conclusion, our approach eliminates the need for cadaveric pancreatic tissue.

Comparison of clinical and laboratory characteristics in children with type 1 diabetes according to pancreatic autoantibodies

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Ji Hae Choi

2010-03-01

Full Text Available Purpose:The purpose of this study was to determine whether there is any difference in the clinical and laboratory characteristics of patients with autoantibody-positive and patients with autoantibody-negative type 1 diabetes at initial presentation. Methods:We analyzed 96 patients under 18 years of age with newly diagnosed type 1 diabetes. One or both of the pancreatic autoantibodies-glutamic acid decarboxylase autoantibodies (GADA and insulin autoantibody (IAA-were measured in all patients, and we reviewed clinical and laboratory characteristics according to the presence of these autoantibodies. Results:GADA was examined in 48 of 87 patients, and 55.2% of patients were positive. IAA was checked in 88 patients, and 39.8% were positive. Both GADA and IAA were measured in 83 patients, and 22.8% had both antibodies. The patients who had one or both autoantibodies (autoantibody-positive group were younger than those not having any autoantibody (autoantibody-negative group. The autoantibody-positive group had lower BMI, corrected sodium level, and serum effective osmolarity, compared to the autoantibody-negative group (P&lt;0.05. Similar differences were found between the GADA-positive and GADA-negative groups. However, there were no significant differences between the IAA- positive and IAA-negative groups. Conclusion:The prevalence of pancreatic autoantibodies was significantly higher in the under-6 years age group than in the other age groups. These findings suggest that measurement of autoantibodies at the initial diagnosis of diabetes is very useful for detecting immune-mediated type 1 diabetes and providing intensive insulin therapy, especially in younger children.

Reduced incretin effect in type 2 diabetes: cause or consequence of the diabetic state?

DEFF Research Database (Denmark)

Knop, Filip K; Vilsbøll, Tina; Højberg, Patricia V

2007-01-01

We aimed to investigate whether the reduced incretin effect observed in patients with type 2 diabetes is a primary event in the pathogenesis of type 2 diabetes or a consequence of the diabetic state. Eight patients with chronic pancreatitis and secondary diabetes (A1C mean [range] of 6.9% [6...... intravenous glucose infusion, respectively. The incretin effect (100% x [beta-cell secretory response to oral glucose tolerance test - intravenous beta-cell secretory response]/beta-cell secretory response to oral glucose tolerance test) was significantly (P ... with chronic pancreatitis and secondary diabetes (31 +/- 4%) compared with patients with chronic pancreatitis and NGT (68 +/- 3) and healthy subjects (60 +/- 4), respectively. In the type 2 diabetes group, the incretin effect amounted to 36 +/- 6%, significantly (P

Escala de Alvarado como herramienta diagnóstica para apendicitis aguda

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Iván Pimienta Concepción

2017-06-01

Full Text Available Introducción: La apendicitis aguda es la enfermedad intrabdominal más frecuente tratada de urgencia. Resulta de interés la utilización de la Escala de Alvarado en el diagnóstico de esta patología por su contribución a la disminución de apendicectomías negativas. Objetivo: Determinar la validez de la Escala de Alvarado como herramienta diagnóstica para apendicitis aguda en pacientes atendidos en el Servicio de Cirugía General del Hospital IESS Ambato. Métodos: Se realizó una investigación observacional, descriptiva y transversal en pacientes hospitalizados con cuadro de dolor abdominal y sospecha de apendicitis aguda, valorados en el Servicio de Cirugía General en el Hospital General IESS Ambato en el período junio 2015 a noviembre del año 2015. Resultados: De acuerdo al resultado histopatológico predominó la apendicitis aguda supurada con (n=83, 54.9%; seguida de apendicitis aguda gangrenosa (n=35, 23.2%; apendicitis aguda precoz (n=15, 9.9%; mientras que el resultado normal y apendicitis aguda gangrenosa perforada se encontraron con los mismos valores (n=9, 5.9%. Conclusiones: Existió un puntaje elevado de la Escala de Alvarado para el diagnóstico de apendicitis aguda según la severidad de los hallazgos descritos en el resultado histopatológico posterior a la apendicectomía. El resultado histopatológico de mayor frecuencia fue la apendicitis aguda supurada, con un riesgo medio en la Escala de Alvarado, la cual es más sensible en periodos de gravedad.

Tratamiento quirúrgico de la pancreatitis aguda con técnica de Puestow modificada

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Vázquez Merayo, Enrique; Moreno Pissau, Francisco; Labrada Arjona, Eduardo; Vázquez Martínez, Yovany Enrique

2014-01-01

La pancreatitis crónica representa uno de los mayores desafíos de la Gastroenterología, y su etiología sigue siendo difícil de establecer en 10-30 % de los pacientes. Se presenta un paciente masculino, de 13 años, con diagnóstico de pancreatitis crónica de tipo inmunológico, con estenosis del conducto pancreático principal. Necesitó tratamiento quirúrgico pancreaticoyeyunostomía longitudinal en Y de Roux, conocido como técnica de Puestow modificada. Se logró mejoría clínica, normalidad de sus...

Pancreatic islet-like clusters from bone marrow mesenchymal stem cells of human first-trimester abortus can cure streptozocin-induced mouse diabetes.

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Zhang, Yihua; Shen, Wenzheng; Hua, Jinlian; Lei, Anmin; Lv, Changrong; Wang, Huayan; Yang, Chunrong; Gao, Zhimin; Dou, Zhongying

2010-12-01

Bone marrow mesenchymal stem cells (BMSCs) have been reported to possess low immunogenicity and cause immunosuppression of recipients when allografted. They can differentiate into insulin-producing cells and may be a valuable source for islet formation. However, the extremely low differentiating rate of adult BMSCs toward insulin-producing cells and the insufficient insulin secretion of the differentiated BMSCs in vitro prevent their clinical use in diabetes treatment. Little is known about the potential of cell replacement therapy with human BMSCs. Previously, we isolated and identified human first-trimester fetal BMSCs (hfBMSCs). Under a novel four-step induction procedure established in this study, the hfBMSCs effectively differentiated into functional pancreatic islet-like cell clusters that contained 62 ± 14% insulin-producing cells, expressed a broad gene profile related to pancreatic islet β-cell development, and released high levels of insulin (2.245 ± 0.222 pmol/100 clusters per 30 min) and C-peptide (2.200 ± 0.468 pmol/100 clusters per 30 min) in response to 25 mmol/L glucose stimulus in vitro. The pancreatic islet-like cell clusters normalized the blood glucose level of diabetic model mice for at least 9 weeks when xenografted; blood glucose levels in these mice rose abnormally again when the grafts were removed. Examination of the grafts indicated that the transplanted cells survived in recipients and produced human insulin and C-peptide in situ. These results demonstrate that hfBMSCs derived from a human first-trimester abortus can differentiate into pancreatic islet-like cell clusters following an established four-step induction. The insulin-producing clusters present advantages in cell replacement therapy of type 1 diabetic model mice.

Mesenchymal stem cells and differentiated insulin producing cells are new horizons for pancreatic regeneration in type I diabetes mellitus.

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Domouky, Ayat M; Hegab, Ashraf S; Al-Shahat, Amal; Raafat, Nermin

2017-06-01

Diabetes mellitus has become the third human killer following cancer and cardiovascular disease. Millions of patients, often children, suffer from type 1 diabetes (T1D). Stem cells created hopes to regenerate damaged body tissues and restore their function. This work aimed at clarifying and comparing the therapeutic potential of differentiated and non-differentiated mesenchymal stem cells (MSCs) as a new line of therapy for T1D. 40 Female albino rats divided into group I (control): 10 rats and group II (diabetic), III and IV, 10 rats in each, were injected with streptozotocin (50mg/kg body weight). Group III (MSCs) were transplanted with bone marrow derived MSCs from male rats and group IV (IPCs) with differentiated insulin producing cells. Blood and pancreatic tissue samples were taken from all rats for biochemical and histological studies. MSCs reduced hyperglycemia in diabetic rats on day 15 while IPCs normalizes blood glucose level on day 7. Histological and morphometric analysis of pancreas of experimental diabetic rats showed improvement in MSCs-treated group but in IPCs-treated group, β-cells insulin immunoreactions were obviously returned to normal, with normal distribution of β-cells in the center and other cells at the periphery. Meanwhile, most of the pathological lesions were still detected in diabetic rats. MSCs transplantation can reduce blood glucose level in recipient diabetic rats. IPCs initiate endogenous pancreatic regeneration by neogenesis of islets. IPCs are better than MSCs in regeneration of β-cells. So, IPCs therapy can be considered clinically to offer a hope for patients suffering from T1D. Copyright © 2017 Elsevier Ltd. All rights reserved.

Issues in Hypertriglyceridemic Pancreatitis - An Update

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Scherer, John; Singh, Vijay; Pitchumoni, C. S; Yadav, Dhiraj

2014-01-01

Hypertriglyceridemia (HTG) is a well established but underestimated cause of acute (AP) and recurrent AP (RAP). The clinical presentation of HTG-induced pancreatitis (HTG pancreatitis) is similar to other causes. Pancreatitis secondary to HTG is typically seen in the presence of one or more secondary factors (uncontrolled diabetes, alcoholism, medications, pregnancy) in a patient with an underlying common genetic abnormality of lipoprotein metabolism (Familial combined hyperlipidemia or Familial HTG). Less commonly, a patient with rare genetic abnormality (Familial chylomicronemic syndrome) with or without an additional secondary factor is encountered. The risk of AP in patients with serum triglycerides >1000 mg/dl and >2000 mg/dl is ∼5% and 10-20% respectively. It is not clear whether HTG pancreatitis is more severe than when it is due to other causes. Clinical management of HTG pancreatitis is similar to that of other causes. Insulin infusion in diabetic patients with HTG can rapidly reduce triglyceride levels. Use of apheresis is still experimental and better designed studies are needed to clarify its role in management of HTG pancreatitis. Diet, lifestyle changes, control of secondary factors are key to the treatment and medications are useful adjuncts to long term management of triglyceride levels. Control of triglyceride levels to well below 500 mg/dl can effectively prevent recurrences of pancreatitis. PMID:24172179

A study of the pancreatic islet β-cell function and insulin resistance of type2 diabetic gastroparesis

International Nuclear Information System (INIS)

Zou Gang; Shao Hao; Lu Zeyuan; Ding Yuzhen; Chen Guanrong; Fu Juan

2005-01-01

Objective: To study the pancreatic islet β-cell function and insulin resistance of diabetic gastroparesis (DGP). Methods: 31 subjects with normal glucose tolerance (NGT), 32 subjects with impaired glucose tolerance (IGT), 38 subjects with type 2 diabetes mellitus (T2DM) and 31 subjects with DGP were en-rolled in the study, assessed by steamed bread meal tests, the plasma glucose and insulin at 0, 30, 60, 120 and 180 min were respectively measured by using glucose oxidase and radioimmunoassay, investigate the changes of area under insulin cure (INSAUC), Homa-insulin resistance (Homa-IR) index and modified β-cell function index (MBCI). Results: The INSAUC of IGT, T2DM, NGT and DGP fell in turn, there were signif-icantly differences among the groups. The Homa-IR index of NGT, IGT, DGP and T2DM rose in turn, there were significantly differences among the groupsexcept between T2DM and DGP. Conclusions: The pancreatic islet β-cell function of DGP was worse that NGT, IGT and T2DM, and the insulin resistance was stronger than NGT and IGT. (authors)

Pancreatite aguda experimental induzida pela L-arginina: avaliação histológica e bioquímica Experimental acute pancreatitis induced by L-arginine: a histological and biochemical evaluation

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Odery Ramos Jr.

2005-03-01

Full Text Available RACIONAL: Doses excessivas de aminoácidos básicos como a L-arginina têm a capacidade de lesar o pâncreas de ratos. OBJETIVO: Descrever e avaliar as características bioquímicas e histológicas da pancreatite aguda induzida pela L-arginina em ratos durante a instalação, desenvolvimento e reparação do processo inflamatório pancreático. MATERIAL E MÉTODOS: A amostra constituiu-se de 105 ratos machos, da linhagem Wistar. Aos ratos do grupo experimento (n = 70 administrou-se injeção intraperitonial de 500 mg/100 g de peso corporal de L-arginina. No grupo controle (n = 35 foi injetada solução salina isotônica. Analisaram-se 10 animais do grupo experimento e 5 do grupo controle em cada período de 6 h, 12 h, 24 h, 48 h, 72 h, 7 dias e 14 dias. Durante os tempos determinados coletou-se sangue para exames laboratoriais e o pâncreas para análise em microscopia óptica. RESULTADOS: Doze a 24 horas após a injeção de L-arginina os níveis séricos de amilase atingiram valores máximos, comparados àqueles dos ratos controle, decrescendo gradualmente, alcançou-os na 48ªhora sendo significativamente menor após 72 horas e 7 dias. A atividade enzimática retornou a níveis basais após 14 dias. Os valores de amilase estavam normais em todos os tempos avaliados nos animais do grupo controle. Na microscopia óptica, após injeção de L-arginina, observou-se arquitetura pancreática histologicamente preservada no período de 6 horas, evidenciando-se em 24 horas importante edema intersticial. Após 48 horas, a arquitetura acinar estava parcialmente destruída com necrose celular focal, atingindo sua máxima severidade ao ultrapassar 72 horas. No 7º dia a necrose tecidual e o edema haviam diminuído, iniciando-se a regeneração da arquitetura acinar. Observou-se a reconstrução estrutural pancreática após 14 dias. No grupo controle não se encontraram alterações histológicas pancreáticas. CONCLUSÃO: A pancreatite aguda experimental

Comportamiento de la otitis media aguda

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Gladys Fuentes Fernández

Full Text Available Introducción: la otitis media aguda es una complicación de las infecciones respiratorias agudas altas, frecuente en los niños menores de 5 años. Objetivos: caracterizar su comportamiento, según edad y sexo, e identificar algunos factores de riesgo en este grupo de edad. Métodos: se realizó un estudio descriptivo retrospectivo de 554 niños ingresados en el hospital Pediátrico de Centro Habana con el diagnóstico de otitis media aguda, durante los años 2006-2010. Los datos se recogieron de las historias clínicas. Resultados: la otitis media aguda fue más frecuente en el sexo masculino (58,7 % y en los menores de 1 año (53,1 %. El antecedente de bajo peso (33,9 % y la prematuridad (27,5 %, la asistencia a círculos infantiles (43,5 % y el hábito de fumar de los padres (58,4 %, además del antecedente de ingresos hospitalarios por otitis media en el mes previo a la aparición del episodio actual (59,0 %, constituyeron los principales factores de riesgo en el presente estudio. Conclusiones: la otitis media es una causa frecuente de ingresos hospitalarios, y se identifican como principales factores de riesgo la asistencia a círculos infantiles y el tabaquismo de algunos de los padres.

TYK2, a Candidate Gene for Type 1 Diabetes, Modulates Apoptosis and the Innate Immune Response in Human Pancreatic β-Cells

DEFF Research Database (Denmark)

Marroqui, Laura; Dos Santos, Reinaldo Sousa; Fløyel, Tina

2015-01-01

histocompatibility complex (MHC) class I proteins, a hallmark of early β-cell inflammation in type 1 diabetes. Importantly, TYK2 inhibition prevented PIC-induced β-cell apoptosis via the mitochondrial pathway of cell death. The present findings suggest that TYK2 regulates apoptotic and proinflammatory pathways...... in pancreatic β-cells via modulation of IFNα signaling, subsequent increase in MHC class I protein, and modulation of chemokines such as CXCL10 that are important for recruitment of T cells to the islets.......Pancreatic β-cells are destroyed by an autoimmune attack in type 1 diabetes. Linkage and genome-wide association studies point to >50 loci that are associated with the disease in the human genome. Pathway analysis of candidate genes expressed in human islets identified a central role for interferon...

Chronic pancreatitis.

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Kleeff, Jorg; Whitcomb, David C; Shimosegawa, Tooru; Esposito, Irene; Lerch, Markus M; Gress, Thomas; Mayerle, Julia; Drewes, Asbjørn Mohr; Rebours, Vinciane; Akisik, Fatih; Muñoz, J Enrique Domínguez; Neoptolemos, John P

2017-09-07

Chronic pancreatitis is defined as a pathological fibro-inflammatory syndrome of the pancreas in individuals with genetic, environmental and/or other risk factors who develop persistent pathological responses to parenchymal injury or stress. Potential causes can include toxic factors (such as alcohol or smoking), metabolic abnormalities, idiopathic mechanisms, genetics, autoimmune responses and obstructive mechanisms. The pathophysiology of chronic pancreatitis is fairly complex and includes acinar cell injury, acinar stress responses, duct dysfunction, persistent or altered inflammation, and/or neuro-immune crosstalk, but these mechanisms are not completely understood. Chronic pancreatitis is characterized by ongoing inflammation of the pancreas that results in progressive loss of the endocrine and exocrine compartment owing to atrophy and/or replacement with fibrotic tissue. Functional consequences include recurrent or constant abdominal pain, diabetes mellitus (endocrine insufficiency) and maldigestion (exocrine insufficiency). Diagnosing early-stage chronic pancreatitis is challenging as changes are subtle, ill-defined and overlap those of other disorders. Later stages are characterized by variable fibrosis and calcification of the pancreatic parenchyma; dilatation, distortion and stricturing of the pancreatic ducts; pseudocysts; intrapancreatic bile duct stricturing; narrowing of the duodenum; and superior mesenteric, portal and/or splenic vein thrombosis. Treatment options comprise medical, radiological, endoscopic and surgical interventions, but evidence-based approaches are limited. This Primer highlights the major progress that has been made in understanding the pathophysiology, presentation, prevalence and management of chronic pancreatitis and its complications.

Pancreatic Endoderm-Derived From Diabetic Patient-Specific Induced Pluripotent Stem Cell Generates Glucose-Responsive Insulin-Secreting Cells.

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Rajaei, Bahareh; Shamsara, Mehdi; Amirabad, Leila Mohammadi; Massumi, Mohammad; Sanati, Mohammad Hossein

2017-10-01

Human-induced pluripotent stem cells (hiPSCs) can potentially serve as an invaluable source for cell replacement therapy and allow the creation of patient- and disease-specific stem cells without the controversial use of embryos and avoids any immunological incompatibility. The generation of insulin-producing pancreatic β-cells from pluripotent stem cells in vitro provides an unprecedented cell source for personal drug discovery and cell transplantation therapy in diabetes. A new five-step protocol was introduced in this study, effectively induced hiPSCs to differentiate into glucose-responsive insulin-producing cells. This process mimics in vivo pancreatic organogenesis by directing cells through stages resembling definitive endoderm, primitive gut-tube endoderm, posterior foregut, pancreatic endoderm, and endocrine precursor. Each stage of differentiation were characterized by stage-specific markers. The produced cells exhibited many properties of functional β-cells, including expression of critical β-cells transcription factors, the potency to secrete C-peptide in response to high levels of glucose and the presence of mature endocrine secretory granules. This high efficient differentiation protocol, established in this study, yielded 79.18% insulin-secreting cells which were responsive to glucose five times higher than the basal level. These hiPSCs-derived glucose-responsive insulin-secreting cells might provide a promising approach for the treatment of type I diabetes mellitus. J. Cell. Physiol. 232: 2616-2625, 2017. © 2016 Wiley Periodicals, Inc. © 2016 Wiley Periodicals, Inc.

Surgical treatment of chronic pancreatitis in young patients.

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Zhou, Feng; Gou, Shan-Miao; Xiong, Jiong-Xin; Wu, He-Shui; Wang, Chun-You; Liu, Tao

2014-10-01

The main treatment strategies for chronic pancreatitis in young patients include therapeutic endoscopic retrograde cholangio-pancreatography (ERCP) intervention and surgical intervention. Therapeutic ERCP intervention is performed much more extensively for its minimally invasive nature, but a part of patients are referred to surgery at last. Historical and follow-up data of 21 young patients with chronic pancreatitis undergoing duodenum-preserving total pancreatic head resection were analyzed to evaluate the outcomes of therapeutic ERCP intervention and surgical intervention in this study. The surgical complications of repeated therapeutic ERCP intervention and surgical intervention were 38% and 19% respectively. During the first therapeutic ERCP intervention to surgical intervention, 2 patients developed diabetes, 5 patients developed steatorrhea, and 5 patients developed pancreatic type B pain. During the follow-up of surgical intervention, 1 new case of diabetes occurred, 1 case of steatorrhea recovered, and 4 cases of pancreatic type B pain were completely relieved. In a part of young patients with chronic pancreatitis, surgical intervention was more effective than therapeutic ERCP intervention on delaying the progression of the disease and relieving the symptoms.

Fetal pancreatic beta-cell function in pregnancies complicated by maternal diabetes mellitus: relationship to fetal acidemia and macrosomia.

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Salvesen, D R; Brudenell, J M; Proudler, A J; Crook, D; Nicolaides, K H

1993-05-01

Our purpose was to investigate the relationship between fetal pancreatic beta-cell function and fetal acidemia and macrosomia in pregnancies complicated by maternal diabetes mellitus. A cross-sectional study at the Harris Birthright Research Centre for Fetal Medicine, London, was performed. In 32 pregnancies complicated by maternal diabetes mellitus cordocentesis was performed at 36 to 39 weeks' gestation for the measurement of umbilical venous blood pH, PO2, PCO2, lactate, and glucose concentration; plasma insulin immunoreactivity; and insulin/glucose ratio. A reference range for plasma insulin and insulin/glucose ratio was constructed by studying fetal blood samples from 80 women who did not have diabetes mellitus. Mean umbilical venous blood pH was significantly lower and plasma insulin immunoreactivity and insulin/glucose ratio were significantly higher than the appropriate normal mean for gestation. There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p < 0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p < 0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p < 0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p < 0.0001). Fetal pancreatic beta-cell hyperplasia is implicated in the pathogenesis of both fetal acidemia and macrosomia.

Protective effect of ganoderma lucidum polysaccharides on pancreatic islet in type 2 diabetes mellitus rats

International Nuclear Information System (INIS)

Tang Zhigang; Xue Hua; Qiao Jin; Gu Jinhua; Xu Jiliang

2010-01-01

Objective: To investigate the protective effects of ganoderma lucidum polysaccharides (GLPs) on pancreatic islet in T2DM rats. Method: SD rats were fed high-fat diet for 4 weeks and then were injected STZ (30 mg/kg) to induce the type 2 diabetes mellitus(T2DM). Once the T2DM model were set successfully, rats were divided into six groups randomly: the normal group (NG), diabetes mellitus group (DMG), GPLs low dosage group (GLPs-LG), GPLs middle dosage group (GLPs-MG), GLPs high dosage group (GLPs-HG) and the berberine group (BerG). They received GLPs with different dosages (200, 400, or 800 mg/kg) and berberine (30 mg/kg) continually for 10 weeks. At 10th weekend, the following indexes of rats in each group were measured respectively: blood glucose, insulin sensivity index (ISI), the contents of NO, SOD, MDA, GSH-Px, CAT in pancreas tissue. At the same time pathological change of pancreas was evaluated by hematoxylin/eosin staining and immunohistochemistry of insulin. Result: As compared with the diabetic model, the decrease of blood glucose with GLPs treatment for 10 weeks were observed. There was also notably increased antioxidant enzyme activity such as superoxide dismutase (SOD), catalase (CAT) as well as decreased MDA content in the pancreatic homogenate. Under light microscope, GLPs-HG treated T2DM showed significantly ameliorated pathological changes, increased islet area and enhanced insulin staining intensity in islets. Conclusion: GLPs has protective effect on the STZ-induced islet injury in T2DM rats through increasing antioxidant enzyme activity and reducing oxidative stress. (authors)

EPConDB: a web resource for gene expression related to pancreatic development, beta-cell function and diabetes.

Science.gov (United States)

Mazzarelli, Joan M; Brestelli, John; Gorski, Regina K; Liu, Junmin; Manduchi, Elisabetta; Pinney, Deborah F; Schug, Jonathan; White, Peter; Kaestner, Klaus H; Stoeckert, Christian J

2007-01-01

EPConDB (http://www.cbil.upenn.edu/EPConDB) is a public web site that supports research in diabetes, pancreatic development and beta-cell function by providing information about genes expressed in cells of the pancreas. EPConDB displays expression profiles for individual genes and information about transcripts, promoter elements and transcription factor binding sites. Gene expression results are obtained from studies examining tissue expression, pancreatic development and growth, differentiation of insulin-producing cells, islet or beta-cell injury, and genetic models of impaired beta-cell function. The expression datasets are derived using different microarray platforms, including the BCBC PancChips and Affymetrix gene expression arrays. Other datasets include semi-quantitative RT-PCR and MPSS expression studies. For selected microarray studies, lists of differentially expressed genes, derived from PaGE analysis, are displayed on the site. EPConDB provides database queries and tools to examine the relationship between a gene, its transcriptional regulation, protein function and expression in pancreatic tissues.

Kill two birds with one stone: making multi-transgenic pre-diabetes mouse models through insulin resistance and pancreatic apoptosis pathogenesis

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Siyuan Kong

2018-04-01

Full Text Available Background Type 2 diabetes is characterized by insulin resistance accompanied by defective insulin secretion. Transgenic mouse models play an important role in medical research. However, single transgenic mouse models may not mimic the complex phenotypes of most cases of type 2 diabetes. Methods Focusing on genes related to pancreatic islet damage, peripheral insulin resistance and related environmental inducing factors, we generated single-transgenic (C/EBP homology protein, CHOP mice (CHOP mice, dual-transgenic (human islet amyloid polypeptide, hIAPP; CHOP mice (hIAPP-CHOP mice and triple-transgenic (11β-hydroxysteroid dehydrogenase type 1, 11β-HSD1; hIAPP; CHOP mice (11β-HSD1-hIAPP- CHOP mice. The latter two types of transgenic (Tg animals were induced with high-fat high-sucrose diets (HFHSD. We analyzed the diabetes-related symptoms and histology features of the transgenic animals. Results Comparing symptoms on the spot-checked points, we determined that the triple-transgene mice were more suitable for systematic study. The results of intraperitoneal glucose tolerance tests (IPGTT of triple-transgene animals began to change 60 days after induction (p < 0.001. After 190 days of induction, the body weights (p < 0.01 and plasma glucose of the animals in Tg were higher than those of the animals in Negative Control (Nc. After sacrificed, large amounts of lipid were found deposited in adipose (p < 0.01 and ectopically deposited in the non-adipose tissues (p < 0.05 or 0.01 of the animals in the Tg HFHSD group. The weights of kidneys and hearts of Tg animals were significantly increased (p < 0.01. Serum C peptide (C-P was decreased due to Tg effects, and insulin levels were increased due to the effects of the HFHSD in the Tg HFHSD group, indicating that damaged insulin secretion and insulin resistance hyperinsulinemia existed simultaneously in these animals. The serum corticosterone of Tg was slightly higher than those of Nc due to the

Nutritional and Metabolic Derangements in Pancreatic Cancer and Pancreatic Resection.

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Gilliland, Taylor M; Villafane-Ferriol, Nicole; Shah, Kevin P; Shah, Rohan M; Tran Cao, Hop S; Massarweh, Nader N; Silberfein, Eric J; Choi, Eugene A; Hsu, Cary; McElhany, Amy L; Barakat, Omar; Fisher, William; Van Buren, George

2017-03-07

Pancreatic cancer is an aggressive malignancy with a poor prognosis. The disease and its treatment can cause significant nutritional impairments that often adversely impact patient quality of life (QOL). The pancreas has both exocrine and endocrine functions and, in the setting of cancer, both systems may be affected. Pancreatic exocrine insufficiency (PEI) manifests as weight loss and steatorrhea, while endocrine insufficiency may result in diabetes mellitus. Surgical resection, a central component of pancreatic cancer treatment, may induce or exacerbate these dysfunctions. Nutritional and metabolic dysfunctions in patients with pancreatic cancer lack characterization, and few guidelines exist for nutritional support in patients after surgical resection. We reviewed publications from the past two decades (1995-2016) addressing the nutritional and metabolic status of patients with pancreatic cancer, grouping them into status at the time of diagnosis, status at the time of resection, and status of nutritional support throughout the diagnosis and treatment of pancreatic cancer. Here, we summarize the results of these investigations and evaluate the effectiveness of various types of nutritional support in patients after pancreatectomy for pancreatic adenocarcinoma (PDAC). We outline the following conservative perioperative strategies to optimize patient outcomes and guide the care of these patients: (1) patients with albumin 10% should postpone surgery and begin aggressive nutrition supplementation; (2) patients with albumin endocrine and exocrine pancreatic insufficiency alongside implementation of appropriate treatment to improve the patient's quality of life.

Negotiating the complexities of exocrine and endocrine dysfunction in chronic pancreatitis.

Science.gov (United States)

Duggan, Sinead N

2017-11-01

Chronic pancreatitis is a chronic inflammatory disease of the pancreas characterised by irreversible morphological change and typically causing pain and/or permanent loss of function. This progressive, irreversible disease results in destruction of healthy pancreatic tissue and the development of fibrous scar tissue. Gradual loss of exocrine and endocrine function follows, along with clinical manifestations such as steatorrhoea, abdominal pain and diabetes. Nutrition in chronic pancreatitis has been described as a problem area and, until recently, there was little research on the topic. It is often asserted that >90 % of the pancreas must be damaged before exocrine insufficiency occurs; however, an exploration of the original studies from the 1970s found that the data do not support this assertion. The management of steatorrhoea with pancreatic enzyme replacement therapy is the mainstay of nutritional management, and early identification and treatment is a key. The presence of steatorrhoea, coupled with poor dietary intake (due to intractable abdominal pain, gastrointestinal side effects and often alcoholism) renders the chronic pancreatitis patients at considerable risk for undernutrition, muscle depletion and fat-soluble vitamin deficiency. Premature osteoporosis/osteopenia afflicts two-thirds of patients as a consequence of poor dietary intake of calcium and vitamin D, low physical activity, low sunlight exposure, heavy smoking, as well as chronic low-grade inflammation. Bone metabolism studies show increased bone formation as well as bone resorption in chronic pancreatitis, indicating that bone turnover is abnormally high. Loss of the pancreatic islet cells occurs later in the disease process as the endocrine cells are diffusely distributed throughout the pancreatic parenchyma. Patients may develop type 3c (pancreatogenic) diabetes, which is complicated by concurrent decreased glucagon secretion, and hence an increased risk of hypoglycaemia. Diabetes control is

Pancreatic Islet Protein Complexes and Their Dysregulation in Type 2 Diabetes

DEFF Research Database (Denmark)

Pedersen, Helle Krogh; Gudmundsdottir, Valborg; Brunak, Søren

2017-01-01

Type 2 diabetes (T2D) is a complex disease that involves multiple genes. Numerous risk loci have already been associated with T2D, although many susceptibility genes remain to be identified given heritability estimates. Systems biology approaches hold potential for discovering novel T2D genes by ...... starting point when evaluating an individual's alterations at the genome, transcriptome, or proteome level in relation to T2D in clinical settings.......Type 2 diabetes (T2D) is a complex disease that involves multiple genes. Numerous risk loci have already been associated with T2D, although many susceptibility genes remain to be identified given heritability estimates. Systems biology approaches hold potential for discovering novel T2D genes...... by considering their biological context, such as tissue-specific protein interaction partners. Pancreatic islets are a key T2D tissue and many of the known genetic risk variants lead to impaired islet function, hence a better understanding of the islet-specific dysregulation in the disease-state is essential...

Evaluation of Porcine Pancreatic Islets Transplanted in the Kidney Capsules of Diabetic Mice Using a Clinically Approved Superparamagnetic Iron Oxide (SPIO) and a 1.5T MR Scanner

International Nuclear Information System (INIS)

Kim, Hoe Suk; Kim, Hyoung Su; Park, Kyong Soo; Moon, Woo Kyung

2010-01-01

To evaluate transplanted porcine pancreatic islets in the kidney capsules of diabetic mice using a clinically approved superparamagnetic iron oxide (SPIO) and a 1.5T MR scanner. Various numbers of porcine pancreatic islets labeled with Resovist, a carboxydextran-coated SPIO, were transplanted into the kidney capsules of normal mice and imaged with a 3D FIESTA sequence using a 1.5T clinical MR scanner. Labeled (n = 3) and unlabeled (n = 2) islets were transplanted into the kidney capsules of streptozotocin-induced diabetic mice. Blood glucose levels and MR signal intensities were monitored for 30 days post-transplantation. There were no significant differences in viability or insulin secretion between labeled and unlabeled islets. A strong correlation (γ 2 > 0.94) was evident between the number of transplanted islets and T 2 relaxation times quantified by MRI. Transplantation with labeled or unlabeled islets helped restore normal sustained glucose levels in diabetic mice, and nephrectomies induced the recurrence of diabetes. The MR signal intensity of labeled pancreatic islets decreased by 80% over 30 days. The transplantation of SPIO-labeled porcine islets into the kidney capsule of diabetic mice allows to restore normal glucose levels, and these islets can be visualized and quantified using a 1.5T clinical MR scanner

The evolution of the surgical treatment of chronic pancreatitis.

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Andersen, Dana K; Frey, Charles F

2010-01-01

To establish the current status of surgical therapy for chronic pancreatitis, recent published reports are examined in the context of the historical advances in the field. The basis for decompression (drainage), denervation, and resection strategies for the treatment of pain caused by chronic pancreatitis is reviewed. These divergent approaches have finally coalesced as the head of the pancreas has become apparent as the nidus of chronic inflammation. The recent developments in surgical methods to treat the complications of chronic pancreatitis and the results of recent prospective randomized trials of operative approaches were reviewed to establish the current best practices. Local resection of the pancreatic head, with or without duct drainage, and duodenum-preserving pancreatic head resection offer outcomes as effective as pancreaticoduodenectomy, with lowered morbidity and mortality. Local resection or excavation of the pancreatic head offers the advantage of lowest cost and morbidity and early prevention of postoperative diabetes. The late incidences of recurrent pain, diabetes, and exocrine insufficiency are equivalent for all 3 surgical approaches. Local resection of the pancreatic head appears to offer best outcomes and lowest risk for the management of the pain of chronic pancreatitis.

Exocrine pancreatic function in hepatocyte nuclear factor 1β-maturity-onset diabetes of the young (HNF1B-MODY) is only moderately reduced: compensatory hypersecretion from a hypoplastic pancreas.

Science.gov (United States)

Tjora, E; Wathle, G; Erchinger, F; Engjom, T; Molven, A; Aksnes, L; Haldorsen, I S; Dimcevski, G; Raeder, H; Njølstad, P R

2013-08-01

To examine the exocrine pancreatic function in carriers of the hepatocyte nuclear factor 1β gene (HNF1B) mutation by direct testing. Patients with HNF1B mutations and control subjects were assessed using rapid endoscopic secretin tests and secretin-stimulated magnetic resonance imaging. Seven patients and 25 controls underwent endoscopy, while eight patients and 20 controls had magnetic resonance imaging. Ductal function was assessed according to peak bicarbonate concentrations and acinar function was assessed according to peak digestive enzyme activities in secretin-stimulated duodenal juice. The association of pancreatic exocrine function and diabetes status with pancreatic gland volume was examined. The mean increase in secretin-stimulated duodenal fluid was smaller in patients than controls (4.0 vs 6.4 ml/min; P = 0.003). We found lower ductal function in patients than controls (median peak bicarbonate concentration: 73 vs 116 mEq/L; P function (median peak lipase activity: 6.4 vs 33.5 kU/ml; P = 0.01; median peak elastase activity: 0.056 vs 0.130 U/ml; P = 0.01). Pancreatic fluid volume outputs correlated significantly with pancreatic gland volumes (r² = 0.71, P = 0.008) in patients. The total fluid output to pancreatic gland volume ratios were higher in patients than controls (4.5 vs 1.3 ml/cm³; P = 0.03), suggesting compensatory hypersecretion in the remaining gland. Carriers of the HNF1B mutation have lower exocrine pancreatic function involving both ductal and acinar cells. Compensatory hypersecretion suggests that the small pancreas of HNF1B mutation carriers is attributable to hypoplasia, not atrophy. © 2013 The Authors. Diabetic Medicine © 2013 Diabetes UK.

Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function

Science.gov (United States)

Neve, Bernadette; Fernandez-Zapico, Martin E.; Ashkenazi-Katalan, Vered; Dina, Christian; Hamid, Yasmin H.; Joly, Erik; Vaillant, Emmanuel; Benmezroua, Yamina; Durand, Emmanuelle; Bakaher, Nicolas; Delannoy, Valerie; Vaxillaire, Martine; Cook, Tiffany; Dallinga-Thie, Geesje M.; Jansen, Hans; Charles, Marie-Aline; Clément, Karine; Galan, Pilar; Hercberg, Serge; Helbecque, Nicole; Charpentier, Guillaume; Prentki, Marc; Hansen, Torben; Pedersen, Oluf; Urrutia, Raul; Melloul, Danielle; Froguel, Philippe

2005-01-01

KLF11 (TIEG2) is a pancreas-enriched transcription factor that has elicited significant attention because of its role as negative regulator of exocrine cell growth in vitro and in vivo. However, its functional role in the endocrine pancreas remains to be established. Here, we report, for the first time, to our knowledge, the characterization of KLF11 as a glucose-inducible regulator of the insulin gene. A combination of random oligonucleotide binding, EMSA, luciferase reporter, and chromatin immunoprecipitation assays shows that KLF11 binds to the insulin promoter and regulates its activity in beta cells. Genetic analysis of the KLF11 gene revealed two rare variants (Ala347Ser and Thr220Met) that segregate with diabetes in families with early-onset type 2 diabetes, and significantly impair its transcriptional activity. In addition, analysis of 1,696 type 2 diabetes mellitus and 1,776 normoglycemic subjects show a frequent polymorphic Gln62Arg variant that significantly associates with type 2 diabetes mellitus in North European populations (OR = 1.29, P = 0.00033). Moreover, this variant alters the corepressor mSin3A-binding activity of KLF11, impairs the activation of the insulin promoter and shows lower levels of insulin expression in pancreatic beta cells. In addition, subjects carrying the Gln62Arg allele show decreased plasma insulin after an oral glucose challenge. Interestingly, all three nonsynonymous KLF11 variants show increased repression of the catalase 1 promoter, suggesting a role in free radical clearance that may render beta cells more sensitive to oxidative stress. Thus, both functional and genetic analyses reveal that KLF11 plays a role in the regulation of pancreatic beta cell physiology, and its variants may contribute to the development of diabetes. PMID:15774581

Ameliorative Activity of Ethanol Extract of Artocarpus heterophyllus Stem Bark on Pancreatic β-Cell Dysfunction in Alloxan-Induced Diabetic Rats.

Science.gov (United States)

Ajiboye, Basiru O; Ojo, Oluwafemi A; Adeyonu, Oluwatosin; Imiere, Oluwatosin D; Fadaka, Adewale O; Osukoya, Adetutu O

2017-10-01

This study sought to investigate the ameliorative effects of ethanol extract Artocarpus heterophyllus (EAH) in alloxan-induced diabetic rats. The rats were divided into 6 groups, with groups 1 and 2 serving as nondiabetic and diabetic control, respectively; group 3 serving as diabetic rats treated with 5 mg/kg glibenclamide; and groups 4 to 6 were diabetic rats treated with 50, 100, and 150 mg/kg of EAH, respectively. Assays determined were serum insulin, lipid peroxidation, and antioxidant enzyme activities. EAH stem bark reduced fasting blood glucose and lipid peroxidation levels and increased serum insulin levels and activities of antioxidant enzymes. Data obtained demonstrated the ability of EAH stem bark to ameliorate pancreatic β-cell dysfunction in alloxan-induced diabetic rats.

Pancreas volume and fat fraction in children with Type 1 diabetes.

Science.gov (United States)

Regnell, S E; Peterson, P; Trinh, L; Broberg, P; Leander, P; Lernmark, Å; Månsson, S; Elding Larsson, H

2016-10-01

People with Type 1 diabetes have smaller pancreases than healthy individuals. Several diseases causing pancreatic atrophy are associated with pancreatic steatosis, but pancreatic fat in Type 1 diabetes has not been measured. This cross-sectional study aimed to compare pancreas size and fat fraction in children with Type 1 diabetes and controls. The volume and fat fraction of the pancreases of 22 children with Type 1 diabetes and 29 controls were determined using magnetic resonance imaging. Pancreas volume was 27% smaller in children with diabetes (median 34.9 cm(3) ) than in controls (47.8 cm(3) ; P Pancreas volume correlated positively with age in controls (P = 0.033), but not in children with diabetes (P = 0.649). Pancreas volume did not correlate with diabetes duration, but it did correlate positively with units of insulin/kg body weight/day (P = 0.048). A linear model of pancreas volume as influenced by age, body surface area and insulin units/kg body weight/day found that insulin dosage correlated with pancreas volume after controlling for both age and body surface area (P = 0.009). Pancreatic fat fraction was not significantly different between the two groups (1.34% vs. 1.57%; P = 0.891). Our findings do not indicate that pancreatic atrophy in Type 1 diabetes is associated with an increased pancreatic fat fraction, unlike some other diseases featuring reduced pancreatic volume. We speculate that our results may support the hypotheses that much of pancreatic atrophy in Type 1 diabetes occurs before the clinical onset of the disease and that exogenous insulin administration decelerates pancreatic atrophy after diabetes onset. © 2016 Diabetes UK.

Pneumonia eosinofílica aguda com evolução para síndroma de dificuldade respiratória aguda: caso clínico

OpenAIRE

J.P.F. Baptista; P.C. Casanova; J.P.A. Sousa; P.J. Martins; A. Simões; V. Fernandes; J. Souto; J.J. Costa; A. Rebelo; L. Carvalho; J. Pimentel

2004-01-01

RESUMO: Os autores apresentam um caso de pneumonia eosinofílica aguda (PEA) associada a síndroma de dificuldade respiratória aguda grave num adolescente previamente saudável, medicado com nitrofurantoína. A PEA deve ser incluída no diagnóstico diferencial da pneumonia adquirida na comunidade, bem como na lista das patologias causadoras de síndroma de dificuldade respiratória aguda, e o seu diagnóstico deve ser sugerido pela presença de alveolite eosinofílica no líquido de lavagem broncoalveol...

Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function

DEFF Research Database (Denmark)

Neve, Bernadette; Fernandez-Zapico, Martin E; Ashkenazi-Katalan, Vered

2005-01-01

in beta cells. Genetic analysis of the KLF11 gene revealed two rare variants (Ala347Ser and Thr220Met) that segregate with diabetes in families with early-onset type 2 diabetes, and significantly impair its transcriptional activity. In addition, analysis of 1,696 type 2 diabetes mellitus and 1......,776 normoglycemic subjects show a frequent polymorphic Gln62Arg variant that significantly associates with type 2 diabetes mellitus in North European populations (OR = 1.29, P = 0.00033). Moreover, this variant alters the corepressor mSin3A-binding activity of KLF11, impairs the activation of the insulin promoter...... and shows lower levels of insulin expression in pancreatic beta cells. In addition, subjects carrying the Gln62Arg allele show decreased plasma insulin after an oral glucose challenge. Interestingly, all three nonsynonymous KLF11 variants show increased repression of the catalase 1 promoter, suggesting...

Serum metabolomics differentiating pancreatic cancer from new-onset diabetes

Science.gov (United States)

He, Xiangyi; Zhong, Jie; Wang, Shuwei; Zhou, Yufen; Wang, Lei; Zhang, Yongping; Yuan, Yaozong

2017-01-01

To establish a screening strategy for pancreatic cancer (PC) based on new-onset diabetic mellitus (NO-DM), serum metabolomics analysis and a search for the metabolic pathways associated with PC related DM were performed. Serum samples from patients with NO-DM (n = 30) and patients with pancreatic cancer and NO-DM were examined by liquid chromatography-mass spectrometry. Data were analyzed using principal components analysis (PCA) and orthogonal projection to latent structures (OPLS) of the most significant metabolites. The diagnostic model was constructed using logistic regression analysis. Metabolic pathways were analyzed using the web-based tool MetPA. PC patients with NO-DM were older and had a lower BMI and shorter duration of DM than those with NO-DM. The metabolomic profiles of patients with PC and NO-DM were significantly different from those of patients with NO-DM in the PCA and OPLS models. Sixty two differential metabolites were identified by the OPLS model. The logistic regression model using a panel of two metabolites including N_Succinyl_L_diaminopimelic_acid and PE (18:2) had high sensitivity (93.3%) and specificity (93.1%) for PC. The top three metabolic pathways associated with PC related DM were valine, leucine and isoleucine biosynthesis and degradation, primary bile acid biosynthesis, and sphingolipid metabolism. In conclusion, screening for PC based on NO-DM using serum metabolomics in combination with clinic characteristics and CA19-9 is a potential useful strategy. Several metabolic pathways differed between PC related DM and type 2 DM. PMID:28418859

Pancreatic size and fat content in diabetes: A systematic review and meta-analysis of imaging studies.

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Tiago Severo Garcia

Full Text Available Imaging studies are expected to produce reliable information regarding the size and fat content of the pancreas. However, the available studies have produced inconclusive results. The aim of this study was to perform a systematic review and meta-analysis of imaging studies assessing pancreas size and fat content in patients with type 1 diabetes (T1DM and type 2 diabetes (T2DM.Medline and Embase databases were performed. Studies evaluating pancreatic size (diameter, area or volume and/or fat content by ultrasound, computed tomography, or magnetic resonance imaging in patients with T1DM and/or T2DM as compared to healthy controls were selected. Seventeen studies including 3,403 subjects (284 T1DM patients, 1,139 T2DM patients, and 1,980 control subjects were selected for meta-analyses. Pancreas diameter, area, volume, density, and fat percentage were evaluated.Pancreatic volume was reduced in T1DM and T2DM vs. controls (T1DM vs. controls: -38.72 cm3, 95%CI: -52.25 to -25.19, I2 = 70.2%, p for heterogeneity = 0.018; and T2DM vs. controls: -12.18 cm3, 95%CI: -19.1 to -5.25, I2 = 79.3%, p for heterogeneity = 0.001. Fat content was higher in T2DM vs. controls (+2.73%, 95%CI 0.55 to 4.91, I2 = 82.0%, p for heterogeneity<0.001.Individuals with T1DM and T2DM have reduced pancreas size in comparison with control subjects. Patients with T2DM have increased pancreatic fat content.

Recurrent pancreatitis secondary to sphincter of Oddi dysfunction: case report

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Jeannette Calzadilla

2016-10-01

Full Text Available Resumen La disfunción del esfínter de Oddi es una patología poco frecuente que es causa de aproximadamente el 20% de las pancreatitis recurrentes idiopáticas. Para sospechar de su existencia es obligatorio haber descartado todas las otras causas de pancreatitis aguda. Luego, sobre la base de la historia clínica, exámenes de laboratorio y estudio con imágenes, se debe realizar una clasificación del tipo de disfunción. Según ello, es necesario llevar a cabo una manometría, considerada el gold estándar para el diagnóstico, y guiar el método de tratamiento, siendo el de elección la esfinterotomía endoscópica. En el presente artículo se discute un caso de pancreatitis recurrente, que luego de un minucioso estudio, y habiendo descartado otras etiologías, se diagnosticó como causa la disfunción del esfínter de Oddi tipo pancreática. Se resolvió mediante esfinterotomía endoscópica, presentando una evolución favorable y sin recurrencia de la sintomatología.

STAT5 activity in pancreatic beta-cells influences the severity of diabetes in animal models of type 1 and 2 diabetes

DEFF Research Database (Denmark)

Jackerott, Malene; Møldrup, Annette; Thams, Peter

2006-01-01

Pancreatic beta-cell growth and survival and insulin production are stimulated by growth hormone and prolactin through activation of the transcription factor signal transducer and activator of transcription (STAT)5. To assess the role of STAT5 activity in beta-cells in vivo, we generated transgen...... and type 2 diabetes....... reduced beta-cell proliferation at 6 months of age. The inhibitory effect of high-fat diet or leptin on insulin secretion was diminished in isolated islets from RIP-DNSTAT5 mice compared with wild-type islets. Upon multiple low-dose streptozotocin treatment, RIP-DNSTAT5 mice exhibited higher plasma...... of glucose tolerance, whereas RIP-CASTAT5 mice were more glucose tolerant and less hyperleptinemic than wild-type mice. Although the pancreatic insulin content and relative beta-cell area were increased in high-fat diet-fed RIP-DNSTAT5 mice compared with wild-type or RIP-CASTAT5 mice, RIP-DNSTAT5 mice showed...

Pancreatitis caused by Clostridium perfringens infection with extensive retropneumoperitoneum

International Nuclear Information System (INIS)

Merchante, E.; Garcia, F. J.; Perez, H.; Marquez, J. L.

2001-01-01

We present a case of primary emphysematous pancreatitis caused by Clostridium perfringens infection (also Known as spontaneous pancreatic gas gangrene) in a 66-year-old man with diabetes and a history of recurrent pancreatitis. One notable feature is the absence of a focal distribution, which is seen on radiological studies to be accompanied by extensive retropneumoperitoneum, with dissemination of the gas toward the mesenteric root and pelvic extra peritoneal spaces. This wide diffusion is aided by the C. perfringens toxins and the pancreatic enzymes released, leading to a fulminate course, an elevated rate of early mortality among the cases reviewed. The early diagnosis of this disease is fundamental, enabling aggressive medical treatment and emergency surgery. Diabetes is a known risk factor for anaerobic infection, including C. perfringens, as in the case of emphysematous cholecystitis. A diseased pancreas or pancreatic duct facilitates the development of infections since it eliminates poorly the microorganisms that reach it from the duodenum. Gas gangrene secondary to necrosis-related super infection or pancreatic collections is uncommon, and spontaneous or primary cases are exceptionally are. (Author) 13 refs

Pancreatic duct stones in patients with chronic pancreatitis: surgical outcomes.

Science.gov (United States)

Liu, Bo-Nan; Zhang, Tai-Ping; Zhao, Yu-Pei; Liao, Quan; Dai, Meng-Hua; Zhan, Han-Xiang

2010-08-01

Pancreatic duct stone (PDS) is a common complication of chronic pancreatitis. Surgery is a common therapeutic option for PDS. In this study we assessed the surgical procedures for PDS in patients with chronic pancreatitis at our hospital. Between January 2004 and September 2009, medical records from 35 patients diagnosed with PDS associated with chronic pancreatitis were retrospectively reviewed and the patients were followed up for up to 67 months. The 35 patients underwent ultrasonography, computed tomography, or both, with an overall accuracy rate of 85.7%. Of these patients, 31 underwent the modified Puestow procedure, 2 underwent the Whipple procedure, 1 underwent simple stone removal by duct incision, and 1 underwent pancreatic abscess drainage. Of the 35 patients, 28 were followed up for 4-67 months. There was no postoperative death before discharge or during follow-up. After the modified Puestow procedure, abdominal pain was reduced in patients with complete or incomplete stone clearance (P>0.05). Steatorrhea and diabetes mellitus developed in several patients during a long-term follow-up. Surgery, especially the modified Puestow procedure, is effective and safe for patients with PDS associated with chronic pancreatitis. Decompression of intraductal pressure rather than complete clearance of all stones predicts postoperative outcome.

Risk of Recurrent Pancreatitis and Progression to Chronic Pancreatitis After a First Episode of Acute Pancreatitis.

Science.gov (United States)

Ahmed Ali, Usama; Issa, Yama; Hagenaars, Julia C; Bakker, Olaf J; van Goor, Harry; Nieuwenhuijs, Vincent B; Bollen, Thomas L; van Ramshorst, Bert; Witteman, Ben J; Brink, Menno A; Schaapherder, Alexander F; Dejong, Cornelis H; Spanier, B W Marcel; Heisterkamp, Joos; van der Harst, Erwin; van Eijck, Casper H; Besselink, Marc G; Gooszen, Hein G; van Santvoort, Hjalmar C; Boermeester, Marja A

2016-05-01

Patients with a first episode of acute pancreatitis can develop recurrent or chronic pancreatitis (CP). However, little is known about the incidence or risk factors for these events. We performed a cross-sectional study of 669 patients with a first episode of acute pancreatitis admitted to 15 Dutch hospitals from December 2003 through March 2007. We collected information on disease course, outpatient visits, and hospital readmissions, as well as results from imaging, laboratory, and histology studies. Standardized follow-up questionnaires were sent to all available patients to collect information on hospitalizations and interventions for pancreatic disease, abdominal pain, steatorrhea, diabetes mellitus, medications, and alcohol and tobacco use. Patients were followed up for a median time period of 57 months. Primary end points were recurrent pancreatitis and CP. Risk factors were evaluated using regression analysis. The cumulative risk was assessed using Kaplan-Meier analysis. Recurrent pancreatitis developed in 117 patients (17%), and CP occurred in 51 patients (7.6%). Recurrent pancreatitis developed in 12% of patients with biliary disease, 24% of patients with alcoholic etiology, and 25% of patients with disease of idiopathic or other etiologies; CP occurred in 3%, 16%, and 10% of these patients, respectively. Etiology, smoking, and necrotizing pancreatitis were independent risk factors for recurrent pancreatitis and CP. Acute Physiology and Chronic Health Evaluation II scores at admission also were associated independently with recurrent pancreatitis. The cumulative risk for recurrent pancreatitis over 5 years was highest among smokers at 40% (compared with 13% for nonsmokers). For alcohol abusers and current smokers, the cumulative risks for CP were similar-approximately 18%. In contrast, the cumulative risk of CP increased to 30% in patients who smoked and abused alcohol. Based on a retrospective analysis of patients admitted to Dutch hospitals, a first

The insulinotropic effect of GIP is impaired in patients with chronic pancreatitis and secondary diabetes mellitus as compared to patients with chronic pancreatitis and normal glucose tolerance

DEFF Research Database (Denmark)

Knop, Filip K; Vilsbøll, Tina; Højberg, Patricia V

2007-01-01

patients with chronic pancreatitis (CP) and normal glucose tolerance (NGT) (fasting plasma glucose (FPG): 5.5 (4.5-6.0) mM (mean (range); HbA(1c): 5.8 (5.4-6.3) %) and 8 patients with CP and secondary diabetes not requiring insulin (FPG: 7.1 (6.0-8.8) mM; HbA(1c): 7.0 (5.8-10.0) %) during three 15-m...

Comparative occurrence of diabetes in canine, feline, and few wild animals and their association with pancreatic diseases and ketoacidosis with therapeutic approach

OpenAIRE

Kamal Niaz; Faheem Maqbool; Fazlullah Khan; Fatima Ismail Hassan; Saeideh Momtaz; Mohammad Abdollahi

2018-01-01

Diabetes mellitus (DM) is a chronic metabolic disorder in which blood glucose level raises that can result in severe complications. However, the incidence increased mostly by obesity, pregnancy, persistent corpus luteum, and diestrus phase in humans and animals. This review has focused on addressing the possible understanding and pathogenesis of spontaneous DM in canine, feline, and few wild animals. Furthermore, pancreatic associated disorders, diabetic ketoacidosis, hormonal and drug intera...

VIH: Infeccion aguda, pesquisa y manejo

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Cortés S. Esteban, Dr.

2014-05-01

Si bien existe una relativa facilidad para realizar el diagnóstico de un paciente con la infección crónica por VIH, existe por otro lado una relativa dificultad para realizar el diagnóstico de la infección aguda en etapas tempranas de la infección. Esta situación es de importancia desde el punto de vista de la Salud Pública por cuanto en la infección aguda es cuando se producen las viremias más elevadas y por tanto la mayor facilidad para que el sujeto sea infectante y disemine la infección viral.

Growth Factor Mediated Signaling in Pancreatic Pathogenesis

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Nandy, Debashis; Mukhopadhyay, Debabrata, E-mail: mukhopadhyay.debabrata@mayo.edu [Department of Biochemistry and Molecular Biology, College of Medicine, Mayo Clinic, 200 First Street SW, Guggenheim 1321C, Rochester, MN 55905 (United States)

2011-02-24

Functionally, the pancreas consists of two types of tissues: exocrine and endocrine. Exocrine pancreatic disorders mainly involve acute and chronic pancreatitis. Acute pancreatitis typically is benign, while chronic pancreatitis is considered a risk factor for developing pancreatic cancer. Pancreatic carcinoma is the fourth leading cause of cancer related deaths worldwide. Most pancreatic cancers develop in the exocrine tissues. Endocrine pancreatic tumors are more uncommon, and typically are less aggressive than exocrine tumors. However, the endocrine pancreatic disorder, diabetes, is a dominant cause of morbidity and mortality. Importantly, different growth factors and their receptors play critical roles in pancreatic pathogenesis. Hence, an improved understanding of how various growth factors affect pancreatitis and pancreatic carcinoma is necessary to determine appropriate treatment. This chapter describes the role of different growth factors such as vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), platelet derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), and transforming growth factor (TGF) in various pancreatic pathophysiologies. Finally, the crosstalk between different growth factor axes and their respective signaling mechanisms, which are involved in pancreatitis and pancreatic carcinoma, are also discussed.

Growth Factor Mediated Signaling in Pancreatic Pathogenesis

International Nuclear Information System (INIS)

Nandy, Debashis; Mukhopadhyay, Debabrata

2011-01-01

Functionally, the pancreas consists of two types of tissues: exocrine and endocrine. Exocrine pancreatic disorders mainly involve acute and chronic pancreatitis. Acute pancreatitis typically is benign, while chronic pancreatitis is considered a risk factor for developing pancreatic cancer. Pancreatic carcinoma is the fourth leading cause of cancer related deaths worldwide. Most pancreatic cancers develop in the exocrine tissues. Endocrine pancreatic tumors are more uncommon, and typically are less aggressive than exocrine tumors. However, the endocrine pancreatic disorder, diabetes, is a dominant cause of morbidity and mortality. Importantly, different growth factors and their receptors play critical roles in pancreatic pathogenesis. Hence, an improved understanding of how various growth factors affect pancreatitis and pancreatic carcinoma is necessary to determine appropriate treatment. This chapter describes the role of different growth factors such as vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), platelet derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), and transforming growth factor (TGF) in various pancreatic pathophysiologies. Finally, the crosstalk between different growth factor axes and their respective signaling mechanisms, which are involved in pancreatitis and pancreatic carcinoma, are also discussed

Reduced Expression of the Liver/Beta-Cell Glucose Transporter Isoform in Glucose-Insensitive Pancreatic Beta Cells of Diabetic Rats

Science.gov (United States)

Thorens, Bernard; Weir, Gordon C.; Leahy, John L.; Lodish, Harvey F.; Bonner-Weir, Susan

1990-09-01

Rats injected with a single dose of streptozocin at 2 days of age develop non-insulin-dependent diabetes 6 weeks later. The pancreatic beta islet cells of these diabetic rats display a loss of glucose-induced insulin secretion while maintaining sensitivity to other secretagogues such as arginine. We analyzed the level of expression of the liver/beta-cell glucose transporter isoform in diabetic islets by immunofluorescence staining of pancreas sections and by Western blotting of islet lysates. Islets from diabetic animals have a reduced expression of this beta-cell-specific glucose transporter isoform and the extent of reduction is correlated with the severity of hyperglycemia. In contrast, expression of this transporter isoform in liver is minimally modified by the diabetes. Thus a decreased expression of the liver/beta-cell glucose transporter isoform in beta cells is associated with the impaired glucose sensing characteristic of diabetic islets; our data suggest that this glucose transporter may be part of the beta-cell glucose sensor.

Uso de plasmaféresis en pancreatitis hipertrigliceridémica

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Fernando Jerkovich

2014-02-01

Full Text Available La hipertrigliceridemia es causa de 1-4% de las pancreatitis agudas. Presentamos el caso de una mujer de 42 años con antecedentes de obesidad, diabetes mellitus tipo 2, hipertrigliceridemia e hipercolesterolemia (9365 mg/dl y 1822 mg/dl, respectivamente, 1 mes previo a la consulta. Concurrió a nuestro hospital por cuadro de dolor abdominal de 5 días de evolución de tipo cólico con progresión continua en las últimas 48 horas. Se realizó tomografía de abdomen que informó imágenes compatibles con pancreatitis. A las 36 horas de su ingreso se inició la primera sesión de plasmaféresis con una reducción de triglicéridos y colesterol del 25 y 30% respectivamente y una segunda sesión al día siguiente con descenso de triglicéridos a 996 mg/dl y colesterol a 238 mg/dl. Durante su internación presentó bacteriemia por Klebsiella pneumoniae, sin colección ni necrosis pancreática detectables por tomografía de abdomen, y luego neumonía intrahospitalaria, ambas infecciones con buena respuesta a antibioticoterapia. Al alta, los triglicéridos habían descendido a 652 mg/dl, el colesterol a 167 mg/dl, el dolor abdominal había cedido y la paciente presentaba buena tolerancia por vía oral. Observamos una reducción del 90% de triglicéridos y 87% de colesterol luego de dos sesiones de plasmaféresis, comparado con 70% de reducción en promedio en la mayoría de los estudios consultados. En los mismos, no hemos encontrado la presencia de bacteriemia ni neumonía hospitalaria como complicaciones.

Parenteral nutrition versus enteral nutrition in severe acute pancreatitis Nutrição parenteral versus enteral em pacientes com pancreatite aguda grave

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Josiel Paiva Vieira

2010-10-01

Full Text Available PURPOSE: To compare the effect of parenteral versus enteral nutritional support in severe acute pancreatitis, with respect to efficacy, safety, morbidity, mortality and length of hospitalization. METHODS: The study was comprised of 31 patients, divided into a parenteral group (n=16 and an enteral group (n=15, who met severity criteria for abdominal tomography (Balthazar classes C, D, and E. The patients were compared by demographics, disease etiology, antibiotic prophylaxis, use or not of somatostatin, nutritional support, complications and disease progression. RESULTS: There was no statistical difference in the average duration of nutritional support, somatostatin, or antibiotics in the two groups. Imipenem was the drug of choice for prophylaxis of pancreatic infections in both groups. More complications occurred in the parenteral group, although the difference was not statistically significant (p=0.10. Infectious complications, such as catheter sepsis and infections of the pancreatic tissue, were significantly more frequent in the parenteral group (p=0.006. There was no difference in average length of hospitalization in the two groups. There were three deaths in the parenteral group and none in the enteral group. CONCLUSION: Enteral nutritional support is associated with fewer septic complications compared to parenteral nutritional support.OBJETIVO: Comparar o efeito do suporte nutricional parenteral versus enteral, em pancreatite aguda grave, com relação à eficácia, à segurança, à morbi-mortalidade e ao tempo de internação. MÉTODOS: Foram estudados 31 pacientes distribuídos em grupo parenteral (n=16, no período de 1995 a 1998 e grupo enteral (n=15, no período de 1999 a 2002, que preencheram os critérios de gravidade pela tomografia de abdome (Balthazar C,D,E. Os pacientes foram comparados quanto aos dados demográficos, etiologia, antibioticoprofilaxia, somatostatina, suporte nutricional, complicações e evolução. RESULTADOS

Current status and outlook of pancreatic islets transplantation research

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Wang Wei; Ye Bin

2006-01-01

Diabetes is a common disease, severely harmful to the human's health and life quality. The pancreatic islets transplantation can correct the patient's hyperglycemia, stop or even reverse the progress of the complication and thus decrease the mortality of diabetic patients. It is the most safe and efficient therapy for diabetes. Since the Edmonton Protocol got success in pancreatic islet transplantation in 2000, it has been more and more interested because of its great clinical curative effect. Research strategy of islet transplantation is now focussed on increasing the acquired islets with normal viability, selecting the best transplantation pathway, and improving the immunosuppression protocol. The shortage of human pancreatic donor is an ever unsolved problem in clinical application. The potential resolutions may include acquisition from xenogenic-islets; islets originated from stem cells, and islets from the living-donor human pancreas. The islets transplantation will open a new application field for interventional radiology. (authors)

D-saccharic acid-1,4-lactone ameliorates alloxan-induced diabetes mellitus and oxidative stress in rats through inhibiting pancreatic beta-cells from apoptosis via mitochondrial dependent pathway

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Bhattacharya, Semantee [Department of Life Sciences and Biotechnology, Jadavpur University, 188, Raja S C Mullick Road, Kolkata 700 032 (India); Manna, Prasenjit [Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata-700054 (India); Gachhui, Ratan [Department of Life Sciences and Biotechnology, Jadavpur University, 188, Raja S C Mullick Road, Kolkata 700 032 (India); Sil, Parames C., E-mail: parames@bosemain.boseinst.ac.in [Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata-700054 (India)

2011-12-15

Oxidative stress plays a vital role in diabetic complications. To suppress the oxidative stress mediated damage in diabetic pathophysiology, a special focus has been given on naturally occurring antioxidants present in normal diet. D-saccharic acid 1,4-lactone (DSL), a derivative of D-glucaric acid, is present in many dietary plants and is known for its detoxifying and antioxidant properties. The aim of the present study was to evaluate the beneficial role of DSL against alloxan (ALX) induced diabetes in the pancreas tissue of Swiss albino rats. A dose-dependent study for DSL (20-120 mg/kg body weight) was carried out to find the effective dose of the compound in ALX-induced diabetic rats. ALX exposure elevated the blood glucose, glycosylated Hb, decreased the plasma insulin and disturbed the intra-cellular antioxidant machineries whereas oral administration of DSL at a dose of 80 mg/kg body weight restored these alterations close to normal. Investigating the mechanism of the protective activity of DSL we observed that it prevented the pancreatic {beta}-cell apoptosis via mitochondria-dependent pathway. Results showed decreased mitochondrial membrane potential, enhanced cytochrome c release in the cytosol and reciprocal regulation of Bcl-2 family proteins in the diabetic rats. These events were also found to be associated with increased level of Apaf-1, caspase 9, and caspase 3 that ultimately led to pancreatic {beta}-cell apoptosis. DSL treatment, however, counteracted these changes. In conclusion, DSL possesses the capability of ameliorating the oxidative stress in ALX-induced diabetes and thus could be a promising approach in lessening diabetic complications. Highlights: Black-Right-Pointing-Pointer Oxidative stress is suggested as a key event in the pathogenesis of diabetes. Black-Right-Pointing-Pointer D-saccharic acid 1,4-lactone (DSL) reduces the alloxan-induced diabetes mellitus. Black-Right-Pointing-Pointer DSL normalizes cellular antioxidant machineries

D-saccharic acid-1,4-lactone ameliorates alloxan-induced diabetes mellitus and oxidative stress in rats through inhibiting pancreatic beta-cells from apoptosis via mitochondrial dependent pathway

International Nuclear Information System (INIS)

Bhattacharya, Semantee; Manna, Prasenjit; Gachhui, Ratan; Sil, Parames C.

2011-01-01

Oxidative stress plays a vital role in diabetic complications. To suppress the oxidative stress mediated damage in diabetic pathophysiology, a special focus has been given on naturally occurring antioxidants present in normal diet. D-saccharic acid 1,4-lactone (DSL), a derivative of D-glucaric acid, is present in many dietary plants and is known for its detoxifying and antioxidant properties. The aim of the present study was to evaluate the beneficial role of DSL against alloxan (ALX) induced diabetes in the pancreas tissue of Swiss albino rats. A dose-dependent study for DSL (20–120 mg/kg body weight) was carried out to find the effective dose of the compound in ALX-induced diabetic rats. ALX exposure elevated the blood glucose, glycosylated Hb, decreased the plasma insulin and disturbed the intra-cellular antioxidant machineries whereas oral administration of DSL at a dose of 80 mg/kg body weight restored these alterations close to normal. Investigating the mechanism of the protective activity of DSL we observed that it prevented the pancreatic β-cell apoptosis via mitochondria-dependent pathway. Results showed decreased mitochondrial membrane potential, enhanced cytochrome c release in the cytosol and reciprocal regulation of Bcl-2 family proteins in the diabetic rats. These events were also found to be associated with increased level of Apaf-1, caspase 9, and caspase 3 that ultimately led to pancreatic β-cell apoptosis. DSL treatment, however, counteracted these changes. In conclusion, DSL possesses the capability of ameliorating the oxidative stress in ALX-induced diabetes and thus could be a promising approach in lessening diabetic complications. Highlights: ► Oxidative stress is suggested as a key event in the pathogenesis of diabetes. ► D-saccharic acid 1,4-lactone (DSL) reduces the alloxan-induced diabetes mellitus. ► DSL normalizes cellular antioxidant machineries disturbed due to alloxan toxicity. ► DSL inhibits pancreatic β-cells apoptosis

Pancreatic cancer: associations of inflammatory potential of diet, cigarette smoking and long-standing diabetes.

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Antwi, Samuel O; Oberg, Ann L; Shivappa, Nitin; Bamlet, William R; Chaffee, Kari G; Steck, Susan E; Hébert, James R; Petersen, Gloria M

2016-05-01

Epidemiologic studies show strong associations between pancreatic cancer (PC) and inflammatory stimuli or conditions such as cigarette smoking and diabetes, suggesting that inflammation may play a key role in PC. Studies of dietary patterns and cancer outcomes also suggest that diet might influence an individual's risk of PC by modulating inflammation. We therefore examined independent and joint associations between inflammatory potential of diet, cigarette smoking and long-standing (≥5 years) type II diabetes in relation to risk of PC. Analyses included data from 817 cases and 1756 controls. Inflammatory potential of diet was measured using the dietary inflammatory index (DII), calculated from dietary intake assessed via a 144-item food frequency questionnaire, and adjusted for energy intake. Information on smoking and diabetes were obtained via risk factor questionnaires. Associations were examined using multivariable-adjusted logistic regression. Higher DII scores, reflecting a more proinflammatory diet, were associated with increased risk of PC [odds ratio (OR)Quintile 5 versus 1 = 2.54, 95% confidence interval (CI) = 1.87-3.46, P trend diet may act as cofactor with cigarette smoking and diabetes to increase risk of PC beyond the risk of any of these factors alone. © The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Oxidative stress as a mechanism of diabetes in diabetic BB prone rats: effect of secoisolariciresinol diglucoside (SDG).

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Prasad, K

2000-06-01

Secoisolariciresinol diglucoside (SDG) isolated from flaxseed has antioxidant activity and has been shown to prevent hypercholesterolemic atherosclerosis. An investigation was made of the effects of SDG on the development of diabetes in diabetic prone BioBreeding rats (BBdp rats), a model of human type I diabetes [insulin dependent diabetes mellitus (IDDM)] to determine if this type of diabetes is due to oxidative stress and if SDG can prevent the incidence of diabetes. The rats were divided into three groups: Group I, BioBreeding normal rats (BBn rats) (n = 10); group II, BBdp untreated (n = 11); and group III, BBdp treated with SDG 22 mg/kg body wt, orally) (n = 14). Oxidative stress was determined by measuring lipid peroxidation product malondialdehyde (MDA) an index of level of reactive oxygen species in blood and pancreas; and pancreatic chemiluminescence (Pancreatic-CL), a measure of antioxidant reserve. Incidence of diabetes was 72.7% in untreated and 21.4% in SDG-treated group as determined by glycosuria and hyperglycemia. SDG prevented the development of diabetes by approximately 71%. Development of diabetes was associated with an increase in serum and pancreatic MDA and a decrease in antioxidant reserve. Prevention in development of diabetes by SDG was associated with a decrease in serum and pancreatic-MDA and an increase in antioxidant reserve. These results suggest that IDDM is mediated through oxidative stress and that SDG prevents the development of diabetes.

Nutrición enteral total vs. nutrición parenteral total en pacientes con pancreatitis aguda grave Total enteral nutrition vs. total parenteral nutrition in patients with severe acute pancreatitis

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M. Casas

2007-05-01

Full Text Available Objetivo: comparar la eficacia de la instauración precoz de nutrición enteral total (NET frente a nutrición parenteral total (NPT en pacientes con pancreatitis aguda grave (PAG. Métodos: estudio prospectivo aleatorio. Se incluyeron consecutivamente 22 pacientes con PAG aplicando los criterios APACHE II, valores de PCR y graduación de Balthazar en la TC. El grupo I (n = 11 recibió NPT y el grupo II (n = 12 NET. Se valoró la respuesta inflamatoria (PCR, TNF-alfa, IL-6, las proteínas viscerales (pre-albúmina, albúmina, la tasa de complicaciones (síndrome de respuesta inflamatoria sistémica, fallo multiorgánico, infecciones, las intervenciones quirúrgicas, la estancia hospitalaria y la mortalidad. Resultados: no hubo diferencias significativas en los primeros 10 días entre los dos grupos en la evolución de los criterios APACHE II, en las concentraciones de PCR, TNF-alfa e IL-6 ni tampoco en los valores de pre-albúmina y albúmina. Siete pacientes del grupo I presentaron complicaciones graves frente a 4 del grupo II. Requirieron intervención quirúrgica 3 pacientes del grupo I. La estancia hospitalaria fue similar en los dos grupos. Dos pacientes del grupo I fallecieron. Conclusiones: se ha observado una tendencia a una mejor evolución de los pacientes con PAG que utilizaron NET frente a los que utilizaron NPT.Objective: to compare the efficacy of early total enteral nutrition (TEN vs. total parenteral nutrition (TPN in patients with severe acute pancreatitis (SAP. Methods: a total of 22 consecutive patients with SAP were randomized to receive TPN (group I or TEN (group II. SAP was defined applying APACHE II score, C-reactive protein (CRP measurements and/or Balthazar CT scan score. Acute inflammatory response (CRP, TNF-alpha, IL-6, visceral proteins (pre-albumin, albumin, complications (systemic inflammatory response syndrome, multiorgan failure, infections, surgical interventions, length of hospital stay and mortality were

Resultados do tratamento da pancreatite aguda grave

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Franz Robert Apodaca-Torrez

Full Text Available OBJETIVO: Avaliar os resultados do Protocolo de Atendimento de pacientes com diagnóstico de pancreatite aguda grave. MÉTODOS: Foram analisados, consecutivamente, a partir de janeiro de 2002, idade, sexo, etiologia, tempo de internação, tipo de tratamento e mortalidade de 37 pacientes portadores de pancreatite aguda grave. RESULTADOS: A idade dos pacientes variou de 20 a 88 anos (média de 50 anos; 27% foram do sexo feminino e 73% do masculino. O tempo médio global de internação foi 47 dias. Treze pacientes foram tratados cirurgicamente; a média de operações realizadas foi duas por paciente. Ocorreram seis óbitos dentre os pacientes submetidos ao tratamento cirúrgico (46% e dois óbitos no grupo submetido somente ao tratamento clínico (8,3%. A mortalidade global foi 21% CONCLUSÃO: Após a modificação na forma de abordagem dos pacientes com pancreatite aguda grave, houve diminuição da mortalidade e uma tendência para a conduta expectante.

Inhibition of cyclooxygenase-2 in experimental severe acute pancreatitis Inibição da Ciclo-Oxigenase-2 na pancreatite aguda grave experimental

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José Luiz Jesus de Almeida

2006-08-01

Full Text Available BACKGROUND: The standard treatment for acute pancreatitis (AP is still based on supportive care. The search for a new drug that could change the natural history of the disease is a continuing challenge for many researchers. The aim of this study is to evaluate the effect of a cyclooxygenase-2 (COX-2 inhibitor on experimental AP in rats. METHODS: The animals were divided into 2 groups: Group 1 (n = 30-animals with taurocholate-induced AP treated with parecoxib (40 mg/kg. Group 2 (n = 30-animals with taurocholate-induced AP that received saline. The COX-2 inhibitor (parecoxib was injected immediately after AP induction, through the penis dorsal vein. The parameters evaluated were histology, serum levels of amylase, IL-6 and IL-10, and mortality rate. RESULTS: The serum levels of IL-6 and IL-10 in the parecoxib-treated group were lower than the control group. The amylase serum levels and the mortality rate remained unchanged in the treated animals. Histologic morphology also was unaltered, except for fat necrosis, which was higher in parecoxib-treated rats. CONCLUSION: Inhibition of Cox-2 decreases the systemic release of inflammatory cytokines, but has a poor effect on the direct pancreas injury caused by taurocholate.INTRODUÇÃO: O tratamento padrão para a pancreatite aguda permanece baseado em medidas de suporte. A busca por uma droga que altere a história natural da doença ainda é um desafio para muitos pesquisadores. O objetivo deste estudo é avaliar o efeito de um inibidor da COX-2 na pancreatite aguda grave experimental (PA em ratos. MÉTODO: Os animais foram divididos em dois Grupos: Grupo 1 (n=30 - animais com PA induzida por taurocolato e tratados com parecoxib (40mg/Kg. Grupo 2 (n=30 - animais com PA induzida por taurocolato que receberam solução salina. O inibidor de COX-2 (parecoxib foi injetado imediatamente após a indução, através da veia dorsal do pênis. Os parâmetros avaliados foram histologia, níveis séricos de

Anti-diabetic potential of the essential oil of Pinus koraiensis leaves toward streptozotocin-treated mice and HIT-T15 pancreatic β cells.

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Joo, Hye-Eun; Lee, Hyo-Jung; Sohn, Eun Jung; Lee, Min-Ho; Ko, Hyun-Suk; Jeong, Soo-Jin; Lee, Hyo-Jeong; Kim, Sung-Hoon

2013-01-01

The metabolic syndrome creates risk factors for coronary heart disease, diabetes, fatty liver, obesity and several cancers. Our group has already reported that the essential oil from leaves of Pinus koraiensis SIEB (EOPK) exerted antihyperlipidemic effects by upregulating the low-density lipoprotein receptor and inhibiting acyl-coenzyme A, cholesterol acyltransferases. We evaluated in the current study the anti-diabetic effects of EOPK on mice with streptozotocin (STZ)-induced type I diabetes and on HIT-T15 pancreatic β cells. EOPK significantly protected HIT-T15 cells from STZ-induced cytotoxicity and reduced the blood glucose level in STZ-induced diabetic mice when compared with the untreated control. EOPK consistently and significantly suppressed the α-amylase activity in a dose-dependent manner and enhanced the expression of insulin at the mRNA level in STZ-treated HIT-T15 cells, while the expression of insulin was attenuated. EOPK also significantly abrogated the population of reactive oxygen species when compared to the untreated control in STZ-treated HIT-T15 cells. Furthermore, EOPK significantly reduce nitric oxide production, suppressed the phosphorylation of endothelial nitric oxide (NO) synthase and suppressed the production of vascular endothelial growth factor (VEGF) in STZ-treated HIT-T15 cells, implying its potential application to diabetic retinopathy. Overall, our findings suggest that EOPK had hypoglycemic potential by inhibiting reactive oxygene species (ROS), endothelial NO synthase (eNOS) and VEGF in STZ-treated mice and HIT-T15 pancreatic β cells as a potent anti-diabetic agent.

Pterocarpan-Enriched Soy Leaf Extract Ameliorates Insulin Sensitivity and Pancreatic β-Cell Proliferation in Type 2 Diabetic Mice

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Un-Hee Kim

2014-11-01

Full Text Available In Korea, soy (Glycine max (L. Merr. leaves are eaten as a seasonal vegetable or pickled in soy sauce. Ethyl acetate extracts of soy leaves (EASL are enriched in pterocarpans and have potent α-glucosidase inhibitory activity. This study investigated the molecular mechanisms underlying the anti-diabetic effect of EASL in C57BL/6J mice with high-fat diet (HFD-induced type 2 diabetes. Mice were randomly divided into normal diet (ND, HFD (60 kcal% fat diet, EASL (HFD with 0.56% (wt/wt EASL, and Pinitol (HFD with 0.15% (wt/wt pinitol groups. Weight gain and abdominal fat accumulation were significantly suppressed by EASL. Levels of plasma glucose, HbA1c, and insulin in the EASL group were significantly lower than those of the HFD group, and the pancreatic islet of the EASL group had greater size than those of the HFD group. EASL group up-regulated neurogenin 3 (Ngn3, paired box 4 (Pax4, and v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA, which are markers of pancreatic cell development, as well as insulin receptor substrate 1 (IRS1, IRS2, and glucose transporter 4 (GLUT4, which are related to insulin sensitivity. Furthermore, EASL suppressed genes involved in hepatic gluconeogenesis and steatosis. These results suggest that EASL improves plasma glucose and insulin levels in mice with HDF-induced type 2 diabetes by regulating β-cell proliferation and insulin sensitivity.

Comparative occurrence of diabetes in canine, feline, and few wild animals and their association with pancreatic diseases and ketoacidosis with therapeutic approach.

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Niaz, Kamal; Maqbool, Faheem; Khan, Fazlullah; Hassan, Fatima Ismail; Momtaz, Saeideh; Abdollahi, Mohammad

2018-04-01

Diabetes mellitus (DM) is a chronic metabolic disorder in which blood glucose level raises that can result in severe complications. However, the incidence increased mostly by obesity, pregnancy, persistent corpus luteum, and diestrus phase in humans and animals. This review has focused on addressing the possible understanding and pathogenesis of spontaneous DM in canine, feline, and few wild animals. Furthermore, pancreatic associated disorders, diabetic ketoacidosis, hormonal and drug interaction with diabetes, and herbal remedies associated with DM are elucidated. Bibliographic search for the present review was done using PubMed, Scopus, and Google Scholar for articles on concurrent DM in small and wild animals. Persistent corpus luteal and pseudopregnancy in female dogs generate gestational DM (GDM). GDM can also be caused by extensive use of drugs/hormones such as glucocorticosteroids. Although many similarities are present between diabetic cats and diabetic humans which present islet amyloidosis, there was a progressive loss of β- and α-cells and the normal number of δ-cells. The most prominent similarity is the occurrence of islet amyloidosis in all cases of diabetic cat and over 90% of human non-insulin dependent DM Type-2. Acute pancreatic necrosis (APN) occurs due to predisposing factors such as insulin antagonism, insulin resistance, alteration in glucose tolerance, obesity, hyperadrenocorticism, and persistent usage of glucocorticoids, as these play a vital role in the progression of APN. To manage such conditions, it is important to deal with the etiological agent, risk factors, diagnosis of diabetes, and hormonal and drug interaction along with its termination with suitable therapy (herbal) protocols. It should be noted that the protocols used for the diagnosis and treatment of human DM are not appropriate for animals. Further investigations regarding diabetic conditions of pets and wild animals are required, which will benefit the health status of

Comparative occurrence of diabetes in canine, feline, and few wild animals and their association with pancreatic diseases and ketoacidosis with therapeutic approach

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Kamal Niaz

2018-04-01

Full Text Available Diabetes mellitus (DM is a chronic metabolic disorder in which blood glucose level raises that can result in severe complications. However, the incidence increased mostly by obesity, pregnancy, persistent corpus luteum, and diestrus phase in humans and animals. This review has focused on addressing the possible understanding and pathogenesis of spontaneous DM in canine, feline, and few wild animals. Furthermore, pancreatic associated disorders, diabetic ketoacidosis, hormonal and drug interaction with diabetes, and herbal remedies associated with DM are elucidated. Bibliographic search for the present review was done using PubMed, Scopus, and Google Scholar for articles on concurrent DM in small and wild animals. Persistent corpus luteal and pseudopregnancy in female dogs generate gestational DM (GDM. GDM can also be caused by extensive use of drugs/hormones such as glucocorticosteroids. Although many similarities are present between diabetic cats and diabetic humans which present islet amyloidosis, there was a progressive loss of β- and α-cells and the normal number of δ-cells. The most prominent similarity is the occurrence of islet amyloidosis in all cases of diabetic cat and over 90% of human non-insulin dependent DM Type-2. Acute pancreatic necrosis (APN occurs due to predisposing factors such as insulin antagonism, insulin resistance, alteration in glucose tolerance, obesity, hyperadrenocorticism, and persistent usage of glucocorticoids, as these play a vital role in the progression of APN. To manage such conditions, it is important to deal with the etiological agent, risk factors, diagnosis of diabetes, and hormonal and drug interaction along with its termination with suitable therapy (herbal protocols. It should be noted that the protocols used for the diagnosis and treatment of human DM are not appropriate for animals. Further investigations regarding diabetic conditions of pets and wild animals are required, which will benefit the

Chronic pancreatitis: from guidelines to clinical practice

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Generoso Uomo

2012-10-01

Full Text Available Introduction The paucity of specific standardized criteria leads to uncertainties in clinical practice regarding the management of chronic pancreatitis (CP.Objectives This paper reports some of the systematic guidelines for the diagnosis and treatment of CP recently elaborated by an Italian multicenter study group. We review recommendations on clinical and nutritional aspects of the disease, assessment of pancreatic function, treatment of exocrine pancreatic failure and secondary diabetes, treatment of pain, and prevention of painful relapses. The review also looks at the role of endoscopy in the management of pancreatic pain, pancreatic stones, duct narrowing and dilation, and complications; the appropriate use of various imaging techniques, including endoscopic ultrasound; and the indications for and techniques used in surgical management of CP.

Oral administration of soybean peptide Vglycin normalizes fasting glucose and restores impaired pancreatic function in Type 2 diabetic Wistar rats.

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Jiang, Hua; Feng, Jueping; Du, Zhongxia; Zhen, Hui; Lin, Mei; Jia, Shaohui; Li, Tao; Huang, Xinyuan; Ostenson, Claes-Goran; Chen, Zhengwang

2014-09-01

Vglycin, a natural 37-residue polypeptide isolated from pea seeds in which six half-cysteine residues are embedded in three pairs of disulfide bonds, is resistant to digestive enzymes and has antidiabetic potential. To investigate the pharmacological activity of Vglycin in vivo and to examine the mechanisms involved, the therapeutic effect of Vglycin in diabetic rats was examined. Diabetes was induced in Wistar rats by high-fat diet and multiple streptozotocin intraperitoneal injections. Diabetic rats were treated daily with Vglycin for 4 weeks. Body weight, food intake, fasting plasma glucose and insulin levels were assayed weekly. Glucose and insulin tolerance tests were conducted on Day 29. Subsequently, levels of p-Akt in the liver and pancreas and cleaved PARP, Pdx-1 and insulin in the pancreas were detected by immunoblotting. The morphology of the pancreas and the insulin expression in the pancreas were analyzed by hematoxylin-eosin staining and immunohistochemistry, respectively. Furthermore, human liver-derived cell lines were used to explore the in vitro effects of Vglycin on insulin sensitivity and glucose uptake. Chronic treatment with Vglycin normalized fasting glucose levels in diabetic rats. The improvement in glucose homeostasis and the increased insulin sensitivity mediated by restored insulin signaling likely contributed to decreased food intake and reduced body weight. Vglycin protected pancreatic cells from damage by streptozotocin. Although insulin synthesis and secretion in impaired β-cell were not significantly elevated, islets morphology was improved in the Vglycin-treated groups. These results suggest that Vglycin could be useful in Type 2 diabetes for restoring impaired insulin signaling, glucose tolerance and pancreatic function. Copyright © 2014 Elsevier Inc. All rights reserved.

Computed tomography of the pancreas in diabetic patients

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Katsumata, Kazuo; Katsumata, Yoshinao; Nakagawa, Takeo; Sakuma, Sadayuki.

1984-01-01

Computed tomography (CT) of the pancreas usually shows either a smooth or granular image in the margin and contents. We have divided these images into three types in both the margin and contents (smooth type, fine-granule type and rough-granule type). These types were analyzed in relation to the clinical features of diabetes mellitus. Four hundred and six controls without diabete, mellitus, gallstones, pancreatitis, liver cirrhosis or malignant tumors were analyzed as a control group, and 121 diabetic patients without these four complications were analyzed as a diabetic group. The following results were obtained. 1. In the control group, the younger obese persons showeds high incidence of the rough-granule type of the pancreatic margin and contents. This decreased with an increase in age. 2. In the diabetic group, the incidence of the rough-granule type of both the pancreatic margin and contents was high among the elderly and older patients. Lean patients did not show the rough-granule type of pancreatic contents. The incidence of the rough-granule type tended to decrease as the clinical features became worse. 3. Pancreata having the rough-granule type of pancreatic contents were considered to be rich in fat tissue. (author)

Computed tomography of the pancreas in diabetic patients

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Katsumata, Kazuo [Katsumata Hospital, Nagoya (Japan); Katsumata, Yoshinao; Nakagawa, Takeo; Sakuma, Sadayuki

1984-08-01

Computed tomography (CT) of the pancreas usually shows either a smooth or granular image in the margin and contents. We have divided these images into three types in both the margin and contents (smooth type, fine-granule type and rough-granule type). These types were analyzed in relation to the clinical features of diabetes mellitus. Four hundred and six controls without diabete, mellitus, gallstones, pancreatitis, liver cirrhosis or malignant tumors were analyzed as a control group, and 121 diabetic patients without these four complications were analyzed as a diabetic group. The following results were obtained. 1. In the control group, the younger obese persons showed high incidence of the rough-granule type of the pancreatic margin and contents. This decreased with an increase in age. 2. In the diabetic group, the incidence of the rough-granule type of both the pancreatic margin and contents was high among the elderly and older patients. Lean patients did not show the rough-granule type of pancreatic contents. The incidence of the rough-granule type tended to decrease as the clinical features became worse. 3. Pancreata having the rough-granule type of pancreatic contents were considered to be rich in fat tissue.

Roles of HNF1α and HNF4α in pancreatic β-cells: lessons from a monogenic form of diabetes (MODY).

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Yamagata, Kazuya

2014-01-01

Mutations in the genes encoding hepatocyte nuclear factor (HNF)1α and HNF4α cause a monogenic form of diabetes mellitus known as maturity-onset diabetes of the young (MODY). The primary cause of MODY is an impairment of glucose-stimulated insulin secretion by pancreatic β-cells, indicating the important roles of HNF1α and HNF4α in β-cells. Large-scale genetic studies have clarified that the common variants of HNF1α and HNF4α genes are also associated with type 2 diabetes, suggesting that they are involved in the pathogenesis of both diseases. Recent experimental studies revealed that HNF1α controls both β-cell function and growth by regulating target genes such as glucose transporter 2, pyruvate kinase, collectrin, hepatocyte growth factor activator, and HNF4α. In contrast, HNF4α mainly regulates the function of β-cells. Although direct target genes of HNF4α in β-cells are largely unknown, we recently identified Anks4b as a novel target of HNF4α that regulates β-cell susceptibility to endoplasmic reticulum stress. Studies of MODY have led to a better understanding of the molecular mechanism of glucose-stimulated insulin secretion by pancreatic β-cells. © 2014 Elsevier Inc. All rights reserved.

GLUT4 in the endocrine pancreas--indicating an impact in pancreatic islet cell physiology?

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Bähr, I; Bazwinsky-Wutschke, I; Wolgast, S; Hofmann, K; Streck, S; Mühlbauer, E; Wedekind, D; Peschke, E

2012-06-01

The glucose transporter GLUT4 is well known to facilitate the transport of blood glucose into insulin-sensitive muscle and adipose tissue. In this study, molecular, immunohistochemical, and Western blot investigations revealed evidence that GLUT4 is also located in the mouse, rat, and human endocrine pancreas. In addition, high glucose decreased and insulin elevated the GLUT4 expression in pancreatic α-cells. In contrast, high glucose increased GLUT4 expression, whereas insulin led to a reduced expression level of the glucose transporter in pancreatic β-cells. In vivo experiments showed that in pancreatic tissue of type 2 diabetic rats as well as type 2 diabetic patients, the GLUT4 expression is significantly increased compared to the nondiabetic control group. Furthermore, type 1 diabetic rats exhibited reduced GLUT4 transcript levels in pancreatic tissue, whereas insulin treatment of type 1 diabetic animals enhanced the GLUT4 expression back to control levels. These data provide evidence for the existence of GLUT4 in the endocrine pancreas and indicate a physiological relevance of this glucose transporter as well as characteristic changes in diabetic disease. © Georg Thieme Verlag KG Stuttgart · New York.

Nefrite Intersticial Aguda Após Exposição a Losartan

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Letícia Schwerz Weinert

2007-07-01

Full Text Available Nefrite intersticial aguda é uma causa comum de perda aguda de função renal. Exposição a drogas é o fator desencadeante mais freqüentemente relatado, porém auto-imunidade e infecções também estão associadas. Os inibidores da enzima de conversão da angiotensina têm sido relatados como possíveis agentes, porém não há relato na literatura de nefrite intersticial com uso de losartan. Descrevemos então, o caso de perda aguda de função renal após exposição a losartan, em paciente com dano renal prévio por nefropatia diabética, cuja biópsia renal diagnosticou nefrite intersticial aguda.

Chronic Pancreatitis: A Changing Etiology?

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Raffaele Pezzilli; Andrea Lioce; Luca Frulloni

2008-01-01

In 1998, Lankisch and Banks reported that the prevalence of chronic pancreatitis appeared to be in the range of 3-10 per 100,000 people in many parts of the world [1]. They also emphasized that the most important medical problems associated with the disease included abdominal pain, steatorrhea, diabetes mellitus and the possibility that chronic pancreatitis may be considered a premalignant condition [2, 3]. In 2002, in a well-written review, Banks pointed out that the two important forms were...

Pancreatic endocrine and exocrine function in children following near-total pancreatectomy for diffuse congenital hyperinsulinism.

Science.gov (United States)

Arya, Ved Bhushan; Senniappan, Senthil; Demirbilek, Huseyin; Alam, Syeda; Flanagan, Sarah E; Ellard, Sian; Hussain, Khalid

2014-01-01

Congenital hyperinsulinism (CHI), the commonest cause of persistent hypoglycaemia, has two main histological subtypes: diffuse and focal. Diffuse CHI, if medically unresponsive, is managed with near-total pancreatectomy. Post-pancreatectomy, in addition to persistent hypoglycaemia, there is a very high risk of diabetes mellitus and pancreatic exocrine insufficiency. International referral centre for the management of CHI. Medically unresponsive diffuse CHI patients managed with near-total pancreatectomy between 1994 and 2012. Near-total pancreatectomy. Persistent hypoglycaemia post near-total pancreatectomy, insulin-dependent diabetes mellitus, clinical and biochemical (faecal elastase 1) pancreatic exocrine insufficiency. Of more than 300 patients with CHI managed during this time period, 45 children had medically unresponsive diffuse disease and were managed with near-total pancreatectomy. After near-total pancreatectomy, 60% of children had persistent hypoglycaemia requiring medical interventions. The incidence of insulin dependent diabetes mellitus was 96% at 11 years after surgery. Thirty-two patients (72%) had biochemical evidence of severe pancreatic exocrine insufficiency (Faecal elastase 1insufficiency was observed in 22 (49%) patients. No statistically significant difference in weight and height standard deviation score (SDS) was found between untreated subclinical pancreatic exocrine insufficiency patients and treated clinical pancreatic exocrine insufficiency patients. The outcome of diffuse CHI patients after near-total pancreatectomy is very unsatisfactory. The incidence of persistent hypoglycaemia and insulin-dependent diabetes mellitus is very high. The presence of clinical rather than biochemical pancreatic exocrine insufficiency should inform decisions about pancreatic enzyme supplementation.

Pancreatic endocrine and exocrine function in children following near-total pancreatectomy for diffuse congenital hyperinsulinism.

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Ved Bhushan Arya

Full Text Available Congenital hyperinsulinism (CHI, the commonest cause of persistent hypoglycaemia, has two main histological subtypes: diffuse and focal. Diffuse CHI, if medically unresponsive, is managed with near-total pancreatectomy. Post-pancreatectomy, in addition to persistent hypoglycaemia, there is a very high risk of diabetes mellitus and pancreatic exocrine insufficiency.International referral centre for the management of CHI.Medically unresponsive diffuse CHI patients managed with near-total pancreatectomy between 1994 and 2012.Near-total pancreatectomy.Persistent hypoglycaemia post near-total pancreatectomy, insulin-dependent diabetes mellitus, clinical and biochemical (faecal elastase 1 pancreatic exocrine insufficiency.Of more than 300 patients with CHI managed during this time period, 45 children had medically unresponsive diffuse disease and were managed with near-total pancreatectomy. After near-total pancreatectomy, 60% of children had persistent hypoglycaemia requiring medical interventions. The incidence of insulin dependent diabetes mellitus was 96% at 11 years after surgery. Thirty-two patients (72% had biochemical evidence of severe pancreatic exocrine insufficiency (Faecal elastase 1<100 µg/g. Clinical exocrine insufficiency was observed in 22 (49% patients. No statistically significant difference in weight and height standard deviation score (SDS was found between untreated subclinical pancreatic exocrine insufficiency patients and treated clinical pancreatic exocrine insufficiency patients.The outcome of diffuse CHI patients after near-total pancreatectomy is very unsatisfactory. The incidence of persistent hypoglycaemia and insulin-dependent diabetes mellitus is very high. The presence of clinical rather than biochemical pancreatic exocrine insufficiency should inform decisions about pancreatic enzyme supplementation.

Hypoglycemic and pancreatic protective effects of Portulaca oleracea extract in alloxan induced diabetic rats.

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Ramadan, Basma K; Schaalan, Mona F; Tolba, Amina M

2017-01-11

Diabetes is a major public health concern. In spite of continuous new drug development to treat diabetes, herbal remedies remain a potential adjunct therapy to maintain better glycemic control while also imparting few side-effects. Portulaca oleracea has been traditionally used to manage several diseases due to the anti-oxidant and anti-atherogenic effects it imparts. To better understand the mechanisms associated with potential protective effect of P. oleracea extract against diabetes, alloxan-induced diabetic rats were used in this study. Forty Wistar rats (male, 7-8-wk-old, 140-160 g) were divided into four groups (n = 10/group): Group I (control), Group II (P. oleracea-treated; gavaged with P. oleracea extract daily [at 250 mg/kg] for 4 weeks), Group III (diabetic control; daily IP injection of alloxan [at 75 mg/kg] for 5 days) and Group IV (P. oleracea-pre-treated diabetic; gavaged with P. oleracea extract daily [at 250 mg/kg] for 4 weeks and then daily IP injection of alloxan [at 75 mg/kg] for 5 days). Body weight, food consumption, blood (serum) levels of glucose, C peptide, Hb A1C, insulin, tumor necrosis factor (TNF)-α and interleukin (IL)-6 were determined for all groups. The results indicated that while Hb A1C, serum levels of glucose, TNF-α and IL-6 were all significantly decreased in the P. oleracea-pre-treated diabetic rats, these hosts also had significant increases in C peptide and insulin compared to levels in the counterpart diabetic rats. These results were confirmed by the histopathological assessments which showed marked improvement of the destructive effect on pancreatic islet cells induced by alloxan. P. oleracea extract is a general tissue protective and regeneartive agent, as evidenced by increasing β-cell mass and therefore improved the glucose metabolism. Thus, stimulation of Portulaca oleracea signaling in β- cells may be a novel therapeutic strategy for diabetes prevention.

Apendicitis Aguda

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Jorge Fallas González

2012-01-01

La apendicitis aguda, descrita desde 1886, es la emergencia quirúrgica más común. Tiene su mayor incidencia durante la adultez joven y su menor incidencia en niños y adultos mayores. Su diagnóstico se basa en una historia clínica completa, un examen físico bien orientado y en una adecuada interpretación de los exámenes de laboratorio y gabinete. A pesar de ser una entidad de resolución quirúrgica, su tratamiento engloba diferentes aspectos médicosAcute appendicitis, described since 1886, is t...

Prospective assessment of the influence of pancreatic cancer resection on exocrine pancreatic function.

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Sikkens, E C M; Cahen, D L; de Wit, J; Looman, C W N; van Eijck, C; Bruno, M J

2014-01-01

Exocrine insufficiency frequently develops in patients with pancreatic cancer owing to tumour ingrowth and pancreatic duct obstruction. Surgery might restore this function by removing the primary disease and restoring duct patency, but it may also have the opposite effect, as a result of resection of functional parenchyma and anatomical changes. This study evaluated the course of pancreatic function, before and after pancreatic resection. This prospective cohort study included patients with tumours in the pancreatic region requiring pancreatic resection in a tertiary referral centre between March 2010 and August 2012. Starting before surgery, exocrine function was determined monthly by measuring faecal elastase 1 levels (normal value over 0.200 µg per g faeces). Endocrine function, steatorrhoea-related symptoms and bodyweight were also evaluated before and after surgery. Subjects were followed from diagnosis until 6 months after surgery, or until death. Twenty-nine patients were included, 12 with pancreatic cancer, 14 with ampullary carcinoma and three with bile duct carcinoma (median tumour size 2.6 cm). Twenty-six patients underwent pancreaticoduodenectomy and three distal pancreatectomy. Thirteen patients had exocrine insufficiency at preoperative diagnosis. After a median follow-up of 6 months, this had increased to 24 patients. Diabetes was present in seven patients at diagnosis, and developed in one additional patient within 1 month after surgery. Most patients with tumours in the pancreatic region requiring pancreatic resection either had exocrine insufficiency at diagnosis or became exocrine-insufficient soon after surgical resection. © 2013 BJS Society Ltd. Published by John Wiley & Sons Ltd.

Nutritional and Metabolic Derangements in Pancreatic Cancer and Pancreatic Resection

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Taylor M. Gilliland

2017-03-01

Full Text Available Pancreatic cancer is an aggressive malignancy with a poor prognosis. The disease and its treatment can cause significant nutritional impairments that often adversely impact patient quality of life (QOL. The pancreas has both exocrine and endocrine functions and, in the setting of cancer, both systems may be affected. Pancreatic exocrine insufficiency (PEI manifests as weight loss and steatorrhea, while endocrine insufficiency may result in diabetes mellitus. Surgical resection, a central component of pancreatic cancer treatment, may induce or exacerbate these dysfunctions. Nutritional and metabolic dysfunctions in patients with pancreatic cancer lack characterization, and few guidelines exist for nutritional support in patients after surgical resection. We reviewed publications from the past two decades (1995–2016 addressing the nutritional and metabolic status of patients with pancreatic cancer, grouping them into status at the time of diagnosis, status at the time of resection, and status of nutritional support throughout the diagnosis and treatment of pancreatic cancer. Here, we summarize the results of these investigations and evaluate the effectiveness of various types of nutritional support in patients after pancreatectomy for pancreatic adenocarcinoma (PDAC. We outline the following conservative perioperative strategies to optimize patient outcomes and guide the care of these patients: (1 patients with albumin < 2.5 mg/dL or weight loss > 10% should postpone surgery and begin aggressive nutrition supplementation; (2 patients with albumin < 3 mg/dL or weight loss between 5% and 10% should have nutrition supplementation prior to surgery; (3 enteral nutrition (EN should be preferred as a nutritional intervention over total parenteral nutrition (TPN postoperatively; and, (4 a multidisciplinary approach should be used to allow for early detection of symptoms of endocrine and exocrine pancreatic insufficiency alongside implementation of

Elevated Medium-Chain Acylcarnitines Are Associated With Gestational Diabetes Mellitus and Early Progression to Type 2 Diabetes and Induce Pancreatic β-Cell Dysfunction.

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Batchuluun, Battsetseg; Al Rijjal, Dana; Prentice, Kacey J; Eversley, Judith A; Burdett, Elena; Mohan, Haneesha; Bhattacharjee, Alpana; Gunderson, Erica P; Liu, Ying; Wheeler, Michael B

2018-05-01

Specific circulating metabolites have emerged as important risk factors for the development of diabetes. The acylcarnitines (acylCs) are a family of metabolites known to be elevated in type 2 diabetes (T2D) and linked to peripheral insulin resistance. However, the effect of acylCs on pancreatic β-cell function is not well understood. Here, we profiled circulating acylCs in two diabetes cohorts: 1 ) women with gestational diabetes mellitus (GDM) and 2 ) women with recent GDM who later developed impaired glucose tolerance (IGT), new-onset T2D, or returned to normoglycemia within a 2-year follow-up period. We observed a specific elevation in serum medium-chain (M)-acylCs, particularly hexanoyl- and octanoylcarnitine, among women with GDM and individuals with T2D without alteration in long-chain acylCs. Mice treated with M-acylCs exhibited glucose intolerance, attributed to impaired insulin secretion. Murine and human islets exposed to elevated levels of M-acylCs developed defects in glucose-stimulated insulin secretion and this was directly linked to reduced mitochondrial respiratory capacity and subsequent ability to couple glucose metabolism to insulin secretion. In conclusion, our study reveals that an elevation in circulating M-acylCs is associated with GDM and early stages of T2D onset and that this elevation directly impairs β-cell function. © 2018 by the American Diabetes Association.

pancreatic steatosis: diagnosis and clinical significance

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Murat Daðdeviren

2017-03-01

Full Text Available Pancreatic steatosis (PS, with increased use of abdominal imaging in recent years generally appears as incidental. But it is a condition that is often overlooked. The reason for this is not yet fully demonstrated the clinical significance of PS while. However, in recent years, there are some studies conducted on the relationship with ps and other disease such as diabetes, metabolic syndrome, acute and chronic pancreatitis and pancreatic cancer. In this review, the etiology, diagnosis, treatment and clinical characteristics of ps were evaluated in the light of recent literature and current approaches. [J Contemp Med 2017; 7(1.000: 107-112

Molecular biology of pancreatic cancer.

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Zavoral, Miroslav; Minarikova, Petra; Zavada, Filip; Salek, Cyril; Minarik, Marek

2011-06-28

In spite of continuous research efforts directed at early detection and treatment of pancreatic cancer, the outlook for patients affected by the disease remains dismal. With most cases still being diagnosed at advanced stages, no improvement in survival prognosis is achieved with current diagnostic imaging approaches. In the absence of a dominant precancerous condition, several risk factors have been identified including family history, chronic pancreatitis, smoking, diabetes mellitus, as well as certain genetic disorders such as hereditary pancreatitis, cystic fibrosis, familial atypical multiple mole melanoma, and Peutz-Jeghers and Lynch syndromes. Most pancreatic carcinomas, however, remain sporadic. Current progress in experimental molecular techniques has enabled detailed understanding of the molecular processes of pancreatic cancer development. According to the latest information, malignant pancreatic transformation involves multiple oncogenes and tumor-suppressor genes that are involved in a variety of signaling pathways. The most characteristic aberrations (somatic point mutations and allelic losses) affect oncogenes and tumor-suppressor genes within RAS, AKT and Wnt signaling, and have a key role in transcription and proliferation, as well as systems that regulate the cell cycle (SMAD/DPC, CDKN2A/p16) and apoptosis (TP53). Understanding of the underlying molecular mechanisms should promote development of new methodology for early diagnosis and facilitate improvement in current approaches for pancreatic cancer treatment.

Repeated Gene Transfection Impairs the Engraftment of Transplanted Porcine Neonatal Pancreatic Cells

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Min Koo Seo

2011-02-01

Full Text Available BackgroundPreviously, we reported that neonatal porcine pancreatic cells transfected with hepatocyte growth factor (HGF gene in an Epstein-Barr virus (EBV-based plasmid (pEBVHGF showed improved proliferation and differentiation compared to those of the control. In this study, we examined if pancreatic cells transfected repeatedly with pEBVHGF can be successfully grafted to control blood glucose in a diabetes mouse model.MethodsNeonatal porcine pancreatic cells were cultured as a monolayer and were transfected with pEBVHGF every other day for a total of three transfections. The transfected pancreatic cells were re-aggregated and transplanted into kidney capsules of diabetic nude mice or normal nude mice. Blood glucose level and body weight were measured every other day after transplantation. The engraftment of the transplanted cells and differentiation into beta cells were assessed using immunohistochemistry.ResultsRe-aggregation of the pancreatic cells before transplantation improved engraftment of the cells and facilitated neovascularization of the graft. Right before transplantation, pancreatic cells that were transfected with pEBVHGF and then re-aggregated showed ductal cell marker expression. However, ductal cells disappeared and the cells underwent fibrosis in a diabetes mouse model two to five weeks after transplantation; these mice also did not show controlled blood glucose levels. Furthermore, pancreatic cells transplanted into nude mice with normal blood glucose showed poor graft survival regardless of the type of transfected plasmid (pCEP4, pHGF, or pEBVHGF.ConclusionFor clinical application of transfected neonatal porcine pancreatic cells, further studies are required to develop methods of overcoming the damage for the cells caused by repeated transfection and to re-aggregate them into islet-like structures.

Gingivitis ulceronecrosante aguda

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Eduardo de la Teja-Ángeles

2015-11-01

Full Text Available La gingivitis ulcerativa necrosante, conocida por sus siglas en inglés como GUN (anteriormente se le conocía como enfermedad de Vincent o “boca de trinchera” por afectar a soldados en guerra, es una enfermedad poco frecuente.1-6 Se caracteriza por ser una infección aguda y dolorosa en la que las encías sangran, hay necrosis de las papilas interdentales y ataque al estado general.

Incretin-based therapies and risk of pancreatic cancer in patients with type 2 diabetes: A meta-analysis of randomized controlled trials.

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Wang, Haining; Liu, Ye; Tian, Qing; Yang, Jin; Lu, Ran; Zhan, Siyan; Haukka, Jari; Hong, Tianpei

2018-04-01

To perform a meta-analysis of randomized controlled trials (RCTs), including 6 recently published large-scale cardiovascular outcome trials (CVOTs), to evaluate the risk of pancreatic cancer with incretin-based therapies in patients with type 2 diabetes (T2DM). For the period January 1, 2007 to May 1, 2017, the PubMed, Embase, Cochrane Central Register and ClininalTrials.gov databases were searched for RCTs in people with T2DM that compared incretin drugs with placebo or other antidiabetic drugs, with treatment and follow-up durations of ≥52 weeks. Two reviewers screened the studies, extracted the data and assessed the risk of bias independently and in duplicate. A total of 33 studies (n = 79 971), including the 6 CVOTs, with 87 pancreatic cancer events were identified. Overall, the pancreatic cancer risk was not increased in patients administered incretin drugs compared with controls (Peto odds ratio [OR] 0.67, 95% confidence interval [CI] 0.44-1.02). In the 6 CVOTs, 79 pancreatic cancer events were identified in 55 248 participants. Pooled estimates of the 6 CVOTs showed an identical tendency (Peto OR 0.65, 95% CI 0.42-1.01). Notably, in the subgroup of participants who received treatment and follow-up for ≥104 weeks, 84 pancreatic cancer events were identified in 59 919 participants, and a lower risk of pancreatic cancer was associated with incretin-based therapies (Peto OR 0.62, 95% CI 0.41-0.95). Treatment with incretin drugs was not associated with an increased risk of pancreatic cancer in people with T2DM. Instead, it might protect against pancreatic malignancy in patients treated for ≥104 weeks. © 2017 John Wiley & Sons Ltd.

Production of pancreatic hormone-expressing endocrine cells from human embryonic stem cells.

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D'Amour, Kevin A; Bang, Anne G; Eliazer, Susan; Kelly, Olivia G; Agulnick, Alan D; Smart, Nora G; Moorman, Mark A; Kroon, Evert; Carpenter, Melissa K; Baetge, Emmanuel E

2006-11-01

Of paramount importance for the development of cell therapies to treat diabetes is the production of sufficient numbers of pancreatic endocrine cells that function similarly to primary islets. We have developed a differentiation process that converts human embryonic stem (hES) cells to endocrine cells capable of synthesizing the pancreatic hormones insulin, glucagon, somatostatin, pancreatic polypeptide and ghrelin. This process mimics in vivo pancreatic organogenesis by directing cells through stages resembling definitive endoderm, gut-tube endoderm, pancreatic endoderm and endocrine precursor--en route to cells that express endocrine hormones. The hES cell-derived insulin-expressing cells have an insulin content approaching that of adult islets. Similar to fetal beta-cells, they release C-peptide in response to multiple secretory stimuli, but only minimally to glucose. Production of these hES cell-derived endocrine cells may represent a critical step in the development of a renewable source of cells for diabetes cell therapy.

The long-term follow up study of acute pancreatitis by means of pancreatic scintigraphy, secretin test and oral glucose tolerance test

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Satoh, Harukuni

1975-01-01

Morphologic and functional alternations of the pancreas following acute pancreatitis were studied in 29 patients. At the time of attack a diagnosis of acute pancreatitis had been confirmed by laparotomy in 27 cases, and by clinical picture and by serum amylase levels in 2 cases. The average duration of follow up was 56.3 months. Normal images were obtained in 17 of 29 cases. According to secretin tests, 4 of these had slight to moderately decreased exocrine function; the test were within normal limits. 12 cases with normal image had abnormal oral glucose tolerance curves similar to those fund in mild to moderate diabetes. 10 of the 12 cases with abnormal scintigrams showed decreased isotope uptake in all or part of the pancreas, while 2 showed no uptake at all. These changes were mast apparent in the tail of the pancreas. Ten of the 12 cases with abnormal images had some degree of decreased exocrine function. All 12 had the abnormal GTT curve of diabetes, 4 who had severe diabetes with markedly decreased exocrine function and poor image of the pancreas. In 4 cases the histopathological findings obtained at the time of laparotomy, were shown to be very consistent with the scintigraphic features. It was demonstrated by both scintigraphs and function tests that the alcoholic factor plays a very important role in the prognosis of acute pancreatitis. Acute pancreatitis resulted in chronic pancreatitis in 4 cases, (14 %) of the remaining 8 cases with abnormal scintigram, it is postulated that the inflamatory process subsided allowing time for cicatrical fibrosis to occur. Follow-up to trace and study of these alternations of the pancreas necessary in future. (Evans, J.)

The long-term follow up study of acute pancreatitis by means of pancreatic scintigraphy, secretin test and oral glucose tolerance test

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Satoh, H [Tohoku Univ., Sendai (Japan). School of Medicine

1975-03-01

Morphologic and functional alternations of the pancreas following acute pancreatitis were studied in 29 patients. At the time of attack a diagnosis of acute pancreatitis had been confirmed by laparotomy in 27 cases, and by clinical picture and by serum amylase levels in 2 cases. The average duration of follow up was 56.3 months. Normal images were obtained in 17 of 29 cases. According to secretin tests, 4 of these had slight to moderately decreased exocrine function; the test were within normal limits. 12 cases with normal image had abnormal oral glucose tolerance curves similar to those fund in mild to moderate diabetes. 10 of the 12 cases with abnormal scintigrams showed decreased isotope uptake in all or part of the pancreas, while 2 showed no uptake at all. These changes were mast apparent in the tail of the pancreas. Ten of the 12 cases with abnormal images had some degree of decreased exocrine function. All 12 had the abnormal GTT curve of diabetes, 4 who had severe diabetes with markedly decreased exocrine function and poor image of the pancreas. In 4 cases the histopathological findings obtained at the time of laparotomy, were shown to be very consistent with the scintigraphic features. It was demonstrated by both scintigraphs and function tests that the alcoholic factor plays a very important role in the prognosis of acute pancreatitis. Acute pancreatitis resulted in chronic pancreatitis in 4 cases, (14 %) of the remaining 8 cases with abnormal scintigram, it is postulated that the inflamatory process subsided allowing time for cicatrical fibrosis to occur. Follow-up to trace and study of these alternations of the pancreas necessary in future.

Emphysematous pancreatitis predisposed by Olanzapine

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Sukhen Samanta

2014-01-01

Full Text Available A 32-year-old male presented to our intensive care unit with severe abdominal pain and was diagnosed as acute pancreatitis after 2 months of olanzapine therapy for bipolar disorder. His serum lipase was 900 u/L, serum triglyceride 560 mg/dL, and blood sugar, fasting and postprandial were 230 and 478 mg/dL, respectively on admission. Contrast enhanced computed tomography (CECT of abdomen was suggestive of acute pancreatitis. Repeat CECT showed gas inside pancreas and collection in peripancreatic area and patient underwent percutaneous drainage and antibiotics irrigation through the drain into pancreas. We describe the rare case of emphysematous pancreatitis due to development of diabetes, hypertriglyceridemia and immunosuppression predisposed by short duration olanzapine therapy.

Interleukin-6 is associated with chronic hyperglycemia and insulin resistance in patients after acute pancreatitis.

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Gillies, Nicola; Pendharkar, Sayali A; Asrani, Varsha M; Mathew, Juby; Windsor, John A; Petrov, Maxim S

2016-01-01

Diabetes is a pervasive disease, with a mounting prevalence and burden on health care systems. Under this collective term of diabetes falls diabetes after diseases of the exocrine pancreas, a condition which was previously under-recognised and often mislabeled as type 2 diabetes mellitus and is now increasingly acknowledged as a stand-alone entity. However, there is a paucity of clinical studies investigating the underlying pathophysiology of diabetes after acute pancreatitis, the most frequent disease of the pancreas. This study aimed to investigate the role of adipocytokines in glucose metabolism after acute pancreatitis. This was a cross-sectional follow-up study of a patient cohort diagnosed with acute pancreatitis. Fasting venous blood samples were collected to analyse markers of glucose metabolism (fasting blood glucose, haemoglobin A1c, homeostasis model assessment (HOMA-IR) as a measure of insulin resistance) and adypocytokines (adiponectin, interleukin-6, leptin, monocyte chemoattractant protein-1, retinol binding protein-4, resistin, and tumor necrosis factor-α). Participants were categorized into two groups: normoglycemia after acute pancreatitis and chronic hyperglycemia after acute pancreatitis (CHAP). Binary logistic regression and linear regression analyses were used to investigate the association between each of the adipocytokines and markers of glucose metabolism. Potential confounders were adjusted for in multivariate analyses. A total of 83 patients with acute pancreatitis were included, of whom 19 developed CHAP. Interleukin-6 was significantly associated with CHAP in both unadjusted and adjusted models (p = 0.030 and p = 0.018, respectively). Further, it was also significantly associated with HOMA-IR in both unadjusted and adjusted models (p = 0.029 and p = 0.037, respectively). Other adipocytokines were not significantly associated with markers of glucose metabolism. Interleukin-6 appears to be implicated in the development of chronic

Pancreatic Endocrine and Exocrine Function in Children following Near-Total Pancreatectomy for Diffuse Congenital Hyperinsulinism

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Arya, Ved Bhushan; Senniappan, Senthil; Demirbilek, Huseyin; Alam, Syeda; Flanagan, Sarah E.; Ellard, Sian; Hussain, Khalid

2014-01-01

Context Congenital hyperinsulinism (CHI), the commonest cause of persistent hypoglycaemia, has two main histological subtypes: diffuse and focal. Diffuse CHI, if medically unresponsive, is managed with near-total pancreatectomy. Post-pancreatectomy, in addition to persistent hypoglycaemia, there is a very high risk of diabetes mellitus and pancreatic exocrine insufficiency. Setting International referral centre for the management of CHI. Patients Medically unresponsive diffuse CHI patients managed with near-total pancreatectomy between 1994 and 2012. Intervention Near-total pancreatectomy. Main Outcome Measures Persistent hypoglycaemia post near-total pancreatectomy, insulin-dependent diabetes mellitus, clinical and biochemical (faecal elastase 1) pancreatic exocrine insufficiency. Results Of more than 300 patients with CHI managed during this time period, 45 children had medically unresponsive diffuse disease and were managed with near-total pancreatectomy. After near-total pancreatectomy, 60% of children had persistent hypoglycaemia requiring medical interventions. The incidence of insulin dependent diabetes mellitus was 96% at 11 years after surgery. Thirty-two patients (72%) had biochemical evidence of severe pancreatic exocrine insufficiency (Faecal elastase 1pancreatectomy is very unsatisfactory. The incidence of persistent hypoglycaemia and insulin-dependent diabetes mellitus is very high. The presence of clinical rather than biochemical pancreatic exocrine insufficiency should inform decisions about pancreatic enzyme supplementation. PMID:24840042

Delta-like Ligand-4-Notch Signaling Inhibition Regulates Pancreatic Islet Function and Insulin Secretion

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Fabienne Billiard

2018-01-01

Full Text Available Although Notch signaling has been proposed as a therapeutic target for type-2 diabetes, liver steatosis, and atherosclerosis, its direct effect on pancreatic islets remains unknown. Here, we demonstrated a function of Dll4-Notch signaling inhibition on the biology of insulin-producing cells. We confirmed enhanced expression of key Notch signaling genes in purified pancreatic islets from diabetic NOD mice and showed that treatment with anti-Dll4 antibody specifically abolished Notch signaling pathway activation. Furthermore, we showed that Notch inhibition could drive proliferation of β-islet cells and confer protection from the development of STZ-induced diabetes. Importantly, inhibition of the Dll4 pathway in WT mice increased insulin secretion by inducing the differentiation of pancreatic β-islet cell progenitors, as well as the proliferation of insulin-secreting cells. These findings reveal a direct effect of Dll4-blockade on pancreatic islets that, in conjunction with its immunomodulatory effects, could be used for unmet medical needs hallmarked by inefficient insulin action.

Morphological assessment of pancreatic islet hormone content following aerobic exercise training in rats with poorly controlled Type 1 diabetes mellitus.

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McDonald, Matthew W; Murray, Michael R; Hall, Katharine E; Noble, Earl G; Melling, C W James

2014-01-01

Regular exercise has been shown to improve many complications of Type 1 diabetes mellitus (T1DM) including enhanced glucose tolerance and increased cardiac function. While exercise training has been shown to increase insulin content in pancreatic islets of rats with T1DM, experimental models were severely hyperglycemic and not undergoing insulin treatment. Further, research to date has yet to determine how exercise training alters glucagon content in pancreatic islets. The purpose of the present investigation was to determine the impact of a 10-week aerobic training program on pancreatic islet composition in insulin-treated rats with T1DM. Second, it was determined whether the acute, exercise-mediated reduction in blood glucose experienced in rats with T1DM would become larger in magnitude following aerobic exercise training. Diabetes was induced in male Sprague-Dawley rats by multiple low dose injections of streptozotocin (20mg/kg i.p.) and moderate intensity aerobic exercise training was performed on a motorized treadmill for one hour per day for a total of 10 weeks. Rats with T1DM demonstrated significantly less islet insulin, and significantly more islet glucagon hormone content compared with non-T1DM rats, which did not significantly change following aerobic training. The reduction in blood glucose in response to a single exercise bout was similar across 10 weeks of training. Results also support the view that different subpopulations of islets exist, as small islets (<50 μm diameter) had significantly more insulin and glucagon in rats with and without T1DM.

PANCREATIC AND EXTRA-PANCREATIC EFFECTS OF INCRETINS AND PERSPECTIVES FOR STUDYING ENTEROINSULIN HORMONAL SYSTEM DURING GESTATIONAL DISORDER OF CARBOHYDRATE METABOLISM

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T. V. Saprina

2013-01-01

Full Text Available The absence of an ideal medicine for the treatment of patients with type 2 diabetes, that would be able to provide not only high quality and constant monitoring of glycemia without increasing body weight, with no risk of hypoglycemia, with no negative impact on the heart, kidneys, liver, but could also ensure the preservation of the secretory function of β-cells, makes scientists continue to search for new opportunities to influence the occurrence and progression of T2D.Gastric inhibitory polypeptide (GIP and glucagon-like peptide-1 (GLP-1 are the two primary incretin hormones secreted from the intestine on ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic β-cells. Within the pancreas, GIP and GLP-1 together promote β-cell proliferation and inhibit apoptosis, thereby expanding pancreatic β-cell mass, while GIP enhances postprandial glucagon response and GLP-1 suppresses it. In adipose tissues, GIP but not GLP-1 facilitates fat deposition. In bone, GIP promotes bone formation while GLP-1 inhibits bone absorption. In the brain, both GIP and GLP-1 are thought to be involved in memory formation as well as the control of appetite. In addition to these differences, secretion of GIP and GLP-1 and their insulinotropic effects on β-cells have been shown to differ in patients with type 2 diabetes compared to healthy subjects.Enteroinsulin hormones' role in the development of gestational disorder of carbohydrate metabolism is poorly understood.In a review article we analyze the publications that summarize what is known about the pancreatic and extra-pancreatic GIP and GLP-1-effects compared with healthy subjects and type 2 diabetes patients. The aspects of gestational diabetes pathophysiology and the perspectives for studying enteroinsulin hormonal system during pregnancy are also discussed in the article.

Occult Metabolic Bone Disease in Chronic Pancreatitis

African Journals Online (AJOL)

2017-10-26

Oct 26, 2017 ... KEYWORDS: Chronic pancreatitis, metabolic bone disease, osteomalacia, osteopenia ... with malabsorption, and endocrine dysfunction results in diabetes .... of insufficiency and deficiency were not assessed separately due ...

Transplantation of Human Pancreatic Endoderm Cells Reverses Diabetes Post Transplantation in a Prevascularized Subcutaneous Site

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Andrew R. Pepper

2017-06-01

Full Text Available Beta-cell replacement therapy is an effective means to restore glucose homeostasis in select humans with autoimmune diabetes. The scarcity of “healthy” human donor pancreata restricts the broader application of this effective curative therapy. “β-Like” cells derived from human embryonic stem cells (hESC, with the capacity to secrete insulin in a glucose-regulated manner, have been developed in vitro, with limitless capacity for expansion. Here we report long-term diabetes correction in mice transplanted with hESC-derived pancreatic endoderm cells (PECs in a prevascularized subcutaneous site. This advancement mitigates chronic foreign-body response, utilizes a device- and growth factor-free approach, facilitates in vivo differentiation of PECs into glucose-responsive insulin-producing cells, and reliably restores glycemic control. Basal and stimulated human C-peptide secretion was detected throughout the study, which was abolished upon graft removal. Recipient mice demonstrated physiological clearance of glucose in response to metabolic challenge and safely retrieved grafts contained viable glucose regulatory cells.

Does the pancreatic volume reduction rate using serial computed tomographic volumetry predict new onset diabetes after pancreaticoduodenectomy?

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Yun, Sung Pil; Seo, Hyung-Il; Kim, Suk; Kim, Dong Uk; Baek, Dong Hoon

2017-01-01

Abstract Volume reduction of the pancreatic tissues following a pancreatectomy can lead to the deterioration of glucose homeostasis. This is defined as pancreatogenic diabetes mellitus (DM). The objective of this study was to investigate the occurrence of new-onset DM (NODM) and evaluate the risk factors, including the pancreas volume reduction rate in patients undergoing pancreaticoduodenectomy (PD). Sixty-six patients without preoperative DM underwent PD for periampullary tumors between August 2007 and December 2012 and were included in this analysis. These patients underwent follow-up tests and abdominal computed tomography (CT) scan 7 days, 6 months, 12 months, 24 months, and 36 months after the operation. The pancreas volume reduction rate was calculated by CT volumetry. The patients were divided into 2 groups according to the postoperative development of DM. After PD, newly diagnosed DM occurred in 16 patients (24.2%). The incidence of DM was highest among patients with carcinomas with an advanced T stage. The pancreatic volume reduction rate after 6 and 12 months in the NODM group was significantly higher than the normal glucose group in the univariate analysis. In the multivariate analysis, the pancreatic volume reduction rate 6 months after PD was the only significant predictive factor for the development of NODM (P = 0.002). This study suggests that the pancreatic volume reduction rate 6 months after PD was the only significant predictive factor for the development of NODM. CT volumetry of the pancreas may be useful as a predictor of NODM after PD. PMID:28353594

Long-Term Culture of Self-renewing Pancreatic Progenitors Derived from Human Pluripotent Stem Cells

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Jamie Trott

2017-06-01

Full Text Available Pluripotent stem cells have been proposed as an unlimited source of pancreatic β cells for studying and treating diabetes. However, the long, multi-step differentiation protocols used to generate functional β cells inevitably exhibit considerable variability, particularly when applied to pluripotent cells from diverse genetic backgrounds. We have developed culture conditions that support long-term self-renewal of human multipotent pancreatic progenitors, which are developmentally more proximal to the specialized cells of the adult pancreas. These cultured pancreatic progenitor (cPP cells express key pancreatic transcription factors, including PDX1 and SOX9, and exhibit transcriptomes closely related to their in vivo counterparts. Upon exposure to differentiation cues, cPP cells give rise to pancreatic endocrine, acinar, and ductal lineages, indicating multilineage potency. Furthermore, cPP cells generate insulin+ β-like cells in vitro and in vivo, suggesting that they offer a convenient alternative to pluripotent cells as a source of adult cell types for modeling pancreatic development and diabetes.

Effect of atorvastatin on pancreatic Beta-cell function and insulin resistance in type 2 diabetes mellitus patients: a randomized pilot study.

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Goyal, Aman; Singh, Surender; Tandon, Nikhil; Gupta, Nandita; Gupta, Yogendra Kumar

2014-12-01

Statins are commonly used for the management of dyslipidemia in type 2 diabetes mellitus patients. We hypothesized that atorvastatin could modulate the beta-cell function by altering the levels of proapoptotic and antiapoptotic lipoproteins and could also have an effect on insulin resistance. The aim of the present pilot study was to assess the effect of atorvastatin 10 mg on pancreatic beta-cell function and insulin resistance in patients with hyperlipidemia and type 2 diabetes by using the homeostasis model assessment-2 (HOMA2) index. Fifty-one type 2 diabetes patients receiving oral antidiabetes drugs, not taking statins, with baseline low-density lipoprotein cholesterol between 2.6 mmol/L and 4.1 mmol/L were included. Forty-three patients (21 in placebo group and 22 in atorvastatin group) completed the study and were taken up for final analysis. Fasting blood samples were obtained at baseline and at 12 weeks to determine levels of blood glucose, lipid profile, insulin, C-peptide and glycosylated hemoglobin (A1C). Atorvastatin nonsignificantly increased fasting serum insulin (+14.29%, p=0.18), accompanied by marginal nonsignificant increases in fasting plasma glucose and A1C. There was a decrease in HOMA2 percent beta-cell function (-2.9%, p=0.72) and increase in HOMA2 insulin resistance (+14%, p=0.16) in the atorvastatin group as compared with baseline, but the difference was not statistically significant. Atorvastatin in the dose used failed to produce significant change in pancreatic beta-cell function and insulin resistance in type 2 diabetes patients as assessed by the HOMA2 index. The possible explanations include absence of lipotoxicity at prevailing levels of dyslipidemia at baseline or inadequacy of statin dose used in the study. (Clinical Trials Registry-India: CTRI/2008/091/000099). Copyright © 2014 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.

Pneumonia aguda fibrinosa e organizante

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Cláudia Santos

2010-07-01

Full Text Available Resumo: O padrão histológico de Pneumonia Aguda Fibrinosa e Organizante (AFOP – Acute Fibrinous And Organizing Pneumonia, descrito por Beasley em 2002, caracteriza-se pela existência de fibrina intra-alveolar sob a forma de bolas de fibrina e pneumonia organizativa difusa. A apresentação clínica desta doença intersticial pulmonar pode ser aguda ou subaguda, diferindo no entanto dos outros padrões histológicos habitualmente associados a lesão pulmonar aguda – Lesão Alveolar Difusa (DAD, Pneumonia Organizativa (OP e Pneumonia Eosinofílica (EP.A propósito deste tema, os autores fazem uma revisão da literatura e descrevem o caso clínico de um doente de 44 anos, com aspectos imagiológicos e evolução pouco habituais. Abstract: The histologic pattern of Acute Fibrinous and Organizing Pneumonia (AFOP, described by Beasley in 2002, is characterized by the existence of intra alveolar fibrin in the form of fibrin “balls” and diffuse organizing pneumonia. Presenting symptoms of this interstitial pulmonary disease can be acute or subacute. However, it differs from the well-recognized histologic patterns of acute pulmonary lesion – Diffuse Alveolar Damage (DAD, Organizing Pneumonia (OP and Eosinophilic Pneumonia (EP.The authors carry out a review of the literature concerning this topic and describe the clinical case of a 44-year-old patient with unusual imaging features and outcome. Palavras-chave: AFOP, bolas de fibrina, pneumonia organizativa, Key-word: AFOP, fibrin balls, organizing pneumonia

Diet and Pancreatic Cancer Prevention

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Ilaria Casari

2015-11-01

Full Text Available Pancreatic cancer is without any doubt the malignancy with the poorest prognosis and the lowest survival rate. This highly aggressive disease is rarely diagnosed at an early stage and difficult to treat due to its resistance to radiotherapy and chemotherapy. Therefore, there is an urgent need to clarify the causes responsible for pancreatic cancer and to identify preventive strategies to reduce its incidence in the population. Some circumstances, such as smoking habits, being overweight and diabetes, have been identified as potentially predisposing factors to pancreatic cancer, suggesting that diet might play a role. A diet low in fat and sugars, together with a healthy lifestyle, regular exercise, weight reduction and not smoking, may contribute to prevent pancreatic cancer and many other cancer types. In addition, increasing evidence suggests that some food may have chemo preventive properties. Indeed, a high dietary intake of fresh fruit and vegetables has been shown to reduce the risk of developing pancreatic cancer, and recent epidemiological studies have associated nut consumption with a protective effect against it. Therefore, diet could have an impact on the development of pancreatic cancer and further investigations are needed to assess the potential chemo preventive role of specific foods against this disease. This review summarizes the key evidence for the role of dietary habits and their effect on pancreatic cancer and focuses on possible mechanisms for the association between diet and risk of pancreatic cancer.

Functional and morphological changes in pancreatic remnant after pancreaticoduodenectomy.

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Fang, Wen-Liang; Su, Cheng-Hsi; Shyr, Yi-Ming; Chen, Tien-Hua; Lee, Rheun-Chuan; Tai, Ling-Chen; Wu, Chew-Wun; Lui, Wing-Yiu

2007-11-01

Pancreatic exocrine insufficiency has been reported to be more common in pancreaticogastrostomy (PG) than in pancreaticojejunostomy (PJ) after pancreaticoduodenectomy (PD). This study aimed to evaluate the long-term outcome after PD between these 2 groups. We evaluated the long-term functional status of 42 surviving patients diagnosed with periampullary lesions who underwent PJ or PG after PD and followed up for more than 1 year. Among these, 23 patients underwent PJ and 19 patients underwent PG. To compare the 2 groups, we analyzed the (1) pancreatic exocrine insufficiency by questioning the presence or absence of steatorrhea, (2) pancreatic endocrine function by measuring glycohemoglobin A1c, fasting blood glucose, and history of new-onset diabetes, (3) nutritional status by measuring serum total protein, albumin, cholesterol, and triglyceride, (4) gastric emptying time, (5) panendoscopic findings, (6) changes of pancreatic duct diameter by computed tomography, and (7) relaparotomy rate. The mean follow-up time for PG and PJ were 37 +/- 23 and 103 +/- 52 months, respectively (P pancreatic exocrine insufficiency, and 11.9% had new-onset diabetes. There was no significant difference between PJ and PG groups. A significantly improved postoperative nutritional state regarding serum total protein and albumin were noticed in both groups. There was no significant difference in terms of gastric emptying time, positive panendoscopic findings, and changes in pancreatic duct diameter. The pancreatic remnant-related relaparotomy rate was higher in the PJ group as compared with the PG group (17.4% vs 0%; P = 0.056). There is no significant difference in pancreatic exocrine or endocrine insufficiency, gastric emptying time, and positive panendoscopic findings between PJ and PG. Pancreaticojejunostomy was associated with a higher pancreatic remnant-related relaparotomy rate; however, because of a shorter follow-up in the PG group, a continuous long-term follow-up is still

Activated macrophages create lineage-specific microenvironments for pancreatic acinar- and β-cell regeneration in mice.

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Criscimanna, Angela; Coudriet, Gina M; Gittes, George K; Piganelli, Jon D; Esni, Farzad

2014-11-01

Although the cells that contribute to pancreatic regeneration have been widely studied, little is known about the mediators of this process. During tissue regeneration, infiltrating macrophages debride the site of injury and coordinate the repair response. We investigated the role of macrophages in pancreatic regeneration in mice. We used a saporin-conjugated antibody against CD11b to reduce the number of macrophages in mice following diphtheria toxin receptor-mediated cell ablation of pancreatic cells, and evaluated the effects on pancreatic regeneration. We analyzed expression patterns of infiltrating macrophages after cell-specific injury or from the pancreas of nonobese diabetic mice. We developed an in vitro culture system to study the ability of macrophages to induce cell-specific regeneration. Depletion of macrophages impaired pancreatic regeneration. Macrophage polarization, as assessed by expression of tumor necrosis factor-α, interleukin 6, interleukin 10, and CD206, depended on the type of injury. The signals provided by polarized macrophages promoted lineage-specific generation of acinar or endocrine cells. Macrophage from nonobese diabetic mice failed to provide signals necessary for β-cell generation. Macrophages produce cell type-specific signals required for pancreatic regeneration in mice. Additional study of these processes and signals might lead to new approaches for treating type 1 diabetes or pancreatitis. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.

Insuficiencia respiratoria aguda

OpenAIRE

Gutiérrez Muñoz, Fernando R.

2010-01-01

La función respiratoria básica es el intercambio gaseoso de oxígeno y dióxido carbono; lo que implica un perfecto equilibrio y control entre los componentes del sistema respiratorio. a insuficiencia respiratoria aguda (IRA) es la incapacidad del sistema respiratorio de cumplir su función básica, que es el intercambio gaseoso de oxígeno y dióxido de carbono. Basic respiratory function is gas exchange of oxygen and carbon dioxide, which implies a perfect balance and control between the compo...

AAV-mediated pancreatic overexpression of Igf1 counteracts progression to autoimmune diabetes in mice.

Science.gov (United States)

Mallol, Cristina; Casana, Estefania; Jimenez, Veronica; Casellas, Alba; Haurigot, Virginia; Jambrina, Claudia; Sacristan, Victor; Morró, Meritxell; Agudo, Judith; Vilà, Laia; Bosch, Fatima

2017-07-01

Type 1 diabetes is characterized by autoimmune destruction of β-cells leading to severe insulin deficiency. Although many improvements have been made in recent years, exogenous insulin therapy is still imperfect; new therapeutic approaches, focusing on preserving/expanding β-cell mass and/or blocking the autoimmune process that destroys islets, should be developed. The main objective of this work was to test in non-obese diabetic (NOD) mice, which spontaneously develop autoimmune diabetes, the effects of local expression of Insulin-like growth factor 1 (IGF1), a potent mitogenic and pro-survival factor for β-cells with immunomodulatory properties. Transgenic NOD mice overexpressing IGF1 specifically in β-cells (NOD-IGF1) were generated and phenotyped. In addition, miRT-containing, IGF1-encoding adeno-associated viruses (AAV) of serotype 8 (AAV8-IGF1-dmiRT) were produced and administered to 4- or 11-week-old non-transgenic NOD females through intraductal delivery. Several histological, immunological, and metabolic parameters were measured to monitor disease over a period of 28-30 weeks. In transgenic mice, local IGF1 expression led to long-term suppression of diabetes onset and robust protection of β-cell mass from the autoimmune insult. AAV-mediated pancreatic-specific overexpression of IGF1 in adult animals also dramatically reduced diabetes incidence, both when vectors were delivered before pathology onset or once insulitis was established. Transgenic NOD-IGF1 and AAV8-IGF1-dmiRT-treated NOD animals had much less islet infiltration than controls, preserved β-cell mass, and normal insulinemia. Transgenic and AAV-treated islets showed less expression of antigen-presenting molecules, inflammatory cytokines, and chemokines important for tissue-specific homing of effector T cells, suggesting IGF1 modulated islet autoimmunity in NOD mice. Local expression of Igf1 by AAV-mediated gene transfer counteracts progression to diabetes in NOD mice. This study suggests a

Chemical strategies for pancreatic β cell differentiation, reprogramming, and regeneration.

Science.gov (United States)

Ma, Xiaojie; Zhu, Saiyong

2017-04-01

Generation of unlimited functional pancreatic β cells is critical for the study of pancreatic biology and treatment of diabetes mellitus. Recent advances have suggested several promising directions, including directed differentiation of pancreatic β cells from pluripotent stem cells, reprogramming of pancreatic β cells from other types of somatic cells, and stimulated proliferation and enhanced functions of existing pancreatic β cells. Small molecules are useful in generating unlimited numbers of functional pancreatic cells in vitro and could be further developed as drugs to stimulate endogenous pancreatic regeneration. Here, we provide an updated summary of recent major achievements in pancreatic β cell differentiation, reprogramming, proliferation, and function. These studies will eventually lead to significant advances in the field of pancreatic biology and regeneration. © The Author 2017. Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Pancreatic Cancer: Multicenter Prospective Data Collection and Analysis by the Hungarian Pancreatic Study Group.

Science.gov (United States)

Lakatos, Gábor; Balázs, Anita; Kui, Balázs; Gódi, Szilárd; Szücs, Ákos; Szentesi, Andrea; Szentkereszty, Zsolt; Szmola, Richárd; Kelemen, Dezső; Papp, Róbert; Vincze, Áron; Czimmer, József; Pár, Gabriella; Bajor, Judit; Szabó, Imre; Izbéki, Ferenc; Halász, Adrienn; Leindler, László; Farkas, Gyula; Takács, Tamás; Czakó, László; Szepes, Zoltán; Hegyi, Péter; Kahán, Zsuzsanna

2016-06-01

Pancreatic cancer is a devastating disease with poor prognosis. There is very limited information available regarding the epidemiology and treatment strategies of pancreatic cancer in Central Europe. The purpose of the study was to prospectively collect and analyze data of pancreatic cancer in the Hungarian population. The Hungarian Pancreatic Study Group (HPSG) organized prospective, uniform data collection. Altogether 354 patients were enrolled from 14 Hungarian centers. Chronic pancreatitis was present in 3.7% of the cases, while 33.7% of the patients had diabetes. Family history for pancreatic cancer was positive in 4.8%. The most frequent presenting symptoms included pain (63.8%), weight loss (63%) and jaundice (52.5%). The reported frequency of smoking and alcohol consumption was lower than expected (28.5% and 27.4%, respectively). The majority of patients (75.6%) were diagnosed with advanced disease. Most patients (83.6%) had a primary tumor located in the pancreatic head. The histological diagnosis was ductal adenocarcinoma in 90.7% of the cases, while neuroendocrine tumor was present in 5.3%. Biliary stent implantation was performed in 166 patients, 59.2% of them received metal stents. Primary tumor resection was performed in 60 (16.9%) patients. Enteral or biliary bypass was done in 35 and 49 patients, respectively. In a multivariate Cox-regression model, smoking status and presence of gemcitabine-based chemotherapy were identified as independent predictors for overall survival. We report the first data from a large cohort of Hungarian pancreatic cancer patients. We identified smoking status and chemotherapy as independent predictors in this cohort.

Tratamiento quirúrgico de la pancreatitis aguda con técnica de Puestow modificada

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Enrique Vázquez Merayo

Full Text Available La pancreatitis crónica representa uno de los mayores desafíos de la Gastroenterología, y su etiología sigue siendo difícil de establecer en 10-30 % de los pacientes. Se presenta un paciente masculino, de 13 años, con diagnóstico de pancreatitis crónica de tipo inmunológico, con estenosis del conducto pancreático principal. Necesitó tratamiento quirúrgico pancreaticoyeyunostomía longitudinal en Y de Roux, conocido como técnica de Puestow modificada. Se logró mejoría clínica, normalidad de sus enzimas en una semana, no hubo complicaciones, tuvo evolución posoperatoria satisfactoria, y una estadía hospitalaria de 14 días. Actualmente se mantiene con 4 años de evolución satisfactoria. La técnica efectuada en el paciente es considerada por muchos como la ideal, por su baja incidencia de mortalidad (menos del 3 % y por el alivio del dolor en más del 75 % de los pacientes. Por ello, se considera que esta técnica quirúrgica pudiera ser una opción terapéutica eficaz para este tipo de paciente.

Plasma Exchange for the Treatment of Transient Extreme Hypertriglyceridemia Associated with Diabetic Ketoacidosis and Acute Pancreatitis

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Davide Donelli

2018-03-01

Full Text Available Diabetic ketoacidosis (DKA can quite frequently present in association with acute pancreatitis (AP caused by transient severe hypertriglyceridemia (HTG. Here we report the case of a patient presenting with DKA, severe HTG and AP who received urgent plasma exchange for HTG control, and who reached adequate serum triglyceride levels only after appropriate DKA management. The treatment of patients presenting with DKA and coexistent AP associated with severe HTG should focus first on appropriate DKA management. Plasma exchange as a treatment for severe HTG in patients with DKA and AP should be evaluated carefully.

Litotripsia Mecánica Intrapancreática en un paciente con pancreatitis crónica y litiasis del Conducto de Wirsung: reporte de un caso y revisión de la literatura

OpenAIRE

Yriberry Ureña, Simón; Monge Zapata, Victor; Salazar Muente, Fernando; Targarona Modena, Javier; Salzar Cabrera, Fernando; Barriga Calle, Eduardo

2008-01-01

Presentamos el caso de una paciente mujer de 34 años con litiasis múltiple del Wirsung sometida a cirugía modificada de Puestow. Dos meses después de la cirugía la paciente ingresa con cuadro de dolor severo compatible con pancreatitis aguda sobrepuesta en pancreatitis crónica. Se observa litiasis gigante de cabeza de páncreas. Se realiza procedimiento terapéutico esfinterotomía de páncreas y litotripsia mecánica. Se describe el procedimiento y se revisa la literatura. The case of a 34 yea...

Severe hypertriglyceridemia-related acute pancreatitis.

Science.gov (United States)

Stefanutti, Claudia; Labbadia, Giancarlo; Morozzi, Claudia

2013-04-01

Acute pancreatitis is a potentially life-threatening complication of severe hypertriglyceridemia. In some cases, inborn errors of metabolism such as lipoprotein lipase deficiency, apoprotein C-II deficiency, and familial hypertriglyceridemia have been reported as causes of severe hypertriglyceridemia. More often, severe hypertriglyceridemia describes various clinical conditions characterized by high plasma levels of triglycerides (>1000 mg/dL), chylomicron remnants, or intermediate density lipoprotein like particles, and/or chylomicrons. International guidelines on the management of acute pancreatitis are currently available. Standard therapeutic measures are based on the use of lipid-lowering agents (fenofibrate, gemfibrozil, niacin, Ω-3 fatty acids), low molecular weight heparin, and insulin in diabetic patients. However, when standard medical therapies have failed, non-pharmacological approaches based upon the removal of triglycerides with therapeutic plasma exchange can also provide benefit to patients with severe hypertriglyceridemia and acute pancreatitis. Plasma exchange could be very helpful in reducing triglycerides levels during the acute phase of hyperlipidemic pancreatitis, and in the prevention of recurrence. The current evidence on management of acute pancreatitis and severe hypertriglyceridemia, focusing on symptoms, treatment and potential complications is reviewed herein. © 2013 The Authors. Therapeutic Apheresis and Dialysis © 2013 International Society for Apheresis.

Mild acute pancreatitis with vildagliptin use

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Ravikant Saraogi

2012-01-01

Full Text Available Vildagliptin has not been associated with the development of acute pancreatitis in postmarketing reports except one case report from Sydney, Australia. We present the case report of 42 year old male, diabetic, with no historyof alcohol use, on vildagliptin 50 mg and metformin 500 mg daily since 6 months, who presented with severe abdominal pain radiating to back, nausea and fever. On evaluation, serum pancreatic enzymes were elevated, triglycerides were not raised and ultrasound showed swollen and echogenic pancreas, loss of peripancreatic fat plane and pancreatic duct was not dilated. Vildagliptin was stopped and the pancreatits resolved. On Follow up, no secondary cause was not identified. This appears to be the first reported case of acute pancreatitis from India probably attributable to use of vildagliptin, thus raising the possibility that this rare reaction may be a class effect of the DPP-4 inhibitors.

Development of biomarker specific of pancreatic beta cells (incretin radiolabelled) for image of beta functional mass in diabetic and obese: study in animal model

International Nuclear Information System (INIS)

Seo, Daniele

2017-01-01

Increased prevalence of obesity worldwide, has become a vast concern, stimulating investigations focusing prevention and therapy of this condition. The association of type 2 diabetes or insulin resistance aggravates the prognosis of obesity. Even patients successfully submitted to bariatric or metabolic surgery, may not be cured of diabetes, as improvement of circulating values of glucose and insulin not necessarily reflects recovery of pancreatic beta cell mass. There is no consensus about how to estimate beta cell mass in vivo. Available tools suffer from low sensitivity and specificity, often being as well cumbersome and expensive. Radiolabeled incretins, such as glucagon-like-peptide 1 (GLP-1) analogs, seem to be promising options for the measurement of beta cell mass in diabetes and insulinoma. The objective of this study was the development of two conjugates of GLP-1 analog, radiolabeled with 99m Technetium, as a noninvasive imaging method for the estimation of pancreatic beta cell mass, in the presence of obesity. Animal models were selected, including hyperlipidic diet-induced obesity, diet restricted obesity, and as controls, alloxan diabetes. Results indicated that both radiotracers achieved over 97% radiochemical yield. The most successful product was 99m Tc-HYNIC-βAla-Exendin-4. Low beta cell mass uptake occurred in diet-induced obesity. Diet-restricted obesity, with substantial shedding of excess body weight, was followed by remarkable decrease of fasting blood glucose, however beta cell mass uptake was only mildly improved. Future studies are recommended in obesity, type 2 diabetes, and dieting, including bariatric and metabolic operations. (author)

Microcristais biliares na pancreatite aguda idiopática: indício para etiologia biliar oculta subjacente

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CHEBLI Júlio Maria Fonseca

2000-01-01

Full Text Available As principais causas de inflamação pancreática no mundo são a litíase biliar e o alcoolismo crônico. Admite-se que 10 a 30% das pancreatites agudas sejam idiopáticas. Sugere-se que parte destas são causadas por microlitíase ou barro biliar, identificados pela presença de microcristais no sedimento biliar. Neste estudo, realizou-se análise microscópica da bile obtida por colangiopancreatografia endoscópica, em pacientes com pancreatite aguda idiopática, pancreatite aguda biliar e pancreatite crônica alcoólica - 20 em cada grupo. Pacientes com pancreatite aguda idiopática e microcristais na bile foram submetidos a colecistectomia. Naqueles inaptos à cirurgia efetuou-se esfincterotomia endoscópica ou tratamento com ácido ursodesoxicólico. Pacientes com pancreatite aguda idiopática sem cristais não receberam tratamento específico. A prevalência de microcristais biliares em pacientes com pancreatite aguda idiopática (75% e pancreatite aguda biliar (90% foi significativamente maior que naqueles com pancreatite crônica alcoólica (15%. A detecção de microcristais apresentou sensibilidade de 90%, especificidade de 85%, valor preditivo positivo de 85,7%, valor preditivo negativo de 89,4% e acurácia de 87,5% em identificar pancreatite de origem biliar. Nos pacientes com pancreatite aguda idiopática recurrente, cursando com microcristais, houve redução significante dos episódios de pancreatite após tratamento específico. No seguimento deste grupo durante 23,3 meses, recidiva ocorreu apenas naqueles que apresentavam "fator biliar persistente" (coledocolitíase ou microcristais. Todos os pacientes com pancreatite aguda idiopática submetidos a colecistectomia apresentavam colecistite crônica, e microlitíase foi observada em um paciente. No seguimento ultra-sonográfico, colelitíase foi detectada em um dos casos. No subgrupo de cinco pacientes com pancreatite aguda idiopática sem microcristais houve uma recidiva. Estudo

Can pancreatic duct-derived progenitors be a source of islet regeneration?

International Nuclear Information System (INIS)

Xia, Bing; Zhan, Xiao-Rong; Yi, Ran; Yang, Baofeng

2009-01-01

The regenerative process of the pancreas is of interest because the main pathogenesis of diabetes mellitus is an inadequate number of insulin-producing β-cells. The functional mass of β-cells is decreased in type 1 diabetes, so replacing missing β-cells or triggering their regeneration may allow for improved type 1 diabetes treatment. Therefore, expansion of the β-cell mass from endogenous sources, either in vivo or in vitro, represents an area of increasing interest. The mechanism of islet regeneration remains poorly understood, but the identification of islet progenitor sources is critical for understanding β-cell regeneration. One potential source is the islet proper, via the dedifferentiation, proliferation, and redifferentiation of facultative progenitors residing within the islet. Neogenesis, or that the new pancreatic islets can derive from progenitor cells present within the ducts has been reported, but the existence and identity of the progenitor cells have been debated. In this review, we focus on pancreatic ductal cells, which are islet progenitors capable of differentiating into islet β-cells. Islet neogenesis, seen as budding of hormone-positive cells from the ductal epithelium, is considered to be one mechanism for normal islet growth after birth and in regeneration, and has suggested the presence of pancreatic stem cells. Numerous results support the neogenesis hypothesis, the evidence for the hypothesis in the adult comes primarily from morphological studies that have in common the production of damage to all or part of the pancreas, with consequent inflammation and repair. Although numerous studies support a ductal origin for new islets after birth, lineage-tracing experiments are considered the 'gold standard' of proof. Lineage-tracing experiments show that pancreatic duct cells act as progenitors, giving rise to new islets after birth and after injury. The identification of differentiated pancreatic ductal cells as an in vivo progenitor for

Can pancreatic duct-derived progenitors be a source of islet regeneration?

Energy Technology Data Exchange (ETDEWEB)

Xia, Bing [Department of Endocrinology, First Hospital of Harbin Medical University, Harbin, Hei Long Jiang Province 150001 (China); Zhan, Xiao-Rong, E-mail: xiaorongzhan@sina.com [Department of Endocrinology, First Hospital of Harbin Medical University, Harbin, Hei Long Jiang Province 150001 (China); Yi, Ran [Department of Endocrinology, First Hospital of Harbin Medical University, Harbin, Hei Long Jiang Province 150001 (China); Yang, Baofeng [Department of Pharmacology, State Key Laboratory of Biomedicine and Pharmacology, Harbin Medical University, Harbin, Hei Long Jiang Province 150001 (China)

2009-06-12

The regenerative process of the pancreas is of interest because the main pathogenesis of diabetes mellitus is an inadequate number of insulin-producing {beta}-cells. The functional mass of {beta}-cells is decreased in type 1 diabetes, so replacing missing {beta}-cells or triggering their regeneration may allow for improved type 1 diabetes treatment. Therefore, expansion of the {beta}-cell mass from endogenous sources, either in vivo or in vitro, represents an area of increasing interest. The mechanism of islet regeneration remains poorly understood, but the identification of islet progenitor sources is critical for understanding {beta}-cell regeneration. One potential source is the islet proper, via the dedifferentiation, proliferation, and redifferentiation of facultative progenitors residing within the islet. Neogenesis, or that the new pancreatic islets can derive from progenitor cells present within the ducts has been reported, but the existence and identity of the progenitor cells have been debated. In this review, we focus on pancreatic ductal cells, which are islet progenitors capable of differentiating into islet {beta}-cells. Islet neogenesis, seen as budding of hormone-positive cells from the ductal epithelium, is considered to be one mechanism for normal islet growth after birth and in regeneration, and has suggested the presence of pancreatic stem cells. Numerous results support the neogenesis hypothesis, the evidence for the hypothesis in the adult comes primarily from morphological studies that have in common the production of damage to all or part of the pancreas, with consequent inflammation and repair. Although numerous studies support a ductal origin for new islets after birth, lineage-tracing experiments are considered the 'gold standard' of proof. Lineage-tracing experiments show that pancreatic duct cells act as progenitors, giving rise to new islets after birth and after injury. The identification of differentiated pancreatic ductal

Balanites aegyptiaca ameliorates insulin secretion and decreases pancreatic apoptosis in diabetic rats: Role of SAPK/JNK pathway.

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Hassanin, Kamel M A; Mahmoud, Mohamed O; Hassan, Hossam M; Abdel-Razik, Abdel-Razik H; Aziz, Lourin N; Rateb, Mostafa E

2018-06-01

SAPK-JNK pathway performs a significant role in the pathogenesis of type 2 diabetes. Balanites aegyptiaca (BA) is used as an anti-diabetic agent in folk medicine however its hypoglycemic mechanism is not fully elucidated. The current study aimed to evaluate the effect of crude extract, butanol, and dichloromethane fractions from BA on the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK-JNK) pathway in experimental diabetic rats. Six groups of male Wistar rats were included: normal control, diabetic, diabetic rats treated with crude, butanol or dichloromethane fraction from BA (50 mg/kg BW) and diabetic rats treated with gliclazide as a reference drug for one month. Our results suggested a protective role of treatment of diabetic rats with BA against oxidative stress-induced SAPK-JNK pathway. Moreover, BA treatment produced a reduction in plasma glucose, HbA 1c , lactic acid, lipid profile, malondialdehyde levels and produced an increase in insulin, reduced glutathione levels, catalase and superoxide dismutase activities compared with untreated diabetic rats. Moreover, it decreased apoptosis signal-regulating kinase 1, c-Jun N-terminal kinase 1, protein 53 and increased insulin receptor substrate 1 in rat pancreas while it increased glucose transporter 4 in rat muscle. Analysis of BA extracts by LC-HRMS revealed the presence of different saponins with reported hypoglycemic effect. In conclusion, BA exerted hypoglycemic, hypolipidemic, insulinotropic and antioxidant effects. Additionally, it reduced apoptosis in pancreatic β-cells and increased glucose uptake in muscle. These results suggest that the hypoglycemic effect of BA is due to the inhibition of the SAPK-JNK pathway. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

Efectividad de la magnetoterapia como tratamiento en pacientes con lumbalgia aguda

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Raidel González Rodríguez

2015-05-01

Full Text Available Son numerosos los pacientes aquejados de algias vertebrales, tanto lumbares como dorsales y cervicales. Se realizó esta investigación con el objetivo de determinar la efectividad de la magnetoterapia como tratamiento en la lumbalgia aguda, en pacientes atendidos en el policlínico universitario “Raúl Sánchez” de la provincia de Pinar del Río, Cuba. Se realizó un estudio descriptivo, prospectivo, de corte transversal en pacientes con lumbalgia aguda, pertenecientes a dicha área de salud. La muestra quedó conformada por 68 pacientes de ambos sexos con lumbalgia aguda, diagnosticados clínicamente y mayores de 17 años de edad. En la investigación predominó el sexo femenino (67,6 % y el rango de edad estuvo entre 40 y 49 años. El esfuerzo físico fue el principal factor desencadenante (47,1 %. Con el tratamiento de la magnetoterapia aplicado a los pacientes se redujeron los estadios del dolor. La mayoría de los pacientes presentaron una respuesta clínica excelente y mejoraron los síntomas entre los siete y diez días (61,8 %. No se reportaron efectos adversos. La magnetoterapia resultó efectiva en el tratamiento de pacientes aquejados de lumbalgia aguda

Is islet transplantation a realistic approach to curing diabetes?

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Jin, Sang-Man; Kim, Kwang-Won

2017-01-01

Since the report of type 1 diabetes reversal in seven consecutive patients by the Edmonton protocol in 2000, pancreatic islet transplantation has been reappraised based on accumulated clinical evidence. Although initially expected to therapeutically target long-term insulin independence, islet transplantation is now indicated for more specific clinical benefits. With the long-awaited report of the first phase 3 clinical trial in 2016, allogeneic islet transplantation is now transitioning from an experimental to a proven therapy for type 1 diabetes with problematic hypoglycemia. Islet autotransplantation has already been therapeutically proven in chronic pancreatitis with severe abdominal pain refractory to conventional treatments, and it holds promise for preventing diabetes after partial pancreatectomy due to benign pancreatic tumors. Based on current evidence, this review focuses on islet transplantation as a realistic approach to treating diabetes.

Mutations in PTF1A cause pancreatic and cerebellar agenesis

NARCIS (Netherlands)

Sellick, GS; Barker, KT; Stolte-Dijkstra, [No Value; Fleischmann, C; Coleman, RJ; Garrett, C; Gloyn, AL; Edghill, EL; Hattersley, AT; Wellauer, PK; Goodwin, G; Houlston, RS

2004-01-01

Individuals with permanent neonatal diabetes mellitus usually present within the first three months of life and require insulin treatment(1,2). We recently identified a locus on chromosome 10p13-p12.1 involved in permanent neonatal diabetes mellitus associated with pancreatic and cerebellar agenesis

Expansion of Adult Human Pancreatic Tissue Yields Organoids Harboring Progenitor Cells with Endocrine Differentiation Potential

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Cindy J.M. Loomans

2018-03-01

Full Text Available Summary: Generating an unlimited source of human insulin-producing cells is a prerequisite to advance β cell replacement therapy for diabetes. Here, we describe a 3D culture system that supports the expansion of adult human pancreatic tissue and the generation of a cell subpopulation with progenitor characteristics. These cells display high aldehyde dehydrogenase activity (ALDHhi, express pancreatic progenitors markers (PDX1, PTF1A, CPA1, and MYC, and can form new organoids in contrast to ALDHlo cells. Interestingly, gene expression profiling revealed that ALDHhi cells are closer to human fetal pancreatic tissue compared with adult pancreatic tissue. Endocrine lineage markers were detected upon in vitro differentiation. Engrafted organoids differentiated toward insulin-positive (INS+ cells, and circulating human C-peptide was detected upon glucose challenge 1 month after transplantation. Engrafted ALDHhi cells formed INS+ cells. We conclude that adult human pancreatic tissue has potential for expansion into 3D structures harboring progenitor cells with endocrine differentiation potential. : In the context of β cell replacement therapy for diabetes, de Koning and colleagues describe a 3D culture platform that supports ex vivo expansion of human pancreatic tissue as organoids. These organoids harbor a subpopulation of ALDHhi cells that display proliferative capacity and can differentiate to an endocrine fate. Keywords: pancreas, organoid, human, ALDH, endocrine differentiation, beta cells, insulin, progenitor, fetal, diabetes

Pancreatic islet transplantation

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Corrêa-Giannella Maria

2009-09-01

Full Text Available Abstract Background No formulation of exogenous insulin available to date has yet been able to mimic the physiological nictemeral rhythms of this hormone, and despite all engineering advancements, the theoretical proposal of developing a mechanical replacement for pancreatic β cell still has not been reached. Thus, the replacement of β cells through pancreas and pancreatic islet transplantation are the only concrete alternatives for re-establishing the endogenous insulin secretion in type 1 diabetic patients. Since only 1 to 1.5% of the pancreatic mass corresponds to endocrine tissue, pancreatic islets transplantation arises as a natural alternative. Data from the International Islet Transplant Registry (ITR from 1983 to December 2000 document a total of 493 transplants performed around the world, with progressively worse rates of post-transplant insulin independence. In 2000, the "Edmonton Protocol" introduced several modifications to the transplantation procedure, such as the use of a steroid-free immunosuppression regimen and transplantation of a mean islet mass of 11,000 islet equivalents per kilogram, which significantly improved 1-year outcomes. Although the results of a 5-year follow-up in 65 patients demonstrated improvement in glycemic instability in a significant portion of them, only 7.5% of the patients have reached insulin independence, indicating the need of further advances in the preservation of the function of transplanted islet. In addition to the scarcity of organs available for transplantation, islets transplantation still faces major challenges, specially those related to cell loss during the process of islet isolation and the losses related to the graft site, apoptosis, allorejection, autoimmunity, and immunosuppression. The main strategies to optimize islet transplantation aim at improving all these aspects. Conclusion Human islet transplantation should be regarded as an intervention that can decrease the frequency of

Early postoperative and late metabolic morbidity after pancreatic resections: An old and new challenge for surgeons - A review.

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Beger, Hans G; Mayer, Benjamin

2018-02-16

The metrics for measuring early postoperative morbidity after resection of pancreatic neoplastic tumors are overall morbidity, severe surgery-related morbidity, frequency of reoperation and reintervention, in-hospital, 30-day and 90-day mortality and length of hospital stay. Thirty-day readmission after discharge is additionally an indispensable criterion to assess quality of surgery. The metrics for surgery-associated long-term results after pancreatic resections are survival times, new onset of diabetes (DM), impaired glucose tolerance, exocrine pancreatic insufficiency, body mass index and GI motility dysfunctions. Following pancreaticoduodenectomy (PD) performed on pancreatic normo-glycemic patients for malignant and benign tumors, 4-30% develop postoperative new onset of diabetes. Long-term persistence of diabetes mellitus is observed after surgery for benign tumors in 14% and in 15.5% of patients after cancer resection. Pancreatic exocrine insufficiency after PD is observed in the early postoperative period in 23-80% of patients. Persistence of exocrine dysfunctions exists in 25% and 49% of patients. Following left-sided pancreatic resection, new onset DM is observed in 14% of cases; an exocrine insufficiency persisting in the long-term outcome is observed in 16-28% of patients. Copyright © 2018 Elsevier Inc. All rights reserved.

Growth Hormone-Releasing Hormone in Diabetes

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Leonid Evsey Fridlyand

2016-10-01

Full Text Available Growth hormone-releasing hormone (GHRH is produced by the hypothalamus and stimulates growth hormone synthesis and release in the anterior pituitary gland. In addition GHRH is an important regulator of cellular functions in many cells and organs. Expression of GHRH G-Protein Coupled Receptor (GHRHR has been demonstrated in different peripheral tissues and cell types including pancreatic islets. Among the peripheral activities, recent studies demonstrate a novel ability of GHRH analogs to increase and preserve insulin secretion by beta-cells in isolated pancreatic islets, which makes them potentially useful for diabetes treatment. This review considers the role of GHRHR in the beta-cell and addresses the unique engineered GHRH agonists and antagonists for treatment of Type 2 diabetes mellitus. We discuss the similarity of signaling pathways activated by GHRHR in pituitary somatotrophs and in pancreatic beta-cells and possible ways as to how the GHRHR pathway can interact with glucose and other secretagogues to stimulate insulin secretion. We also consider the hypothesis that novel GHRHR agonists can improve glucose metabolism in Type 2 diabetes by preserving the function and survival of pancreatic beta-cells. Wound healing and cardioprotective action with new GHRH agonists suggesting that they may prove useful in ameliorating certain diabetic complications. These findings highlight the future potential therapeutic effectiveness of modulators of GHRHR activity for the development of new therapeutic approaches in diabetes and its complications.

Correlation of the results of radiotherapy of pancreatic cancer with different clinical factors

Energy Technology Data Exchange (ETDEWEB)

Barkanov, A I [Akademiya Meditsinskikh Nauk SSSR, Moscow. Onkologicheskij Nauchnyj Tsentr

1983-01-01

Altogether 124 patients with pancreatic cancer radiation treated at doses of 50-80 Gy. With the period of medical history from 1 to 6 months in 82.1 % of the patients, 6-12 months in 74.4 % and over 12 months in 61.9 % of the patients the mean survival time after radiotherapy was respectively 20.1, 15.5 and 14.3 months, i.e. radiotherapeutic results got worse with the increase of the period of disease. Better survival results were obtained for pancreatic head cancer (14.7 months), worse results in its total involvement (10.4 months). Optimum time between operation and irradiation depending on the degree of jaundice was 0.5-1.5 months. With concomitant pancreatitis irradiation was combined with i.v. administration of contrykal that helped to alleviate the pain syndrome. Irradiation of pancreatic cancer complicated by diabetes mellitus facilitates the course of diabetes during follow-up.

Maturation and function of human embryonic stem cell-derived pancreatic progenitors in macroencapsulation devices following transplant into mice.

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Bruin, Jennifer E; Rezania, Alireza; Xu, Jean; Narayan, Kavitha; Fox, Jessica K; O'Neil, John J; Kieffer, Timothy J

2013-09-01

Islet transplantation is a promising cell therapy for patients with diabetes, but it is currently limited by the reliance upon cadaveric donor tissue. We previously demonstrated that human embryonic stem cell (hESC)-derived pancreatic progenitor cells matured under the kidney capsule in a mouse model of diabetes into glucose-responsive insulin-secreting cells capable of reversing diabetes. However, the formation of cells resembling bone and cartilage was a major limitation of that study. Therefore, we developed an improved differentiation protocol that aimed to prevent the formation of off-target mesoderm tissue following transplantation. We also examined how variation within the complex host environment influenced the development of pancreatic progenitors in vivo. The hESCs were differentiated for 14 days into pancreatic progenitor cells and transplanted either under the kidney capsule or within Theracyte (TheraCyte, Laguna Hills, CA, USA) devices into diabetic mice. Our revised differentiation protocol successfully eliminated the formation of non-endodermal cell populations in 99% of transplanted mice and generated grafts containing >80% endocrine cells. Progenitor cells developed efficiently into pancreatic endocrine tissue within macroencapsulation devices, despite lacking direct contact with the host environment, and reversed diabetes within 3 months. The preparation of cell aggregates pre-transplant was critical for the formation of insulin-producing cells in vivo and endocrine cell development was accelerated within a diabetic host environment compared with healthy mice. Neither insulin nor exendin-4 therapy post-transplant affected the maturation of macroencapsulated cells. Efficient differentiation of hESC-derived pancreatic endocrine cells can occur in a macroencapsulation device, yielding glucose-responsive insulin-producing cells capable of reversing diabetes.

The prevalence of small intestinal bacterial overgrowth in non-surgical patients with chronic pancreatitis and pancreatic exocrine insufficiency (PEI).

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Ní Chonchubhair, Hazel M; Bashir, Yasir; Dobson, Mark; Ryan, Barbara M; Duggan, Sinead N; Conlon, Kevin C

2018-02-24

Small intestinal bacterial overgrowth (SIBO) is a condition characterised by symptoms similar to pancreatic exocrine insufficiency (PEI) in chronic pancreatitis patients. SIBO is thought to complicate chronic pancreatitis in up to 92% of cases; however, studies are heterogeneous and protocols non-standardised. SIBO may be determined by measuring lung air-expiration of either hydrogen or methane which are by-products of small bowel bacterial fermentation of intraluminal substrates such as carbohydrates. We evaluated the prevalence of SIBO among a defined cohort of non-surgical chronic pancreatitics with mild to severe PEI compared with matched healthy controls. Thirty-five patients and 31 age-, gender- and smoking status-matched healthy controls were evaluated for SIBO by means of a fasting glucose hydrogen breath test (GHBT). The relationship between SIBO and clinical symptoms in chronic pancreatitis was evaluated. SIBO was present in 15% of chronic pancreatitis patients, while no healthy controls tested positive (P = 0.029). SIBO was more prevalent in those taking pancreatic enzyme replacement therapy (PERT) (P = 0.016), with proton pump inhibitor use (PPI) (P = 0.022) and in those with alcohol aetiology (P = 0.023). Patients with concurrent diabetes were more often SIBO-positive and this was statistically significant (P = 0.009). There were no statistically significant differences in reported symptoms between patients with and without SIBO, with the exception of 'weight loss', with patients reporting weight loss more likely to have SIBO (P = 0.047). The prevalence of SIBO in this study was almost 15% and consistent with other studies of SIBO in non-surgical chronic pancreatitis patients. These data support the testing of patients with clinically-relevant PEI unresolved by adequate doses of PERT, particularly in those patients with concurrent diabetes. SIBO can be easily diagnosed therefore allowing more specific and more targeted symptom

Diabetes-associated dry eye syndrome in a new humanized transgenic model of type 1 diabetes.

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Imam, Shahnawaz; Elagin, Raya B; Jaume, Juan Carlos

2013-01-01

Patients with Type 1 Diabetes (T1D) are at high risk of developing lacrimal gland dysfunction. We have developed a new model of human T1D using double-transgenic mice carrying HLA-DQ8 diabetes-susceptibility haplotype instead of mouse MHC-class II and expressing the human beta cell autoantigen Glutamic Acid Decarboxylase in pancreatic beta cells. We report here the development of dry eye syndrome (DES) after diabetes induction in our humanized transgenic model. Double-transgenic mice were immunized with DNA encoding human GAD65, either naked or in adenoviral vectors, to induce T1D. Mice monitored for development of diabetes developed lacrimal gland dysfunction. Animals developed lacrimal gland disease (classically associated with diabetes in Non Obese Diabetic [NOD] mice and with T1D in humans) as they developed glucose intolerance and diabetes. Animals manifested obvious clinical signs of dry eye syndrome (DES), from corneal erosions to severe keratitis. Histological studies of peri-bulbar areas revealed lymphocytic infiltration of glandular structures. Indeed, infiltrative lesions were observed in lacrimal/Harderian glands within weeks following development of glucose intolerance. Lesions ranged from focal lymphocytic infiltration to complete acinar destruction. We observed a correlation between the severity of the pancreatic infiltration and the severity of the ocular disease. Our results demonstrate development of DES in association with antigen-specific insulitis and diabetes following immunization with clinically relevant human autoantigen concomitantly expressed in pancreatic beta cells of diabetes-susceptible mice. As in the NOD mouse model and as in human T1D, our animals developed diabetes-associated DES. This specific finding stresses the relevance of our model for studying these human diseases. We believe our model will facilitate studies to prevent/treat diabetes-associated DES as well as human diabetes.

A Suspicious Pancreatic Mass in Chronic Pancreatitis: Pancreatic Actinomycosis

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F. de Clerck

2015-01-01

Full Text Available Introduction. Pancreatic actinomycosis is a chronic infection of the pancreas caused by the suppurative Gram-positive bacterium Actinomyces. It has mostly been described in patients following repeated main pancreatic duct stenting in the context of chronic pancreatitis or following pancreatic surgery. This type of pancreatitis is often erroneously interpreted as pancreatic malignancy due to the specific invasive characteristics of Actinomyces. Case. A 64-year-old male with a history of chronic pancreatitis and repeated main pancreatic duct stenting presented with weight loss, fever, night sweats, and abdominal pain. CT imaging revealed a mass in the pancreatic tail, invading the surrounding tissue and resulting in splenic vein thrombosis. Resectable pancreatic cancer was suspected, and pancreatic tail resection was performed. Postoperative findings revealed pancreatic actinomycosis instead of neoplasia. Conclusion. Pancreatic actinomycosis is a rare type of infectious pancreatitis that should be included in the differential diagnosis when a pancreatic mass is discovered in a patient with chronic pancreatitis and prior main pancreatic duct stenting. Our case emphasizes the importance of pursuing a histomorphological confirmation.

Serie de 8 casos de parotiditis supurada aguda neonatal

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Manuel Díaz Álvarez

Full Text Available La parotiditis supurada aguda es una infección poco frecuente en la práctica del pediatra y neonatólogo. El objetivo es mostrar nuestra experiencia en la atención de serie de casos con parotiditis supurada aguda en el período neonatal, y describir sus características de presentación. Se presentan los hallazgos clínicos en 8 pacientes con parotiditis supurativa neonatal, quienes estuvieron ingresados en el Servicio de Neonatología del Hospital Pediátrico Universitario "Juan Manuel Márquez", durante el período de 22 años (desde el año 1992 hasta el año 2013, y se contrasta con los reportes publicados en la literatura internacional. Las características de presentación de la parotiditis aguda supurada de nuestros casos concuerdan con la literatura revisada en muchos aspectos, y se demuestra que es, además, una infección poco frecuente en el período neonatal. Es la primera publicación sobre esta entidad en neonatos en Cuba, y la mayor serie de casos en el ámbito latinoamericano.

Autoimmunity in diabetics induced by hormonal contaminants of insulin

International Nuclear Information System (INIS)

Bloom, S.R.; Barnes, A.J.; Adrian, T.E.; Polak, J.M.

1979-01-01

Several commercial insulin preparations were found to contain significant quantities of pancreatic glucagon, pancreatic polypeptide (P.P.), vasoactive intestinal peptide (V.I.P.), and somatostatin, though these substances were effectively absent from the new highly purified or monocomponent insulins. Of 448 insulin-dependent diabetics receiving conventional insulins, 63% had circulating antibodies to human P.P., 6% antibodies to V.I.P., 6% to glucagon, and 0.5% to somatostatin. The antibodies were of high affinity and were commonest in the younger diabetics. No antibodies were detected in 167 maturity-onset diabetics, in 125 healthy controls, or in 22 patients treated only with monocomponent insulin. Immuno-cytochemical testing showed that antibody-positive diabetic plasmas reacted specifically against the corresponding hormone-producing pancreatic endocrine cells, against enteroglucagon and somatostatin cells outside the pancreas, and against V.I.P.-containing autonomic nerves throughout the body. The finding of iatrogenic autoimmunity to naturally occurring hormones in large numbers of insulin-dependent diabetics raises important questions about long-term treatment. (author)

Autoimmunity in diabetics induced by hormonal contaminants of insulin

Energy Technology Data Exchange (ETDEWEB)

Bloom, S R; Barnes, A J; Adrian, T E; Polak, J M [Royal Postgraduate Medical School, London (UK)

1979-01-06

Several commercial insulin preparations were found to contain significant quantities of pancreatic glucagon, pancreatic polypeptide (P.P.), vasoactive intestinal peptide (V.I.P.), and somatostatin, though these substances were effectively absent from the new highly purified or monocomponent insulins. Of 448 insulin-dependent diabetics receiving conventional insulins, 63% had circulating antibodies to human P.P., 6% antibodies to V.I.P., 6% to glucagon, and 0.5% to somatostatin. The antibodies were of high affinity and were commonest in the younger diabetics. No antibodies were detected in 167 maturity-onset diabetics, in 125 healthy controls, or in 22 patients treated only with monocomponent insulin. Immuno-cytochemical testing showed that antibody-positive diabetic plasmas reacted specifically against the corresponding hormone-producing pancreatic endocrine cells, against enteroglucagon and somatostatin cells outside the pancreas, and against V.I.P.-containing autonomic nerves throughout the body. The finding of iatrogenic autoimmunity to naturally occurring hormones in large numbers of insulin-dependent diabetics raises important questions about long-term treatment.

Severe Hypertriglyceridemia Possibly Masked Acute Pancreatitis and Led to a Difficult Diagnosis in an Obese Patient with Ketoacidosis-onset Type 2 Diabetes.

Science.gov (United States)

Fujishiro, Midori; Horita, Akiko; Nakagawara, Hiroshi; Mawatari, Takayuki; Kishigami, Yoshifusa; Tominaga, Yoshiteru; Moriyama, Mitsuhiko; Ishihara, Hisamitsu

2017-10-01

A young obese man with ketoacidosis-onset type 2 diabetes mellitus, associated with severe hypertriglyceridemia, was admitted to a local hospital complaining of abdominal pain. Although the abdominal pain worsened, his serum amylase level remained normal with persistent severe hypertriglyceridemia until the second day of hospitalization. The next day, computed tomography showed severe acute pancreatitis (AP) with serum amylase elevation, while the patient's triglyceride level decreased to 558 mg/dL. He was transferred to our hospital and recovered after intensive care. AP accompanied by diabetic ketoacidosis is not rare but an early diagnosis can be difficult to make due to normal amylase levels in the presence of severe hypertriglyceridemia.

The variable phenotype of the p.A16V mutation of cationic trypsinogen (PRSS1) in pancreatitis families

DEFF Research Database (Denmark)

Grocock, Christopher J; Rebours, Vinciane; Delhaye, Myriam

2010-01-01

Pancreatitis (HP); idiopathic disease; or pancreatitis in a single generation. HP was defined as 2 cases in 2 generations. MAIN OUTCOME MEASURES: Onset of painful episodes of pancreatitis, death from pancreatic cancer, diagnosis of diabetes mellitus and exocrine pancreatic failure. RESULTS: Ten families with p...... or Mann-Whitney-U tests. CONCLUSIONS: Penetrance of p.A16V is highly variable and family dependent, suggesting it contributes to a multigenic inheritance of a predisposition to pancreatitis....

Acute pancreatitis with gliptins: Is it a clinical reality?

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Muthukrishnan Jayaraman

2013-01-01

Full Text Available There are reports of acute pancreatitis with the use of dipeptidyl peptidase-4 inhibitors (gliptins. This class of drugs is widely being prescribed for type 2 diabetes mellitus (DM in our country. We evaluated the incidence of acute pancreatitis with the use of gliptins during the period January 2012-June 2013. Patients of type 2 DM on treatment with any of the gliptins (Sitagliptin, vildagliptin, or saxagliptin for at least 1 month duration were included. A total of 185 patients were included (205.3 patient years of follow-up. Five of them had history of acute pancreatitis (all mild >6 months prior to inclusion with complete resolution and no chronic pancreatitis. One patient (0.48 per 100 patient years presented with mild acute pancreatitis which resolved in 8 days. Asymptomatic elevation of serum amylase > 3× upper limit of normal was noted in five patients (2.4 per 100 patient years, without any sonological evidence of pancreatitis, which resolved on withdrawal of gliptins. None of the patients with previous history of pancreatitis had a recurrence of pancreatitis. In a group at low risk of acute pancreatitis, incidence of acute pancreatitis is low with the use of gliptins.

The impact of pancreaticoduodenectomy on endocrine and exocrine pancreatic function: A prospective cohort study based on pre- and postoperative function tests.

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Roeyen, Geert; Jansen, Miet; Hartman, Vera; Chapelle, Thiery; Bracke, Bart; Ysebaert, Dirk; De Block, Christophe

Studies reporting on function after pancreatic surgery are frequently based on diabetes history, fasting glycemia or random glycemia. The aim of this study was to investigate prospectively the evolution of pancreatic function in patients undergoing pancreaticoduodenectomy based on proper pre- and postoperative function tests. It was hypothesised that pancreatic function deteriorates after pancreaticoduodenectomy. Between 2013 and 2016, 78 patients undergoing pancreaticoduodenectomy for oncologic indications had a prospective evaluation of their endocrine and exocrine pancreatic function. Endocrine function was evaluated with the 75 g oral glucose tolerance test (OGTT) and the 1 mg intravenous glucagon test. Exocrine function was evaluated with a 13C-labelled mixed-triglyceride breath test. Tests were performed pre- and postoperatively. In 90.5% (19/21) of patients with preoperatively known diabetes, no change in endocrine function was observed. In contrast, endocrine function improved in 68.1% (15/22) of patients with newly diagnosed diabetes. 40% (14/35) of patients with a preoperative normal OGTT or prediabetes experienced deterioration in function. In multivariate analysis, improvement of newly diagnosed diabetes was correlated with preoperative bilirubin levels (p = 0.045), while progression towards diabetes was correlated with preoperative C-peptidogenic index T 30 (p = 0.037). A total of 20.5% (16/78) of patients had pancreatic exocrine insufficiency preoperatively. Another 51.3% (40/78) of patients deteriorated on exocrine level. In total, 64.1% (50/78) of patients required pancreatic enzyme-replacement therapy postoperatively. Although deterioration of endocrine function was expected after pancreatic resection, improvement is frequently observed in patients with newly diagnosed diabetes. Exocrine function deteriorates after pancreaticoduodenectomy. Copyright © 2017 IAP and EPC. Published by Elsevier B.V. All rights reserved.

An SCFFBXO28 E3 Ligase Protects Pancreatic β-Cells from Apoptosis

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Kanaka Durga Devi Gorrepati

2018-03-01

Full Text Available Loss of pancreatic β-cell function and/or mass is a central hallmark of all forms of diabetes but its molecular basis is incompletely understood. β-cell apoptosis contributes to the reduced β-cell mass in diabetes. Therefore, the identification of important signaling molecules that promote β-cell survival in diabetes could lead to a promising therapeutic intervention to block β-cell decline during development and progression of diabetes. In the present study, we identified F-box protein 28 (FBXO28, a substrate-recruiting component of the Skp1-Cul1-F-box (SCF ligase complex, as a regulator of pancreatic β-cell survival. FBXO28 was down-regulated in β-cells and in isolated human islets under diabetic conditions. Consistently, genetic silencing of FBXO28 impaired β-cell survival, and restoration of FBXO28 protected β-cells from the harmful effects of the diabetic milieu. Although FBXO28 expression positively correlated with β-cell transcription factor NEUROD1 and FBXO28 depletion also reduced insulin mRNA expression, neither FBXO28 overexpression nor depletion had any significant impact on insulin content, glucose-stimulated insulin secretion (GSIS or on other genes involved in glucose sensing and metabolism or on important β-cell transcription factors in isolated human islets. Consistently, FBXO28 overexpression did not further alter insulin content and GSIS in freshly isolated islets from patients with type 2 diabetes (T2D. Our data show that FBXO28 improves pancreatic β-cell survival under diabetogenic conditions without affecting insulin secretion, and its restoration may be a novel therapeutic tool to promote β-cell survival in diabetes.

Incidencia de la enfermedad diarreica aguda en menores de cinco años

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Mayelín Ávila Labrada

2015-05-01

Full Text Available La enfermedad diarreica aguda es motivo frecuente de consulta pediátrica, representando un problema grave de salud pública. Los agentes infecciosos son causa frecuente de diarrea aguda. Se realizó un estudio descriptivo, retrospectivo sobre la prevalencia de la enfermedad diarreica aguda en menores de cinco años, atendidos en la clínica “Simón Bolívar” en la ciudad de Mariara del municipio Diego Ibarra, Carabobo, Venezuela; en el periodo comprendido entre enero de 2008 y diciembre de 2012, lo cual ofreció información de cinco años completos. La prevalencia de la enfermedad diarreica aguda disminuyó significativamente en el intervalo 2009-2011, sin embargo, se caracterizó por tener la mayor prevalencia en los años extremos, 2012 y 2008, por ese orden. Los varones y los del grupo de uno a cuatro años fueron los que más incidieron en cada uno de los años estudiados

A novel peptide nanomedicine for treatment of pancreatogenic diabetes.

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Banerjee, Amrita; Onyuksel, Hayat

2013-08-01

Pancreatogenic diabetes (PD) is a potentially fatal disease that occurs secondary to pancreatic disorders. The current anti-diabetic therapy for PD is fraught with adverse effects that can increase morbidity. Here we investigated the efficacy of novel peptide nanomedicine: pancreatic polypeptide (PP) in sterically stabilized micelles (SSM) for management of PD. PP exhibits significant anti-diabetic efficacy but its short plasma half-life curtails its therapeutic application. To prolong and improve activity of PP in vivo, we evaluated the delivery of PP in SSM. PP-SSM administered to rats with PD, significantly improved glucose tolerance, insulin sensitivity and hepatic glycogen content compared to peptide in buffer. The studies established the importance of micellar nanocarriers in protecting enzyme-labile peptides in vivo and delivering them to target site, thereby enhancing their therapeutic efficacy. In summary, this study demonstrated that PP-SSM is a promising novel anti-diabetic nanomedicine and therefore should be further developed for management of PD. Pancreatic peptide was earlier demonstrated to address pancreatogenic diabetes, but its short half-life represented major difficulties in further development for therapeutic use. PP-SSM (pancreatic polypeptide in sterically stabilized micelles) is a promising novel anti-diabetic nanomedicine that enables prolonged half-life and increased bioactivity of PP, as shown in this novel study, paving the way toward clinical studies in the near future. Copyright © 2013 Elsevier Inc. All rights reserved.

Notas sobre apendicitis aguda

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Martín Méndez S.

1933-04-01

apendicitis aguda y sin embargo, es necesario decirlo claro, nada hay tan complicado y en ocasiones tan oscuro. Sin duda, a medida que los conocimientos clínicos se extienden, se va iluminando el campo, antes inexplorado, de la cirugía apendicular, y hoy día casi todos los médicos y cirujanos tienen un criterio científico muy bien formado para lograr hacer un buen diagnóstico y aconsejar o llevar a cabo una intervención quirúrgica.

Xylitol improves pancreatic islets morphology to ameliorate type 2 diabetes in rats: a dose response study.

Science.gov (United States)

Rahman, Md Atiar; Islam, Md Shahdiul

2014-07-01

Xylitol has been reported as a potential antidiabetic sweetener in a number of recent studies; however, the most effective dietary dose and organ-specific effects are still unclear. Six-week-old male Sprague-Dawley rats were randomly divided into 5 groups: normal control (NC), diabetic control (DBC), diabetic xylitol 2.5% (DXL2.5), diabetic xylitol 5.0% (DXL5), and diabetic xylitol 10.0% (DXL10). Diabetes was induced only in the animals in DBC and DXL groups and considered diabetic when their nonfasting blood glucose level was >300 mg/dL. The DXL groups were fed with 2.5%, 5.0%, and 10% xylitol solution, whereas the NC and DBC groups were supplied with normal drinking water. After 4-wk intervention, body weight, food and fluid intake, blood glucose, serum fructosamine, liver glycogen, serum alanine transaminase, aspartate transaminase, lactate dehydrogenase, creatine kinase, uric acid, creatinine, and most serum lipids were significantly decreased, and serum insulin concentration, glucose tolerance ability, and pancreatic islets morphology were significantly improved in the DXL10 group compared to the DBC group. The data of this study suggest that 10% xylitol has the better antidiabetic effects compared to 2.5% and 5.0% and it can be used as an excellent antidiabetic sweetener and food supplement in antidiabetic foods. Xylitol is widely used as a potential anticariogenic and sweetening agent in a number of oral care and food products when many of its health benefits are still unknown. Due to its similar sweetening power but lower calorific value (2.5 compared with 4 kcal) and lower glycemic index (13 compared with 65) compared to sucrose, recently it has been widely used as a sugar substitute particularly by overweight, obese, and diabetic patients in order to reduce their calorie intake from sucrose. However, the potential antidiabetic effects of xylitol have been discovered recently. The results of this study confirmed the effective dietary dose of xylitol for

Hepatitis viral aguda

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Héctor Rubén Hernández Garcés

1998-10-01

Full Text Available Se realizó una revisión bibliográfica de las hepatitis virales agudas sobre aspectos vinculados a su etiología. Se tuvieron en cuenta además algunos datos epidemiológicos, las formas clínicas más importantes, los exámenes complementarios con especial énfasis en los marcadores virales y el diagnóstico positivoA bibliographical review of acute viral hepatitis was made taking into account those aspects connected with its etiology. Some epidemiological markers, the most important clinical forms, and the complementary examinations with special emphasis on the viral markers and the positive diagnosis were also considered

Size of pancreas in non-insulin-dependent diabetes mellitus: a study based on CT

International Nuclear Information System (INIS)

Shin, Ju Won; Yoon, Soon Min; Yoon, Mi Jin; Song, Moon Gab; Kim, Yoon Suk; Yoon, Young Kyu; Jun, Se June

1997-01-01

To evaluate changes of pancreatic size with aging in control subjects and in non-insulin- dependent diabetic patients. Two groups of non-insulin-dependent diabetic patients were examined; one had been treated with an oral hypoglycemic agent(n=59), and the other with insulin(n=56). The CT findings of 175 patients without clinical evidence of pancreatic disease were included as a normal control. In control subjects, pancreatic size and age correlated. The pancreas was smaller in non-insulin-dependent diabetics than in control subjects and smaller in insulin- treated non-insulin-dependent diabetics than in non-insulin treated patients. The pancreas was smaller in non-insulin-dependent diabetic patients than in control subjects within the same age range

Patient and Disease Characteristics Associated With the Presence of Diabetes Mellitus in Adults With Chronic Pancreatitis in the United States.

Science.gov (United States)

Bellin, Melena D; Whitcomb, David C; Abberbock, Judah; Sherman, Stuart; Sandhu, Bimaljit S; Gardner, Timothy B; Anderson, Michelle A; Lewis, Michele D; Alkaade, Samer; Singh, Vikesh K; Baillie, John; Banks, Peter A; Conwell, Darwin; Cote, Gregory A; Guda, Nalini M; Muniraj, Thiruvengadam; Tang, Gong; Brand, Randall E; Gelrud, Andres; Amann, Stephen T; Forsmark, Christopher E; Wilcox, C Mel; Slivka, Adam; Yadav, Dhiraj

2017-09-01

Diabetes mellitus (DM) is a common complication of chronic pancreatitis (CP). Past studies for DM risk factors in CP have been limited to single centers or highly focused on a single etiology such as alcoholic or hereditary disease. We studied risk factors for DM in a large population of patients with CP of all etiologies enrolled in the North American Pancreatitis 2 studies. Participants (1,171) with CP (n=383 with DM, n=788 without DM) were enrolled prospectively from 26 participating centers. Questionnaires were completed by patients and physicians in a cross-sectional assessment. Patient demographics and disease characteristics were compared for CP with DM vs. without DM. Logistic regression was performed to assess the variables associated with DM diagnosis in a multivariable model. Diabetics were more likely to be black (P=0.02), overweight, or obese (Ppancreatic calcifications (63% vs. 54%, P=0.002), atrophy (44% vs. 32%, Prisk factors for DM were obesity (odds ratio (OR) 2.8, 95% confidence interval (CI) 1.9, 4.2) and exocrine insufficiency (OR 2.4, 95% CI 1.8, 3.2). In this large multicenter cohort of patients with CP, exocrine insufficiency, calcifications, and pancreas surgery conveyed higher odds of having DM. However, the traditional 'type 2 DM' risk factors of obesity and family history were similarly important in conveying risk for DM.

Algunas observaciones sobre la apendicitis aguda en los niños

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Luis Piñeros Suárez

1940-03-01

Full Text Available La apendicitis aguda en los niños, presenta actitudes particulares que diferencian de la apendicitis aguda del adulto y que vienen a formar grupos clínicos casi exclusivamente de la infancia. De una manera general, las formas más graves, las formas fulminantes de la apendicitis aguda se encuentran especialmente en la infancia y en estas formas graves llama poderosamente la atención, la falta de relación entre los signos clínicos observados y la importancia de las lesiones encontradas en el apéndice y el peritoneo, pues en los niños con signos de intensidad media y sin que se hayan presentado los síntomas que en el adulto caracterizan las formas graves de apendicitis, podemos encontrar en las operaciones practicadas en las primeras 24 a 36 horas, peritonitis generalizadas, formas de apendicitis gangrenosas, que no son frecuentes en el adulto y mucho menos en un lapso de tiempo tan corto.

Chronic Pancreatitis in the 21st Century - Research Challenges and Opportunities

Science.gov (United States)

Uc, Aliye; Andersen, Dana K.; Bellin, Melena D.; Bruce, Jason I.; Drewes, Asbjørn M.; Engelhardt, John F.; Forsmark, Christopher E.; Lerch, Markus M.; Lowe, Mark E.; Neuschwander-Tetri, Brent A.; O’Keefe, Stephen J.; Palermo, Tonya M.; Pasricha, Pankaj; Saluja, Ashok K.; Singh, Vikesh K.; Szigethy, Eva M.; Whitcomb, David C.; Yadav, Dhiraj; Conwell, Darwin L.

2016-01-01

A workshop was sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) to focus on research gaps and opportunities in chronic pancreatitis (CP) and its sequelae. This conference marked the 20th year anniversary of the discovery of the cationic trypsinogen (PRSS1) gene mutation for hereditary pancreatitis. The event was held on July 27, 2016, and structured into 4 sessions: (1) pathophysiology; (2) exocrine complications; (3) endocrine complications; and (4) pain. The current state of knowledge was reviewed; many knowledge gaps and research needs were identified that require further investigation. Common themes included the need to design better tools to diagnose CP and its sequelae early and reliably, identify predisposing risk factors for disease progression, develop standardized protocols to distinguish type 3c diabetes mellitus from other types of diabetes and design effective therapeutic strategies through novel cell culture technologies, animal models mimicking human disease, and pain management tools. Gene therapy and cystic fibrosis conductance regulator (CFTR) potentiators as possible treatments for CP were discussed. Importantly, the need for chronic pancreatitis endpoints and intermediate targets for future drug trials was emphasized. PMID:27748719

Enteric hyperoxaluria in chronic pancreatitis.

Science.gov (United States)

Demoulin, Nathalie; Issa, Zaina; Crott, Ralph; Morelle, Johann; Danse, Etienne; Wallemacq, Pierre; Jadoul, Michel; Deprez, Pierre H

2017-05-01

Chronic pancreatitis may lead to steatorrhea, enteric hyperoxaluria, and kidney damage. However, the prevalence and determinants of hyperoxaluria in chronic pancreatitis patients as well as its association with renal function decline have not been investigated.We performed an observational study. Urine oxalate to creatinine ratio was assessed on 2 independent random urine samples in consecutive adult patients with chronic pancreatitis followed at the outpatient clinic from March 1 to October 31, 2012. Baseline characteristics and annual estimated glomerular filtration rate (eGFR) change during follow-up were compared between patients with hyper- and normo-oxaluria.A total of 48 patients with chronic pancreatitis were included. The etiology of the disease was toxic (52%), idiopathic (27%), obstructive (11%), autoimmune (6%), or genetic (4%). Hyperoxaluria (defined as urine oxalate to creatinine ratio >32 mg/g) was found in 23% of patients. Multivariate regression analysis identified clinical steatorrhea, high fecal acid steatocrit, and pancreatic atrophy as independent predictors of hyperoxaluria. Taken together, a combination of clinical steatorrhea, steatocrit level >31%, and pancreatic atrophy was associated with a positive predictive value of 100% for hyperoxaluria. On the contrary, none of the patients with a fecal elastase-1 level >100 μg/g had hyperoxaluria. Longitudinal evolution of eGFR was available in 71% of the patients, with a mean follow-up of 904 days. After adjustment for established determinants of renal function decline (gender, diabetes, bicarbonate level, baseline eGFR, and proteinuria), a urine oxalate to creatinine ratio >32 mg/g was associated with a higher risk of eGFR decline.Hyperoxaluria is highly prevalent in patients with chronic pancreatitis and associated with faster decline in renal function. A high urine oxalate to creatinine ratio in patients with chronic pancreatitis is best predicted by clinical steatorrhea, a high acid

Advances in pancreatic islet transplantation for the treatment of diabetes%胰岛移植治疗糖尿病的现状和进展

Institute of Scientific and Technical Information of China (English)

彭丹凤; 贾伟平

2012-01-01

胰岛移植是治疗糖尿病尤其是1型糖尿病的一种简单有效的方法,相较与胰腺移植,它较为简单和方便,但存在组织来源匮乏和免疫移植排斥等障碍.新的胰岛分离纯化方法提高了供移植的胰岛的纯度和活性.成体干细胞研究、异种移植研究,有望解决移植的供源问题.Edmonton方案在胰岛移植的临床应用中具有里程碑意义.新型的免疫抑制剂和免疫诱导剂的研究可以提高临床胰岛移植的成功率.%Objective Pancreatic islet transplantation is effective in treating diabetes, especially in type 1 diabetes. It can provide diabetes management with good glycemic control and insulin independence. Compared to pancreas transplantation, islet transplantation is technically much simplier and safer. However, currently its clinical use is highly restricted by a series of influence factors, including lack of sufficient donor organs and the side effects of immunosuppressive therapy. With recent advances in methods of islet isolation and purification, we can get better donor organs. Deriving islet cells from other sources such as pigs, human pancreatic duct cells, fetal pancreatic stem cells, and embryonic stem cells will overcome shortage of donor organs. The use of the Edmonton protocol has been proved to be the key procedure of clinical islet transplantation. And study of new immunosuppressive drugs and immunomodulators can provide higher rate of success for clinical islet transplantation.

Diabetes, obesidad y ejercicio físico

OpenAIRE

Cricri, Karina; Corvalán, Juan Manuel; Poletta, Fernando

2011-01-01

El Hospital Italiano de La Plata busca generar una concientización de la Diabetes, enfermedad que afecta alrededor del 7% de la población, con el fin de mejorar la calidad de vida y de evitar o retrasar la aparición de las complicaciones agudas y crónicas. Considerando que en la prevención y el tratamiento de la Diabetes existen cuatro pilares fundamentales: Alimentación, Tratamiento Farmacológico, Ejercicio Físico y Educación se organiza a partir del año 2007 una Campaña gratuita abierta a l...

Pancreatic islet-cell viability, functionality and oxidative status ...

Indian Academy of Sciences (India)

Unknown

Environmental factors such as diet, physical activity, drugs, pollution and life style play an important ... Antibiotics seem to have a correlation with diabetes and pancreatic function. ... altogether have a different effect in vitro than what is seen.

Characterization of Momordica charantia L. polysaccharide and its protective effect on pancreatic cells injury in STZ-induced diabetic mice.

Science.gov (United States)

Zhang, Cong; Chen, Hongman; Bai, Weiqi

2018-04-10

A polysaccharide with a molecular weight of 13,029Da was isolated from Momordica charantia (MCP) fruit and purified by ion-exchange and size-exclusion chromatography. The isolated polysaccharide MCPIIa contained L-Rha, D-GalA, D-Gal, D-Xyl, L-Ara in a molar ratio of 12:3.05:19.89:5.95:56. IR spectrum and NMR studies indicated that the MCPIIa sugar units were linked, via β-glycosidic bonds, to a large number of arabinofuranose, glucuronic acid, and xylopyranosyl residues. In addition, the hypoglycemic effect of MCPIIa was investigated in streptozotocin (STZ)-induced diabetic mice. After STZ-induction, MCPIIa (100, 200, or 300mg/kg body weight) was administered orally, once daily, for 28days. Glycemia in STZ-diabetogenic mice was significantly reduced, and compared with diabetes mellitus (DM) mice, serum insulin concentration increased significantly, following MCPIIa administration. Transmission electron microscopy showed an alleviation of STZ-lesions in pancreatic tissue from mice treated with MCPIIa. These results indicate that MCPIIa may be useful as an anti-diabetic agent. Copyright © 2018 Elsevier B.V. All rights reserved.

Effects of methyl mercury exposure on pancreatic beta cell development and function.

Science.gov (United States)

Schumacher, Lauren; Abbott, Louise C

2017-01-01

Methyl mercury is an environmental contaminant of worldwide concern. Since the discovery of methyl mercury exposure due to eating contaminated fish as the underlying cause of the Minamata disaster, the scientific community has known about the sensitivity of the developing central nervous system to mercury toxicity. Warnings are given to pregnant women and young children to limit consumption of foods containing methyl mercury to protect the embryonic, fetal and postnatally developing central nervous system. However, evidence also suggests that exposure to methyl mercury or various forms of inorganic mercury may also affect development and function of other organs. Numerous reports indicate a worldwide increase in diabetes, particularly type 2 diabetes. Quite recently, methyl mercury has been shown to have adverse effects on pancreatic beta (β) cell development and function, resulting in insulin resistance and hyperglycemia and may even lead to the development of diabetes. This review discusses possible mechanisms by which methyl mercury exposure may adversely affect pancreatic β cell development and function, and the role that methyl mercury exposure may have in the reported worldwide increase in diabetes, particularly type 2 diabetes. While additional information is needed regarding associations between mercury exposure and specific mechanisms of the pathogenesis of diabetes in the human population, methyl mercury's adverse effects on the body's natural sources of antioxidants suggest that one possible therapeutic strategy could involve supplementation with antioxidants. Thus, it is important that additional investigation be undertaken into the role of methyl mercury exposure and reduced pancreatic β cell function. Copyright © 2016 John Wiley & Sons, Ltd. Copyright © 2016 John Wiley & Sons, Ltd.

Pancreatic effects of GLP-1

DEFF Research Database (Denmark)

Kuhre, Rune Ehrenreich; Albrechtsen, Nicolai Jacob Wewer; Holst, Jens Juul

2014-01-01

-dependent manner. But perhaps equally importantly, GLP-1’s glucose lowering effects are attributable to a strong inhibition of glucagon secretion, and, thereby, a reduction of hepatic glucose output. The effects of GLP-1 on insulin secretion are mediated by binding of the hormone to the receptor (GLP-1r......) on the pancreatic β-cell, which increases intracellular cAMP levels and sets in motion a plethora of events that lead to secretion. In contrast, the inhibitory effect of GLP-1 on the α-cell may be indirect, involving paracrine intra-islet regulation by somatostatin and possibly also insulin, although GLP-1 also...... inhibits glucagon secretion in patients with type 1 diabetes mellitus. Besides these acute effects on the endocrine pancreas, GLP-1 also appears to have a positive effect on β-cell mass. In the following we will review GLP-1’s pancreatic effects with particular focus on its effects on pancreatic islets...

Estado oxidante e antioxidante de crianças com bronquiolite aguda

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Rusen Dundaroz

2013-08-01

Full Text Available OBJETIVO: O estresse oxidativo demonstrou contribuir para a patogênese de doenças pulmonares inflamatórias agudas e crônicas. Nosso objetivo foi avaliar o estado oxidante/antioxidante de crianças com bronquiolite aguda por meio de mensuração da capacidade antioxidante total do plasma, estado oxidante total e índice de estresse oxidativo. MÉTODOS: As crianças com bronquiolite aguda encaminhadas para o Departamento de Emergência Pediátrica do hospital universitário entre janeiro e abril 2012 foram comparadas a controles saudáveis de mesma idade. Os pacientes com bronquiolite aguda tiveram essa doença classificada como leve e moderada. O estado oxidante e antioxidante foi avaliado pela mensuração da capacidade antioxidante total do plasma, estado oxidante total e índice de estresse oxidativo. RESULTADOS: Foram incluídas 31 crianças com bronquiolite aguda com idade de três meses a dois anos e 37 crianças saudáveis. O estado oxidante total (EOT foi maior em pacientes com bronquiolite aguda do que no grupo de controle (5,16±1,99 µmol H2O2 em comparação a 3,78±1,78 µmol H2O2 [p = 0,004]. A capacidade antioxidante total (CAT foi significativamente menor em crianças com bronquiolite que no grupo de controle (2,51±0,37 µmol Trolox equivalente/L em comparação a 2,75±0,39 µmol Trolox Eqv/L (p = 0,013. Os pacientes com bronquiolite moderada apresentaram níveis de EOT mais elevados que os com bronquiolite leve e os do grupo de controle (p = 0,03, p < 0,001. Os pacientes com bronquiolite moderada apresentaram níveis de IEO mais elevados que os do grupo de controle (p = 0,015. O nível de saturação de oxigênio de pacientes com bronquiolite foi inversamente correlacionado ao nível de EOT (r = -0,476, p < 0,05. CONCLUSÃO: O equilíbrio entre os sistemas oxidante e antioxidante é interrompido em crianças com bronquiolite moderada, indicando que o fator de estresse poderá ter um papel na patogênese da doença.

Positron emission tomography study on pancreatic somatostatin receptors in normal and diabetic rats with {sup 68}Ga-DOTA-octreotide: A potential PET tracer for beta cell mass measurement

Energy Technology Data Exchange (ETDEWEB)

Sako, Takeo [Division of Bio-function Dynamics Imaging, RIKEN Center for Life Science Technologies, 6-7-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan); Division of Molecular Imaging, Institute of Biomedical Research and Innovation, 2-2 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan); Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Hyogo 650-0017 (Japan); Hasegawa, Koki; Nishimura, Mie; Kanayama, Yousuke; Wada, Yasuhiro; Hayashinaka, Emi; Cui, Yilong; Kataoka, Yosky [Division of Bio-function Dynamics Imaging, RIKEN Center for Life Science Technologies, 6-7-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan); Senda, Michio [Division of Bio-function Dynamics Imaging, RIKEN Center for Life Science Technologies, 6-7-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan); Division of Molecular Imaging, Institute of Biomedical Research and Innovation, 2-2 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan); Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, Hyogo 650-0017 (Japan); Watanabe, Yasuyoshi, E-mail: yywata@riken.jp [Division of Bio-function Dynamics Imaging, RIKEN Center for Life Science Technologies, 6-7-3 Minatojima-minamimachi, Chuo-ku, Kobe, Hyogo 650-0047 (Japan)

2013-12-06

Highlights: •PET images showed high uptake of {sup 68}Ga-DOTA-octreotide in the normal pancreas. •{sup 68}Ga-DOTA-octreotide specifically binds to somatostatin receptors in the pancreas. •The pancreatic uptake of {sup 68}Ga-DOTA-octreotide was decreased in the diabetic rats. •{sup 68}Ga-DOTA-octreotide could be a candidate PET probe to measure the beta cell mass. -- Abstract: Diabetes mellitus (DM) is a metabolic disorder characterized by hyperglycemia, and the loss or dysfunction of pancreatic beta cells has been reported before the appearance of clinical symptoms and hyperglycemia. To evaluate beta cell mass (BCM) for improving the detection and treatment of DM at earlier stages, we focused on somatostatin receptors that are highly expressed in the pancreatic beta cells, and developed a positron emission tomography (PET) probe derived from octreotide, a metabolically stable somatostatin analog. Octreotide was conjugated with 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA), a chelating agent, and labeled with {sup 68}Gallium ({sup 68}Ga). After intravenous injection of {sup 68}Ga-DOTA-octreotide, a 90-min emission scan of the abdomen was performed in normal and DM model rats. The PET studies showed that {sup 68}Ga-DOTA-octreotide radioactivity was highly accumulated in the pancreas of normal rats and that the pancreatic accumulation was significantly reduced in the rats administered with an excess amount of unlabeled octreotide or after treatment with streptozotocin, which was used for the chemical induction of DM in rats. These results were in good agreement with the ex vivo biodistribution data. These results indicated that the pancreatic accumulation of {sup 68}Ga-DOTA-octreotide represented specific binding to the somatostatin receptors and reflected BCM. Therefore, PET imaging with {sup 68}Ga-DOTA-octreotide could be a potential tool for evaluating BCM.

Altered Expression of Somatostatin Receptors in Pancreatic Islets from NOD Mice Cultured at Different Glucose Concentrations In Vitro and in Islets Transplanted to Diabetic NOD Mice In Vivo

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Eva Ludvigsen

2011-01-01

Full Text Available Somatostatin acts via five receptors (sst1-5. We investigated if the changes in pancreatic islet sst expression in diabetic NOD mice compared to normoglycemic mice are a consequence of hyperglycemia or the ongoing immune reaction in the pancreas. Pancreatic islets were isolated from NOD mice precultured for 5 days and further cultured for 3 days at high or low glucose before examined. Islets were also isolated from NOD mice and transplanted to normal or diabetic mice in a number not sufficient to cure hyperglycemia. After three days, the transplants were removed and stained for sst1-5 and islet hormones. Overall, changes in sst islet cell expression were more common in islets cultured in high glucose concentration in vitro as compared to the islet transplantation in vivo to diabetic mice. The beta and PP cells exhibited more frequent changes in sst expression, while the alpha and delta cells were relatively unaffected by the high glucose condition. Our findings suggest that the glucose level may alter sst expressed in islets cells; however, immune mechanisms may counteract such changes in islet sst expression.

Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes

OpenAIRE

Zhang, Xuebao; Zhang, Kezhong

2012-01-01

Diabetes mellitus (DM), a metabolic disorder characterized by hyperglycemia, is caused by insufficient insulin production due to excessive loss of pancreatic β cells (type I diabetes) or impaired insulin signaling due to peripheral insulin resistance (type II diabetes). Pancreatic β cell is the only insulin-secreting cell type that has highly developed endoplasmic reticulum (ER) to cope with high demands of insulin synthesis and secretion. Therefore, ER homeostasis is crucial to the proper fu...

Otomastoidite Aguda em Criança

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João Araújo

2017-09-01

Full Text Available Criança de 2 anos, sexo masculino, diagnóstico de otite média aguda bilateral, medicada inicialmente com amoxicilina + clavulanato 90 mg/kg/dia desde há 7 dias, internada por agravamento do quadro à esquerda, com edema e eritema retroauricular, apagamento do sulco retroauricular [...] Recebido: 07/09/2015 · Aceite: 7/01/2016

Leucemia congénita aguda Acute congenital leukemia

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Nilvia Esther González García

2011-06-01

Full Text Available La leucemia aguda durante el período neonatal es poco frecuente de evolución rápida y pronóstico sombrío. Sus características clínicas y biológicas difieren de las encontradas en niños de mayor edad, y su inicio se caracteriza por afectación cutánea, hepatoesplenomegalia, hiperleucocitosis e infiltración del sistema nervioso central. Se han observado pacientes con formas tanto mieloides como linfoides, pero la leucemia mieloide aguda parece predominar en esta etapa de la vida. Se presenta el caso de un paciente con leucemia congénita clasificada morfológicamente, con aparición de manifestaciones clínicas de enfermedad hematológica desde el nacimiento y diagnóstico de leucemia linfoblástica aguda congénita.Acute leukemia during neonatal period is not frequent, of a fast course and gloomy prognosis. Its clinical and biological features differ of that present in older children and it onset is characterized by cutaneous affection, hepatosplenomegaly, hyperleukocytosis and infiltration of central nervous system (CNS. There are patients presenting with myeloid and lymphoid types, but the acute leukemia seems to predominate in this stage of life. This is the case of a patient with acute leukemia morphologically classified, with appearance of clinical manifestations of hematologic disease from birth and a diagnosis of congenital acute lymphoblastic leukemia.

Therapeutic potential of genistein in ovariectomy-induced pancreatic injury in diabetic rats: The regulation of MAPK pathway and apoptosis

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Hadi Yousefi

2017-09-01

Full Text Available Objective(s: Genistein, as a phytoestrogen found in legumes, has several biological activities in general and anti-diabetic activity particularly. In this study, we investigated the effect of genistein on proteins involved in β-cell proliferation, survival and apoptosis to further reveal its anti-diabetic potential in the ovariectomized diabetic rat. Materials and Methods: We used three-month-old female Wistar rats that either underwent ovariectomy (OVX or received a sham surgery (Sham. In a subsequent series of experiments, OVX rats received high-fat diet and low dose STZ to induce diabetes (OVX.D and genistein treatment (OVX.D.G. Western blot analysis was used for the assessment of phosphorylation of ERK1/2 and AKT and expression of Bcl-2 and caspase-3 in pancreas tissue. Hematoxylin-Eosin (H&E staining was used for histopathological assessment. Results: Genistein induced AKT and ERK1/2 phosphorylation protein expression of Bcl-2 in the pancreas. In addition, genistein suppressed protein level of caspase-3. Administration of genistein significantly improved hyperglycemia in ovariectomized diabetic rat, concomitant with improved islet β-cell morphology and mass. Conclusion: These findings suggest that the beneficial antidiabetic effect of genistein partially mediated by directly modulating pancreatic β-cell function via activation of the AKT, ERK1/2, and Bcl-2, as cell survival and anti-apoptotic factors, and decreasing of proapoptotic caspase-3.

Neonatal pancreatic pericytes support β-cell proliferation

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Alona Epshtein

2017-10-01

Conclusions: This study introduces pancreatic pericytes as regulators of neonatal β-cell proliferation. In addition to advancing current understanding of the physiological β-cell replication process, these findings could facilitate the development of protocols aimed at expending these cells as a potential cure for diabetes.

Effect of iron on pancreatic beta cell function and insulin resistance ...

African Journals Online (AJOL)

Background: Increase in total body iron store has been reported in the aetiology and development of diabetes mellitus. The effect of iron supplementation in female with respect to the incidence of diabetes mellitus was investigated on the pancreatic beta cell function and insulin resistance in normal female rats. Methods: ...

Surgical treatment of pain in chronic pancreatitis

Directory of Open Access Journals (Sweden)

Stefanović Dejan

2006-01-01

Full Text Available INTRODUCTION: The principal indication for surgical intervention in chronic pancreatitis is intractable pain. Depending upon the presence of dilated pancreatic ductal system, pancreatic duct drainage procedures and different kinds of pancreatic resections are applied. OBJECTIVE: The objective of the study was to show the most appropriate procedure to gain the most possible benefits in dependence of type of pathohistological process in chronic pancreatitis. METHOD: Our study included 58 patients with intractable pain caused by chronic pancreatitis of alcoholic genesis. The first group consisted of 30 patients with dilated pancreatic ductal system more than 10 mm. The second group involved 28 patients without dilated pancreatic ductal system. Pain relief, weight gain and glucose tolerance were monitored. RESULTS: All patients of Group I (30 underwent latero-lateral pancreaticojejunal - Puestow operation. 80% of patients had no pain after 6 month, 13.6% had rare pain and 2 patients, i.e. 6.4%, who continued to consume alcohol, had strong pain. Group II consisting of 28 patients was without dilated pancreatic ductal system. This group was subjected to various types of pancreatic resections. Whipple procedure (W was done in 6 patients, pylorus preserving Whipple (PPW in 7 cases, and duodenum preserving cephalic pancreatectomy (DPCP was performed in 15 patients. Generally, 89.2% of patients had no pain 6 month after the operation. An average weight gain was 1.9 kg in W group, 2.8 kg in PPW group and 4.1 kg in DPCP group. Insulin-dependent diabetes was recorded in 66.6% in W group, 57.1% in PPW group and 0% in DPCP group. CONCLUSION: According to our opinion, DPCP may be considered the procedure of choice for surgical treatment of pain in chronic pancreatitis in patients without dilatation of pancreas ductal system because of no serious postoperative metabolic consequences.

New developments in diagnosis and non-surgical treatment of chronic pancreatitis.

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Inui, Kazuo; Yoshino, Junji; Miyoshi, Hironao; Yamamoto, Satoshi; Kobayashi, Takashi

2013-12-01

Chronic pancreatitis is progressive and irreversible, leading to digestive and absorptive disorders by destruction of the exocrine pancreas and to diabetes mellitus by destruction of the endocrine pancreas. When complications such as pancreatolithiasis and pseudocyst occur, elevated pancreatic ductal pressure exacerbates pain and induces other complications, worsening the patient's general condition. Combined treatment with extracorporeal shock-wave lithotripsy and endoscopic lithotripsy is a useful, minimally invasive, first-line treatment approach that can preserve pancreatic exocrine function. Pancreatic duct stenosis elevates intraductal pressure and favor both pancreatolithiasis and pseudocyst formation, making effective treatment vitally important. Endoscopic treatment of benign pancreatic duct stenosis stenting frequently decreases pain in chronic pancreatitis. Importantly, stenosis of the main pancreatic duct increases risk of stone recurrence after treatment of pancreatolithiasis. Recently, good results were reported in treating pancreatic duct stricture with a fully covered self-expandable metallic stent, which shows promise for preventing stone recurrence after lithotripsy in patients with pancreatic stricture. Chronic pancreatitis has many complications including pancreatic carcinoma, pancreatic atrophy, and loss of exocrine and endocrine function, as well as frequent recurrence of stones after treatment of pancreatolithiasis. As early treatment of chronic pancreatitis is essential, the new concept of early chronic pancreatitis, including characteristics findings in endoscopic ultrasonograms, is presented. © 2013 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd.

High fat diet and GLP-1 drugs induce pancreatic injury in mice

Energy Technology Data Exchange (ETDEWEB)

Rouse, Rodney, E-mail: rodney.rouse@fda.hhs.gov; Xu, Lin; Stewart, Sharron; Zhang, Jun

2014-04-15

Glucagon Like Peptide-1 (GLP-1) drugs are currently used to treat type-2 diabetes. Safety concerns for increased risk of pancreatitis and pancreatic ductal metaplasia have accompanied these drugs. High fat diet (HFD) is a type-2 diabetes risk factor that may affect the response to GLP-1 drug treatment. The objective of the present study was to investigate the effects of diet and GLP-1 based drugs on the exocrine pancreas in mice. Experiments were designed in a mouse model of insulin resistance created by feeding a HFD or standard diet (STD) for 6 weeks. The GLP-1 drugs, sitagliptin (SIT) and exenatide (EXE) were administered once daily for additional 6 weeks in both mice fed HFD or STD. The results showed that body weight, blood glucose levels, and serum levels of pro-inflammatory cytokines (TNFα, IL-1β, and KC) were significantly greater in HFD mice than in STD mice regardless of GLP-1 drug treatment. The semi-quantitative grading showed that pancreatic changes were significantly greater in EXE and SIT-treated mice compared to control and that HFD exacerbated spontaneous exocrine pancreatic changes seen in saline-treated mice on a standard diet. Exocrine pancreatic changes identified in this study included acinar cell injury (hypertrophy, autophagy, apoptosis, necrosis, and atrophy), vascular injury, interstitial edema and inflammation, fat necrosis, and duct changes. These findings support HFD as a risk factor to increased susceptibility/severity for acute pancreatitis and indicate that GLP-1 drugs cause pancreatic injury that can be exacerbated in a HFD environment.

High fat diet and GLP-1 drugs induce pancreatic injury in mice

International Nuclear Information System (INIS)

Rouse, Rodney; Xu, Lin; Stewart, Sharron; Zhang, Jun

2014-01-01

Glucagon Like Peptide-1 (GLP-1) drugs are currently used to treat type-2 diabetes. Safety concerns for increased risk of pancreatitis and pancreatic ductal metaplasia have accompanied these drugs. High fat diet (HFD) is a type-2 diabetes risk factor that may affect the response to GLP-1 drug treatment. The objective of the present study was to investigate the effects of diet and GLP-1 based drugs on the exocrine pancreas in mice. Experiments were designed in a mouse model of insulin resistance created by feeding a HFD or standard diet (STD) for 6 weeks. The GLP-1 drugs, sitagliptin (SIT) and exenatide (EXE) were administered once daily for additional 6 weeks in both mice fed HFD or STD. The results showed that body weight, blood glucose levels, and serum levels of pro-inflammatory cytokines (TNFα, IL-1β, and KC) were significantly greater in HFD mice than in STD mice regardless of GLP-1 drug treatment. The semi-quantitative grading showed that pancreatic changes were significantly greater in EXE and SIT-treated mice compared to control and that HFD exacerbated spontaneous exocrine pancreatic changes seen in saline-treated mice on a standard diet. Exocrine pancreatic changes identified in this study included acinar cell injury (hypertrophy, autophagy, apoptosis, necrosis, and atrophy), vascular injury, interstitial edema and inflammation, fat necrosis, and duct changes. These findings support HFD as a risk factor to increased susceptibility/severity for acute pancreatitis and indicate that GLP-1 drugs cause pancreatic injury that can be exacerbated in a HFD environment

Vitamin D and Diabetes

OpenAIRE

PITTAS, ANASTASSIOS G.; DAWSON-HUGHES, BESS

2010-01-01

On the basis of evidence from animal and human studies, vitamin D has emerged as a potential risk modifier for type 1 and type 2 diabetes (type 1 diabetes and type 2 diabetes). Vitamin D is thought to have both direct (through activation of the vitamin D receptor) and indirect (via regulation of calcium homeostasis) effects on various mechanisms related to the pathophysiology of both types of diabetes, including pancreatic beta cell dysfunction, impaired insulin action and systemic inflammati...

Pancreatic Tuberculosis or Autoimmune Pancreatitis

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Ayesha Salahuddin

2014-01-01

Full Text Available Introduction. Isolated pancreatic and peripancreatic tuberculosis is a challenging diagnosis due to its rarity and variable presentation. Pancreatic tuberculosis can mimic pancreatic carcinoma. Similarly, autoimmune pancreatitis can appear as a focal lesion resembling pancreatic malignancy. Endoscopic ultrasound-guided fine needle aspiration provides an effective tool for differentiating between benign and malignant pancreatic lesions. The immune processes involved in immunoglobulin G4 related systemic diseases and tuberculosis appear to have some similarities. Case Report. We report a case of a 59-year-old Southeast Asian male who presented with fever, weight loss, and obstructive jaundice. CT scan revealed pancreatic mass and enlarged peripancreatic lymph nodes. Endoscopic ultrasound-guided fine needle aspiration confirmed the presence of mycobacterium tuberculosis. Patient also had high immunoglobulin G4 levels suggestive of autoimmune pancreatitis. He was started on antituberculosis medications and steroids. Clinically, he responded to treatment. Follow-up imaging showed findings suggestive of chronic pancreatitis. Discussion. Pancreatic tuberculosis and autoimmune pancreatitis can mimic pancreatic malignancy. Accurate diagnosis is imperative as unnecessary surgical intervention can be avoided. Endoscopic ultrasound-guided fine needle aspiration seems to be the diagnostic test of choice for pancreatic masses. Long-term follow-up is warranted in cases of chronic pancreatitis.

Pancreatite aguda biliar na infância

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Flavio Augusto Menin

Full Text Available Acute pancreatitis is an uncommon condition in childhood. Gallstones rarely cause pancreatitis in children. Instead, the leading causes of pancreatitis tend to be trauma, infecctions, drugs, congenital disorders. One rare case of acute gallstone pancreatitis in children is described, showing the diagnosis clinical/radiologic and surgery treatment (videocolecistectomy.

Hyperglycemia regulates TXNIP/TRX/ROS axis via p38 MAPK and ERK pathways in pancreatic cancer.

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Li, Wei; Wu, Zheng; Ma, Qingyong; Liu, Jiangbo; Xu, Qinhong; Han, Liang; Duan, Wanxing; Lv, Yunfu; Wang, Fengfei; Reindl, Katie M; Wu, Erxi

2014-01-01

Approximately 85% of pancreatic cancer patients suffer from glucose intolerance or even diabetes because high glucose levels can contribute to oxidative stress which promotes tumor development. As one of the reactive oxygen species (ROS)-regulating factors, thioredoxin-interacting protein (TXNIP), is involved in the maintenance of thioredoxin (TRX)-mediated redox regulation. In this study, we demonstrated that high glucose levels increased the expression of TXNIP in time- and concentration-dependent manners and modulated the activity of TRX and ROS production in pancreatic cancer cells, BxPC-3 and Panc-1. We also found that glucose activated both p38 MAPK and ERK pathways and inhibitors of these pathways impaired the TXNIP/TRX/ROS axis. Knockdown of TXNIP restored TRX activity and decreased ROS production under high glucose conditions. Moreover, we observed that the integrated optical density (IOD) of TXNIP staining as well as the protein and mRNA expression levels of TXNIP were higher in the tumor tissues of pancreatic cancer patients with diabetes. Taken together, these results indicate that hyperglycemia-induced TXNIP expression is involved in diabetes-mediated oxidative stress in pancreatic cancer via p38 MAPK and ERK pathways.

Pancreatic differentiation of Pdx1-GFP reporter mouse induced pluripotent stem cells.

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Porciuncula, Angelo; Kumar, Anujith; Rodriguez, Saray; Atari, Maher; Araña, Miriam; Martin, Franz; Soria, Bernat; Prosper, Felipe; Verfaillie, Catherine; Barajas, Miguel

2016-12-01

Efficient induction of defined lineages in pluripotent stem cells constitutes the determinant step for the generation of therapeutically relevant replacement cells to potentially treat a wide range of diseases, including diabetes. Pancreatic differentiation has remained an important challenge in large part because of the need to differentiate uncommitted pluripotent stem cells into highly specialized hormone-secreting cells, which has been shown to require a developmentally informed step-by-step induction procedure. Here, in the framework of using induced pluripotent stem cells (iPSCs) to generate pancreatic cells for pancreatic diseases, we have generated and characterized iPSCs from Pdx1-GFP transgenic mice. The use of a GFP reporter knocked into the endogenous Pdx1 promoter allowed us to monitor pancreatic induction based on the expression of Pdx1, a pancreatic master transcription factor, and to isolate a pure Pdx1-GFP + population for downstream applications. Differentiated cultures timely expressed markers specific to each stage and end-stage progenies acquired a rather immature beta-cell phenotype, characterized by polyhormonal expression even among cells highly expressing the Pdx1-GFP reporter. Our findings highlight the utility of employing a fluorescent protein reporter under the control of a master developmental gene in order to devise novel differentiation protocols for relevant cell types for degenerative diseases such as pancreatic beta cells for diabetes. Copyright © 2016 International Society of Differentiation. Published by Elsevier B.V. All rights reserved.

Insulinotropic and anti-inflammatory effects of rosiglitazone in experimental autoimmune diabetes.

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Awara, Wageh M; el-Sisi, Alaa E; el-Refaei, Mohamed; el-Naa, Mona M; el-Desoky, Karima

2005-01-01

Cytokines and nitric oxide (NO) are involved in the pathogenesis of autoimmune diabetes mellitus (DM). Rosiglitazone is an insulin-sensitizing drug that is a ligand for the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). The anti-inflammatory and immunomodulating properties of PPAR-gamma have been documented. The aim of this study is to investigate the effectiveness of rosiglitazone in autoimmune DM and to clarify the possible mechanism(s) involved. Autoimmune DM was induced in adult male Balb/c mice by co-administration of cyclosporin A and multiple low doses of streptozotocin. Diabetic mice were treated daily with rosiglitazone (7 mg/kg, p.o.) for 21 days. Blood glucose level (BGL), serum insulin level and pancreatic levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and NO were measured. Histopathological examination and immunohistochemical determination of CD4 and CD8 T lymphocytes in the pancreatic islets were performed. In addition, analysis of pancreatic protein expression was carried out. The results showed that rosiglitazone treatment resulted in a significant decrease in the BGL and the pancreatic levels of TNF-alpha, IFN-gamma and NO compared to diabetic mice. The serum insulin level was significantly increased after rosiglitazone treatment compared to diabetic mice. The destroyed pancreatic islets were regenerated and became free from both CD4 and CD8 T cells after treatment. Furthermore, many changes in pancreatic protein expression were observed. These results suggest that rosiglitazone has a beneficial effect in the treatment of autoimmune diabetes, an effect that seemed to be a secondary consequence of its anti-inflammatory and immunomodulating properties and might be reflected at the level of protein expression.

In vivo and in vitro evaluation of the effects of Urtica dioica and swimming activity on diabetic factors and pancreatic beta cells.

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Ranjbari, Abbas; Azarbayjani, Mohammad Ali; Yusof, Ashril; Halim Mokhtar, Abdul; Akbarzadeh, Samad; Ibrahim, Mohamed Yousif; Tarverdizadeh, Bahman; Farzadinia, Parviz; Hajiaghaee, Reza; Dehghan, Firouzeh

2016-03-15

Urtica dioica (UD) has been identified as a traditional herbal medicine. This study aimed to investigate the effect of UD extract and swimming activity on diabetic parameters through in vivo and in vitro experiments. Adult WKY male rats were randomly distributed in nine groups: intact control, diabetic control, diabetic + 625 mg/kg, 1.25 g/kg UD, diabetic + 100 mg/kg Metformin, diabetic + swimming, diabetic + swimming 625 mg/kg, 1.25 g/kg UD, and diabetic +100 mg/kg Metformin + swimming. The hearts of the animals were punctured, and blood samples were collected for biochemical analysis. The entire pancreas was exposed for histologic examination. The effect of UD on insulin secretion by RIN-5F cells in 6.25 or 12.5 mM glucose dose was examined. Glucose uptake by cultured L6 myotubes was determined. The serum glucose concentration decreased, the insulin resistance and insulin sensitivity significantly increased in treated groups. These changes were more pronounced in the group that received UD extract and swimming training. Regeneration and less beta cell damage of Langerhans islets were observed in the treated groups. UD treatment increased insulin secretion in the RIN-5F cells and glucose uptake in the L6 myotubes cells. Swimming exercises accompanied by consuming UD aqueous extracts effectively improved diabetic parameters, repaired pancreatic tissues in streptozotocin-induced diabetics in vivo, and increased glucose uptake or insulin in UD-treated cells in vitro.

Pancreatic Cancer-Derived Exosomes Cause Paraneoplastic β-cell Dysfunction.

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Javeed, Naureen; Sagar, Gunisha; Dutta, Shamit K; Smyrk, Thomas C; Lau, Julie S; Bhattacharya, Santanu; Truty, Mark; Petersen, Gloria M; Kaufman, Randal J; Chari, Suresh T; Mukhopadhyay, Debabrata

2015-04-01

Pancreatic cancer frequently causes diabetes. We recently proposed adrenomedullin as a candidate mediator of pancreatic β-cell dysfunction in pancreatic cancer. How pancreatic cancer-derived adrenomedullin reaches β cells remote from the cancer to induce β-cell dysfunction is unknown. We tested a novel hypothesis that pancreatic cancer sheds adrenomedullin-containing exosomes into circulation, which are transported to β cells and impair insulin secretion. We characterized exosomes from conditioned media of pancreatic cancer cell lines (n = 5) and portal/peripheral venous blood of patients with pancreatic cancer (n = 20). Western blot analysis showed the presence of adrenomedullin in pancreatic cancer-exosomes. We determined the effect of adrenomedullin-containing pancreatic cancer exosomes on insulin secretion from INS-1 β cells and human islets, and demonstrated the mechanism of exosome internalization into β cells. We studied the interaction between β-cell adrenomedullin receptors and adrenomedullin present in pancreatic cancer-exosomes. In addition, the effect of adrenomedullin on endoplasmic reticulum (ER) stress response genes and reactive oxygen/nitrogen species generation in β cells was shown. Exosomes were found to be the predominant extracellular vesicles secreted by pancreatic cancer into culture media and patient plasma. Pancreatic cancer-exosomes contained adrenomedullin and CA19-9, readily entered β cells through caveolin-mediated endocytosis or macropinocytosis, and inhibited insulin secretion. Adrenomedullin in pancreatic cancer exosomes interacted with its receptor on β cells. Adrenomedullin receptor blockade abrogated the inhibitory effect of exosomes on insulin secretion. β cells exposed to adrenomedullin or pancreatic cancer exosomes showed upregulation of ER stress genes and increased reactive oxygen/nitrogen species. Pancreatic cancer causes paraneoplastic β-cell dysfunction by shedding adrenomedullin(+)/CA19-9(+) exosomes into

Pancreatic cancer: Incidence, clinical profile, and frequency of ...

African Journals Online (AJOL)

Hana T. Al-Majed

2012-08-09

Aug 9, 2012 ... Diabetes has been postulated to be both a risk factor and a consequence of pancreatic cancer, ... (A.A.. El-Basmi),. Shihab@yahoo.com. (S.H. Al-Mohannadi) ..... A recent meta-analysis reported that obese people may have a ...

Pengaruh Transplantasi Allograf Pancreatic Stem Cell terhadap Kadar Insulin dan C-Peptide Tikus Putih Penderita Diabetes Melitus Tipe I

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Boedi Setiawan

2016-09-01

Full Text Available Diabetes mellitus is one of the degenerative diseases in which the therapy still remains unresolved and is still a serious threat to the global health, including to the health of Indonesian people. The aim of this study was to describe the level of insulin and C-peptide in diabetes mellitus type I white rats treated with pancreatic stem cell allograft through intrapancreatic laparotomy. This study was conducted at the Institute of Tropical Diseases, Universitas Airlangga, Surabaya in a 6 month period (July–December 2014. Twelve male white rats Rattus novergicus Wistar strain, were randomly divided into two groups. The first group (P0 was injected by alloxan, 150 mg/kg body weight, without stem cell therapy. Another group was injected by alloxan, 150 mg/kg body weight, and was treated with 1x106/kg body weight pancreatic stem cell throughintrapancreatic laparotomy (P1. The experiment was finalized on the 31th day of the experiment. The results showed that the blood glucose levels at the end of experiment were highly significantly different p<0.01 between the treatment group that received stem cell therapy (P1 and P0 positive control, although the average value of blood glucose levels was not as normal as on the first day. C-peptide and insulin levels of P0 and P1 group differed significantly (p<0.01. It can be concluded that stem cell therapy through intrapancreatic laparotomy can reduce blood glucose levels and increase the levels of C-peptide and insulin.

Specifying pancreatic endocrine cell fates.

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Collombat, Patrick; Hecksher-Sørensen, Jacob; Serup, Palle; Mansouri, Ahmed

2006-07-01

Cell replacement therapy could represent an attractive alternative to insulin injections for the treatment of diabetes. However, this approach requires a thorough understanding of the molecular switches controlling the specification of the different pancreatic cell-types in vivo. These are derived from an apparently identical pool of cells originating from the early gut endoderm, which are successively specified towards the pancreatic, endocrine, and hormone-expressing cell lineages. Numerous studies have outlined the crucial roles exerted by transcription factors in promoting the cell destiny, defining the cell identity and maintaining a particular cell fate. This review focuses on the mechanisms regulating the morphogenesis of the pancreas with particular emphasis on recent findings concerning the transcription factor hierarchy orchestrating endocrine cell fate allocation.

Lúpus eritematoso sistêmico e pancreatite aguda: relato de dois casos

OpenAIRE

Azevedo, Ana Beatriz Cordeiro de; Brito, Fabiano Almeida; Santos, Flávia Patrícia Sena Teixeira; Ferreira, Gilda Aparecida; Carvalho, Marco Antônio Parreiras de

2003-01-01

A pancreatite aguda é uma manifestação incomum do lúpus eritematoso sistêmico (LES) e a freqüência desta associação não é conhecida. Contudo, a pancreatite aguda é um diagnóstico diferencial importante na avaliação da dor abdominal em pacientes com LES. Os pacientes, normalmente, apresentam dor de intensidade variável, algumas vezes simulando abdome agudo. Vários fatores têm sido implicados na patogênese desta condição, tais como fenômenos autoimunes, vasculite, anticorpos antifosfolípides e ...

Quality of life in patients after total pancreatectomy is comparable with quality of life in patients who undergo a partial pancreatic resection.

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Epelboym, Irene; Winner, Megan; DiNorcia, Joseph; Lee, Minna K; Lee, James A; Schrope, Beth; Chabot, John A; Allendorf, John D

2014-03-01

Quality of life after total pancreatectomy (TP) is perceived to be poor secondary to insulin-dependent diabetes and pancreatic insufficiency. As a result, surgeons may be reluctant to offer TP for benign and premalignant pancreatic diseases. We retrospectively reviewed presenting features, operative characteristics, and postoperative outcomes of all patients who underwent TP at our institution. Quality of life was assessed using institutional questionnaires and validated general, pancreatic disease-related, and diabetes-related instruments (European Organization for Research and Treatment of Cancer Quality of Life Questionnaire [EORTC QLQ-C30 and module EORTC-PAN26], Audit of Diabetes Dependent Quality of Life), and compared with frequency-matched controls, patients after a pancreaticoduodenectomy (PD). Continuous variables were compared using Student t-test or analysis of variance. Categorical variables were compared using χ(2) or Fisher exact test. Between 1994 and 2011, 77 TPs were performed. Overall morbidity was 49%, but only 15.8% patients experienced a major complication. Perioperative mortality was 2.6%. Comparing 17 TP and 14 PD patients who returned surveys, there were no statistically significant differences in quality of life in global health, functional status, or symptom domains of EORTC QLQ-C30 or in pancreatic disease-specific EORTC-PAN26. TP patients had slightly but not significantly higher incidence of hypoglycemic events as compared with PD patients with postoperative diabetes. A negative impact of diabetes assessed by Audit of Diabetes Dependent Quality of Life did not differ between TP and PD. Life domains most negatively impacted by diabetes involved travel and physical activity, whereas self-confidence, friendships and personal relationships, motivation, and feelings about the future remained unaffected. Although TP-induced diabetes negatively impacts select activities and functions, overall quality of life is comparable with that of

Suscetibilidade genética na lesão pulmonar aguda e síndrome da angústia respiratória aguda Genetic susceptibility in acute lung injury and acute respiratory distress syndrome

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Fernando Suparregui Dias

2009-12-01

Full Text Available A lesão pulmonar aguda e sua forma mais grave, a síndrome da angústia respiratória aguda, são o denominador comum de várias doenças que podem provocar uma inflamação exagerada nos pulmões. Nos últimos anos, essa variabilidade tem sido atribuída, pelo menos em parte, a fatores genéticos. O presente estudo tem por objetivos revisar o papel dos principais genes envolvidos na suscetibilidade, morbidade e mortalidade na lesão pulmonar aguda e na síndrome da angústia respiratória aguda. Através de pesquisa nas bases de dados PubMed e LiLACS, empregando-se os unitermos lesão pulmonar aguda, síndrome da angústia respiratória aguda e síndrome da angústia respiratória do adulto em combinação com polimorfismos genéticos, foram selecionados 69 artigos, dos quais 38 foram incluídos nesta revisão. Foram também considerados artigos relevantes extraídos das referências bibliográficas nos artigos selecionados das bases de dados. Os polimorfismos genéticos são variantes gênicas presentes em pelo menos 1% da população. A presença destas variantes genéticas pode influenciar a expressão de mediadores da resposta inflamatória, afetando diretamente a suscetibilidade à lesão pulmonar aguda, a intensidade da inflamação no parênquima pulmonar, a evolução e o desfecho destes pacientes. Estudos de associação com grandes populações e passíveis de reprodução permitirão de modo definitivo a inclusão da genômica no arsenal diagnóstico, prognóstico e terapêutico de pacientes com lesão pulmonar aguda/síndrome da angústia respiratória agudaAcute lung injury and its most severe presentation, acute respiratory distress syndrome, are a common denominator for several diseases which can lead to exaggerated lung inflammation. In the last years this variability has been ascribed, at least partially, to genetic issues. This study aims to review the role of the main genes involved in acute lung injury and acute respiratory

Protective Effects of the Mushroom Lactarius deterrimus Extract on Systemic Oxidative Stress and Pancreatic Islets in Streptozotocin-Induced Diabetic Rats

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Mirjana Mihailović

2015-01-01

Full Text Available The aim of this study was to assess the in vivo effects of the extract of the medicinal mushroom, Lactarius deterrimus, when administered (60 mg/kg, i.p. daily for four weeks to streptozotocin- (STZ- induced diabetic rats. Diabetic rats treated with the L. deterrimus extract displayed several improved biochemical parameters in the circulation: reduced hyperglycemia, lower triglyceride concentration and reduced glycated hemoglobin, glycated serum protein, and advanced glycation end product (AGE levels. This treatment also adjusted the diabetes-induced redox imbalance. Thus, higher activities of the antioxidative enzymes, superoxide dismutase, and catalase in the circulation were accompanied by increased levels of free intracellular thiols and glutathionylated proteins after treatment with the L. deterrimus extract. In addition to a systemic antioxidant effect, the administration of the extract to diabetic rats also had a positive localized effect on pancreatic islets where it decreased AGE formation, and increased the expression of chemokine CXCL12 protein that mediates the restoration of β-cell population through the activation of the serine/threonine-specific Akt protein kinase prosurvival pathway. As a result, the numbers of proliferating cell nuclear antigen- (PCNA- and insulin-positive β-cells were increased. These results show that the ability of the L. deterrimus extract to alleviate oxidative stress and increase β-cell mass represents a therapeutic potential for diabetes management.

Experience in surgical treatment of 19 patients with pancreatic duct stones

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ZHANG Yahui

2015-05-01

Full Text Available ObjectiveTo summarize the experience in the diagnosis and surgical treatment selection of pancreatic duct stones (PDS. MethodsThe medical records of 19 patients with PDS in Rongchang Hospital of Traditional Chinese Medicine from January 2006 to September 20l4 were analyzed retrospectively in terms of clinical characteristics, diagnosis, and treatment. All 19 patients were diagnosed with PDS by imaging examinations such as B-ultrasonography, computed tomography, and magnetic resonance cholangiopancreatography. Besides all cases diagnosed with chronic pancreatitis, 3 cases were accompanied by diabetes, 2 cases by jaundice, 1 case by biliary tract hemorrhage, and 1 case by carcinoma of the pancreatic head. ResultsAll patients received surgeries including 9 cases of pancreatic duodenal resection, 5 cases of both pancreatolithotomy and pancreatic duct jejunum anastomosis, 2 cases of simple resection of pancreatic body and tail, and 2 cases of duodenum-preserving pancreatic head resection. ConclusionSurgery is the most commonly used, curative method for PDS patients. Based on fully analyzing the actual situation of patients, personalized operation treatment can ensure operation success rate and improve patients′ quality of life.

Rice bran water extract attenuates pancreatic abnormalities in high ...

African Journals Online (AJOL)

105 on pancreatic abnormalities in high-fat diet (HFD)-induced obese rats. Methods: Male ... initiation of these metabolic disturbances [2]. Under physiological ..... injury in the zucker diabetic fatty rat fed a chronic high- fat diet. Pancreas 2014 ...

[Severe hypertriglyceridemia--an important cause of pancreatitis].

Science.gov (United States)

Graesdal, Asgeir

2008-05-01

Moderate hypertriglyceridaemia is a risk factor for cardiovascular disease and serious hypertriglyceridaemia, with triglyceride values above 10 mmol/L, increases the risk of pancreatitis. Gallstones and alcohol abuse are regarded as the two most important causes of acute pancreatitis, but the considerable risk posed by hypertriglyceridaemia has probably been underrated. It is therefore crucial to acquire updated knowledge and awareness of the fact that high levels of triglycerides can cause pancreatitis. This article is based on current literature retrieved though a search on the topic and clinical experience. Serious hypertriglyceridaemia is a relatively rare condition and its usual cause is genetic predisposition combined with obesity, diabetes or alcohol abuse. Certain types of medication, as well as pregnancy, are also well known causes. Current literature suggests that hypertriglyceridaemia is the cause of pancreatitis in 1-38% of the cases--a substantial variation. The condition is often accompanied by low amylase values and may therefore be underrated as a cause. Our case reports illustrate that the etiology is complex. Plasmapheresis or LDL-apheresis may be indicated when conservative treatment proves insufficient.

Comprehensive Evaluation of Altered Systemic Metabolism and Pancreatic Cancer Risk

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2015-10-01

09/08/15-08/31/19 0.96 cal. mo. NIH/NCI $168,300 A prospective investigation of the oral microbiome and pancreatic cancer 1.To perform a...and BWHS. 2.To evaluate racial differences in the oral microbiome using 165 AA and 165 EA controls (from the SCCS only), and to identify any racial...risk factors for pancreatic cancer (cigarette smoking, obesity, red meat and processed meat consumption, alcohol consumption, type 2 diabetes) and oral

Clinical application of duodenum-preserving pancreatic head resection

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ZHOU Songqiang

2018-01-01

Full Text Available Objective To investigate the indications and therapeutic effect of duodenum-preserving pancreatic head resection (DPPHR. Methods A retrospective analysis was performed for the clinical data of 17 patients who underwent DPPHR in Fujian Provincial Hospital from January 2013 to February 2017. Among these patients, 6 had chronic pancreatitis with pancreatic duct stones, 2 had chronic pancreatitis with pancreatic pseudocyst, 3 had solid pseudopapillary tumor of the pancreatic head, 3 had intraductal papillary mucinous neoplasm, 2 had serous cystadenoma of the pancreatic head, and 1 had mucinous cystadenoma of the pancreatic head. Results The time of operation was 200-360 minutes (mean 304.0±45.3 minutes, and the intraoperative blood loss was 50-500 ml (mean 267.5±116.1 ml. No patient died in the perioperative period. After surgery, 5 experienced biochemical leak, 2 experienced grade B pancreatic fistula, no patient experienced grade C pancreatic fistula, and 1 experienced gastroplegia; all these patients were cured and discharged after conservative treatment. The length of postoperative hospital stay was 17-78 days (mean 30.8±14.3 days. The 17 patients were followed up for 2 months to 4 years after surgery, and no patient experienced tumor recurrence, new-onset diabetes, dyspepsia, or common bile duct stenosis after surgery. Conclusion Besides ensuring the complete resection of tumor, DPPHR can reduce the incidence rate of surgical trauma and complications and shorten the time of operation and the length of hospital stay. Compared with pancreaticoduodenectomy, DPPHR can better preserve the endocrine and exocrine functions of the pancreas and improve patients′ postoperative quality of life.

[Update on chronic pancreatitis: review article].

Science.gov (United States)

Czul, Frank; Coronel, Emmanuel; Donet, Jean A

2017-01-01

Chronic pancreatitis is a progressive fibro-inflammatory disease of the pancreas characterized by irreversible fibrosis of the gland with eventual failure of exocrine and endocrine functions and hallmark features of abdominal pain, malabsorption, malnutrition, diabetes mellitus and pancreatic calcifications. In many patients this disease results from a complex mix of environmental (eg, alcohol, cigarettes, and occupational chemicals), genetic factors and a few patients with hereditary or autoimmune disease. The management includes medical, endoscopic and surgical approaches with the need for interaction between various specialties, calling for a concerted multidisciplinary approach. This review provides the reader with a comprehensive overview of the studies summarizing the epidemiology, etiology, physiopatology, clinical manifestation, diagnosis and treatments of the disease.

Esofagitis necrosante aguda: análisis retrospectivo Acute esophageal necrosis: a retrospective case series

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R. Ramos

2008-09-01

Full Text Available Introducción: la esofagitis necrosante aguda es una entidad rara. Se reconoce por el aspecto negro difuso del esófago a la endoscopia. Su incidencia e patogénesis se desconoce. Pacientes y métodos: se analizaron retrospectivamente 11 pacientes con esofagitis necrosante aguda desde el punto de vista de los datos clínicos, de laboratorio y endoscopicos en 2 años. Resultados: se analizaron las endoscopias realizadas a 3.976 pacientes, observándose esofagitis necrosante aguda en 11 pacientes. El estado nutricional era malo en 6 pacientes. La resolución completa de la esofagitis se observó en cuatro pacientes. Durante el seguimiento se observó una estenosis en un paciente y un nuevo episodio de esofagitis necrosante aguda en otro paciente. Siete pacientes fallecieron, pero esta elevada mortalidad parece deberse a las enfermedades de base y no es atribuible a las lesiones de la esofagitis necrosante. Conclusiones: la incidencia de esofagitis necrosante aguda en nuestra serie fue 0,28%. La esofagitis necrosante aguda tiene una elevada mortalidad.Background: acute esophageal necrosis has been considered a rare event. It is defined as the presence of diffuse dark pigmentation of the esophagus on upper endoscopy. Its incidence has not yet been established. The pathogenesis remains unknown. Patients and methods: a retrospective analysis of clinical, laboratory, endoscopic, and histological data, and of the clinical course of 11 patients with acute necrotizing esophagitis was carried out over a 2-year period. Results: among 3,976 patients who underwent upper endoscopy, 11 (0.28% with acute esophageal necrosis were identified. Nutritional status was poor for 6 patients. Complete resolution of acute esophageal necrosis without further recurrence was observed in 4. One stricture appeared during follow-up and other patient developed new-onset acute esophageal necrosis. Seven patients died, but no death was directly related to acute esophageal necrosis

Intoxicaciones agudas en pediatría

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Yalena Prado Vizcaíno

2011-12-01

Full Text Available Introducción: las intoxicaciones han sido en los últimos años una importante causa de aumento de la morbilidad y mortalidad en edades pediátricas. Objetivo: determinar el comportamiento clínico de las intoxicaciones agudas en la etapa de enero de 2005 a diciembre de 2009 en el Hospital Pediátrico "William Soler". Métodos: el estudio se realizó en el Hospital "William Soler". Se revisaron las historias clínicas, los registros de intoxicaciones agudas y las tarjetas de codificación de egresos hospitalarios por intoxicaciones de los pacientes llegados al hospital en esta etapa. Resultados: se recibieron en el hospital 886 pacientes. El grupo de mayor frecuencia de intoxicaciones fue el de 1 a 5 años, con predominio del sexo masculino, aunque sin diferencias significativas con respecto al sexo femenino. Las intoxicaciones más frecuentes fueron por medicamentos, fundamentalmente psicofármacos y antibióticos, seguido por alimentos y por productos químicos del hogar. El 30,2 % de los casos fueron ingresados. Conclusiones: estos resultados nos hacen pensar en la necesidad de estar alertas y crear acciones encaminadas a proteger o evitar las intoxicaciones en edades tan vulnerables.

Pielonefritis enfisematosa aguda bilateral: Un desafío terapéutico Acute bilateral emphysematous pyelonephritis: A therapeutic challenge

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Marcelo J. Melero

2007-06-01

Full Text Available La pielonefritis enfisematosa es una forma poco común de infección renal, caracterizada por la presencia de bacterias coliformes productoras de gas que afecta preferentemente a los pacientes diabéticos. Comunicamos el caso de una mujer diabética de 57 años de edad que ingresó en el hospital por un shock séptico, signos de pielonefritis enfisematosa aguda bilateral y cetoacidosis diabética. En los cultivos de las muestras de orina y sangre desarrolló Escherichia coli. La paciente fue tratada exitosamente con antibióticos de amplio espectro por un tiempo prolongado, control diabético y medidas de sostén solamente. No fue necesario el drenaje con catéteres o la nefrectomía para superar esta situación potencialmente letal.Emphysematous pyelonephritis is a rare form of kidney infection characterized by the presence of gas-forming coliform bacteria which affects more frequently diabetic subjects. We report the case of a 57-years-old diabetic woman, who was admitted in septic shock, signs of acute bilateral emphysematous pyelonephritis, and diabetic ketoacidosis. Both blood and urine cultures yielded Escherichia coli. The patient was successfully treated using long-term broad-spectrum antibiotics, diabetic control and supportive measures alone. Catheter drainage and nephrectomy were not necessary to overcome this life threatening situation.

ENDOCRINE PANCREATIC FUNCTION IN ACUTE PANCREATITIS

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P. V. Novokhatny

2014-02-01

Full Text Available Introduction Among the organs of internal secretion pancreas has a special place thanks to active exocrine function and a wide range of physiological actions of produced hormones. Violations of endocrine pancreas arises in 6.5-38 % of patients with acute pancreatitis. However, there is still no clear understanding of the pathogenetic mechanisms of hormonal dysfunction of the pancreas in acute pancreatitis, there is no uniform algorithms for its correction. Aim of the research was to study the endocrine function of pancreas in acute pancreatitis. To define the role of endocrine pancreatic function in the etiology and pathogenesis of the acute pancreatitis. To assess the prospects of the use of pancreatic hormones in the treatment and predicting the outcomes of acute pancreatitis. Materials and methods of the research Survey of publications in specialized periodical medical journals, PubMed sources developed by the National Center for Biotechnology Information. Search in PubMed was carried out in the following databases: MEDLINE, Pre MEDLINE. Results of the research. In a significant proportion of patients who recovered from acute pancreatitis, exocrine and endocrine functional impairments were found. This finding was not detected only in patients after severe acute pancreatitis. Routine evaluation of pancreatic function after acute pancreatitis should be considered. The comparative analysis of the synthetic analogues (somatostatin, calcitonin, leu-enkefalin-dalargin influence on the glucose metabolism of rats in acute pancreatitis of was made. Physiological reaction of beta-cells is preserved in infusion of somatostatin. However, infusion of calcitonin results in the distortion of counterregulatory action of insulin and glucagon. It was detected that pancreatic renin-angiotensin system is markedly activated in the experimental rat models of chronic hypoxia and acute pancreatitis. The activation of the pancreatic renin-angiotensin system by

Small Molecule Kaempferol Promotes Insulin Sensitivity and Preserved Pancreatic β-Cell Mass in Middle-Aged Obese Diabetic Mice

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Alkhalidy, Hana; Moore, William; Zhang, Yanling; Wang, Aihua; Ali, Mostafa; Suh, Kyung-Shin; Zhen, Wei; Cheng, Zhiyong; Jia, Zhenquan; Hulver, Matthew

2015-01-01

Insulin resistance and a progressive decline in functional β-cell mass are hallmarks of developing type 2 diabetes (T2D). Thus, searching for natural, low-cost compounds to target these two defects could be a promising strategy to prevent the pathogenesis of T2D. Here, we show that dietary intake of flavonol kaempferol (0.05% in the diet) significantly ameliorated hyperglycemia, hyperinsulinemia, and circulating lipid profile, which were associated with the improved peripheral insulin sensitivity in middle-aged obese mice fed a high-fat (HF) diet. Kaempferol treatment reversed HF diet impaired glucose transport-4 (Glut4) and AMP-dependent protein kinase (AMPK) expression in both muscle and adipose tissues from obese mice. In vitro, kaempferol increased lipolysis and prevented high fatty acid-impaired glucose uptake, glycogen synthesis, AMPK activity, and Glut4 expression in skeletal muscle cells. Using another mouse model of T2D generated by HF diet feeding and low doses of streptozotocin injection, we found that kaempferol treatment significantly improved hyperglycemia, glucose tolerance, and blood insulin levels in obese diabetic mice, which are associated with the improved islet β-cell mass. These results demonstrate that kaempferol may be a naturally occurring anti-diabetic agent by improving peripheral insulin sensitivity and protecting against pancreatic β-cell dysfunction. PMID:26064984

The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus.

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Gerber, Philipp A; Rutter, Guy A

2017-04-01

Metabolic syndrome is a frequent precursor of type 2 diabetes mellitus (T2D), a disease that currently affects ∼8% of the adult population worldwide. Pancreatic beta-cell dysfunction and loss are central to the disease process, although understanding of the underlying molecular mechanisms is still fragmentary. Recent Advances: Oversupply of nutrients, including glucose and fatty acids, and the subsequent overstimulation of beta cells, are believed to be an important contributor to insulin secretory failure in T2D. Hypoxia has also recently been implicated in beta-cell damage. Accumulating evidence points to a role for oxidative stress in both processes. Although the production of reactive oxygen species (ROS) results from enhanced mitochondrial respiration during stimulation with glucose and other fuels, the expression of antioxidant defense genes is unusually low (or disallowed) in beta cells. Not all subjects with metabolic syndrome and hyperglycemia go on to develop full-blown diabetes, implying an important role in disease risk for gene-environment interactions. Possession of common risk alleles at the SLC30A8 locus, encoding the beta-cell granule zinc transporter ZnT8, may affect cytosolic Zn 2+ concentrations and thus susceptibility to hypoxia and oxidative stress. Loss of normal beta-cell function, rather than total mass, is increasingly considered to be the major driver for impaired insulin secretion in diabetes. Better understanding of the role of oxidative changes, its modulation by genes involved in disease risk, and effects on beta-cell identity may facilitate the development of new therapeutic strategies to this disease. Antioxid. Redox Signal. 26, 501-518.

Type 1 diabetes

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Atkinson, Mark A; Eisenbarth, George S; Michels, Aaron W

2013-01-01

Over the past decade, knowledge of the pathogenesis and natural history of type 1 diabetes has grown substantially, particularly with regard to disease prediction and heterogeneity, pancreatic pathology, and epidemiology. Technological improvements in insulin pumps and continuous glucose monitors help patients with type 1 diabetes manage the challenge of lifelong insulin administration. Agents that show promise for averting debilitating disease-associated complications have also been identifi...

Bases moleculares de las leucemias agudas

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G. Martínez Antuña

2006-04-01

Full Text Available El gran desarrollo de la biología molecular en los últimos años ha contribuido a un importante avance en los conocimientos relacionados con las bases moleculares de las leucemias agudas (LA. Ademas de profundizar en la biología de estas enfermedades y conocer las bases moleculares, ha renido también gran impacto en mejorar el resultado de los tratamientos y disminuir la toxicidad de las terapias.

Knowledge Gaps in Rodent Pancreas Biology: Taking Human Pluripotent Stem Cell-Derived Pancreatic Beta Cells into Our Own Hands.

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Santosa, Munirah Mohamad; Low, Blaise Su Jun; Pek, Nicole Min Qian; Teo, Adrian Kee Keong

2015-01-01

In the field of stem cell biology and diabetes, we and others seek to derive mature and functional human pancreatic β cells for disease modeling and cell replacement therapy. Traditionally, knowledge gathered from rodents is extended to human pancreas developmental biology research involving human pluripotent stem cells (hPSCs). While much has been learnt from rodent pancreas biology in the early steps toward Pdx1(+) pancreatic progenitors, much less is known about the transition toward Ngn3(+) pancreatic endocrine progenitors. Essentially, the later steps of pancreatic β cell development and maturation remain elusive to date. As a result, the most recent advances in the stem cell and diabetes field have relied upon combinatorial testing of numerous growth factors and chemical compounds in an arbitrary trial-and-error fashion to derive mature and functional human pancreatic β cells from hPSCs. Although this hit-or-miss approach appears to have made some headway in maturing human pancreatic β cells in vitro, its underlying biology is vaguely understood. Therefore, in this mini-review, we discuss some of these late-stage signaling pathways that are involved in human pancreatic β cell differentiation and highlight our current understanding of their relevance in rodent pancreas biology. Our efforts here unravel several novel signaling pathways that can be further studied to shed light on unexplored aspects of rodent pancreas biology. New investigations into these signaling pathways are expected to advance our knowledge in human pancreas developmental biology and to aid in the translation of stem cell biology in the context of diabetes treatments.

Functional characterization of the HNF4α isoform (HNF4α8) expressed in pancreatic β-cells

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Ihara, Arisa; Yamagata, Kazuya; Nammo, Takao; Miura, Atsuko; Yuan, Ming; Tanaka, Toshiya; Sladek, Frances M.; Matsuzawa, Yuji; Miyagawa, Jun-ichiro; Shimomura, Iichiro

2005-01-01

Mutations in the hepatocyte nuclear factor (HNF) 4α gene cause a form of maturity-onset diabetes of the young (MODY1), which is a monogenic form of type 2 diabetes characterized by impaired insulin secretion by pancreatic β-cells. HNF4α is a transcription factor expressed in the liver, kidney, intestine, and pancreatic islet. Multiple splice variants of the HNF4α gene have been identified and an isoform of HNF4α8, an N-terminal splice variant, is expressed in pancreatic β-cells. However, expression levels of HNF4α protein in pancreatic β-cells and the transcriptional activity of HNF4α8 are not yet understood. In the present study, we investigated the expression of HNF4α in β-cells and examined its functional properties. Western blotting and immunohistochemical analysis revealed that the expression of HNF4α protein in pancreatic islets and INS-1 cells was much lower than in the liver. A reporter gene assay showed that the transactivation potential of HNF4α8 was significantly weaker than that of HNF4α2, which is a major isoform in the liver, suggesting that the total level of HNF4α activity is very weak in pancreatic β-cells. We also showed that the N-terminal A/B region of HNF4α8 possessed no activation function and C-terminal F region negatively regulated the transcriptional activity of HNF4α8. The information presented here would be helpful for the better understanding of MODY1/HNF4α diabetes

NGAL urinária em pacientes sem e com lesão renal aguda em unidade de terapia intensiva

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Mirian Watanabe

2014-12-01

Full Text Available Objetivo: Avaliar a eficácia diagnóstica e prognóstica da lipocalina associada à gelatinase neutrofílica urinária em pacientes de unidade de terapia intensiva. Métodos: Estudo do tipo coorte, prospectivo, longitudinal desenvolvido em uma unidade de terapia intensiva clínica especializada em cardiologia. Os pacientes foram estratificados segundo os grupos sem e com lesão renal aguda, acompanhados a partir das primeiras 24 horas de internação até a alta hospitalar ou óbito. A creatinina sérica, o fluxo urinário e a lipocalina associada à gelatinase neutrofílica urinária foram coletadas em dois períodos: 24 horas e 48 horas de admissão. Resultados: Foram avaliados 83 pacientes clínicos da unidade de terapia intensiva, com predomínio do gênero masculino (57,8%. Os pacientes foram agrupados em sem lesão renal aguda (N=18, com lesão renal aguda (N=28 ou com lesão renal aguda grave (N=37. Entre os pacientes com lesão renal aguda e lesão renal aguda grave, foram prevalentes os portadores de doenças crônicas, em uso de ventilação mecânica e em terapia de substituição renal, além daqueles com maiores taxas de permanência na unidade de terapia intensiva e hospitalar, e maior mortalidade. O grupo com lesão renal aguda não apresentou alteração significativa da creatinina sérica nas primeiras 24 horas na unidade de terapia intensiva, apesar dos níveis elevados de lipocalina associada à gelatinase neutrofilica urinária demonstrados nos grupos com lesão renal aguda e lesão renal aguda grave (p<0,001. Níveis elevados de lipocalina associada à gelatinase neutrofílica urinária na amostra foram associados ao óbito. Conclusão: A elevação nos níveis de lipocalina associada à gelatinase neutrofílica urinária antecede as variações da creatinina sérica em pacientes com lesão renal aguda e pode ser associada ao óbito.

Transcriptional Regulation of Chemokine Genes: A Link to Pancreatic Islet Inflammation?

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Susan J. Burke

2015-05-01

Full Text Available Enhanced expression of chemotactic cytokines (aka chemokines within pancreatic islets likely contributes to islet inflammation by regulating the recruitment and activation of various leukocyte populations, including macrophages, neutrophils, and T-lymphocytes. Because of the powerful actions of these chemokines, precise transcriptional control is required. In this review, we highlight what is known about the signals and mechanisms that govern the transcription of genes encoding specific chemokine proteins in pancreatic islet β-cells, which include contributions from the NF-κB and STAT1 pathways. We further discuss increased chemokine expression in pancreatic islets during autoimmune-mediated and obesity-related development of diabetes.

Demonstration of the dorsal pancreatic artery by CTA to facilitate superselective arterial infusion of stem cells into the pancreas

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Lin Yuning; Yang Xizhang; Chen Ziqian; Tan Jianming; Zhong Qun; Yang Li; Wu Zhixian

2012-01-01

Purpose: To investigate the diagnostic performance of 64-section CTA in the detection of dorsal pancreatic artery before interventional therapy for patients with diabetes. Materials and methods: The study was approved by the institutional ethics committee; written informed consent was obtained. Forty-two consecutive patients with diabetes received an experimental treatment of autologous bone marrow-derived stem cell transplantation by means of infusion into the dorsal pancreatic artery. All cases underwent abdominal CTA before angiography of pancreatic arteries in order to locate the origin and course of dorsal pancreatic artery. Angiography of coeliac artery, splenic artery, common hepatic artery and superior mesenteric artery were performed both in CTA and DSA. Superselective catheterization of dorsal pancreatic artery was carried out for the infusion of stem cell. Sensitivity, specificity and accuracy for the detection of dorsal pancreatic artery with CTA were calculated using DSA images as the reference standard. Results: Thirty-five and thirty-six dorsal pancreatic arteries were detected by CTA and DSA respectively. Dorsal pancreatic artery was not visualized in either CTA or DSA in 5 patients. The sensitivity, specificity and accuracy for CTA were 94.4%, 83.3% and 92.9%. Conclusion: 64-section CTA is accurate for the detection of dorsal pancreatic artery. It may be useful for the facilitation of superselective arterial infusion of stem cells to pancreas.

Extreme Beta-Cell Deficiency in Pancreata of Dogs with Canine Diabetes.

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Emily J Shields

Full Text Available The pathophysiology of canine diabetes remains poorly understood, in part due to enigmatic clinical features and the lack of detailed histopathology studies. Canine diabetes, similar to human type 1 diabetes, is frequently associated with diabetic ketoacidosis at onset or after insulin omission. However, notable differences exist. Whereas human type 1 diabetes often occurs in children, canine diabetes is typically described in middle age to elderly dogs. Many competing theories have been proposed regarding the underlying cause of canine diabetes, from pancreatic atrophy to chronic pancreatitis to autoimmune mediated β-cell destruction. It remains unclear to what extent β-cell loss contributes to canine diabetes, as precise quantifications of islet morphometry have not been performed. We used high-throughput microscopy and automated image processing to characterize islet histology in a large collection of pancreata of diabetic dogs. Diabetic pancreata displayed a profound reduction in β-cells and islet endocrine cells. Unlike humans, canine non-diabetic islets are largely comprised of β-cells. Very few β-cells remained in islets of diabetic dogs, even in pancreata from new onset cases. Similarly, total islet endocrine cell number was sharply reduced in diabetic dogs. No compensatory proliferation or lymphocyte infiltration was detected. The majority of pancreata had no evidence of pancreatitis. Thus, canine diabetes is associated with extreme β-cell deficiency in both new and longstanding disease. The β-cell predominant composition of canine islets and the near-total absence of β-cells in new onset elderly diabetic dogs strongly implies that similar to human type 1 diabetes, β-cell loss underlies the pathophysiology of canine diabetes.

Nutritional Intake in Low Body Mass Index (BMI Males with Type 1 Diabetes and Fibrocalcific Pancreatic Diabetes: What are the Unmet Needs? A Cross-Sectional Study from a South Indian Tertiary Care Hospital

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Mini Joseph

2017-10-01

Full Text Available Introduction: There is paucity of data on the nutritional intake in low Body Mass Index (BMI Asian Indians with diabetes. Aim: To study the difference in the nutrient intake pattern in low-BMI Type 1 Diabetes Mellitus (T1DM and Fibrocalcific Pancreatic Diabetes (FCPD patients. Materials and Methods: This cross-sectional study consisted of T1DM (n=40 and FCPD (n=20 male patients with similar BMI. Nutritional data was collected using the 24 hour recall method and food diaries. Fasting blood samples were analysed for lipid profile, serum creatinine, glycosylated haemoglobin, albumin, calcium and vitamin D. Stool samples were analysed for pancreatic elastase. Percentage analysis, Independent sample t-test and Pearson coefficient correlation were used to analyse the data. A p-value<0.05 was considered as statistically significant. Results: The FCPD patients, on biochemical analysis, had significantly lower vitamin D levels compared to the T1DM group (p=0.035. However, haemoglobin, triglycerides, low density lipoproteins, creatinine, albumin and calcium were similar between the groups. In the nutrient data, FCPD patients had a significant higher intake of fat (p=0.039, fibre (p<0.001, calcium (p=0.047, phosphorous (p=0.035, and niacin (p=0.001 and calories from fat (p=0.047. The T1DM group had a significantly higher intake of thiamine (p=0.047 and carbohydrates (p=0.014. Conclusion: T1DM and FCPD groups have similar dietary pattern deficit in fibre, calories, macronutrients and micronutrients. Malabsorption and poor glycaemic control in FCPD patients can be attributed to a higher dietary fat intake. A balanced diet can ensure better glycaemic control.

Frey's pancreaticojejunostomy in tropical pancreatitis: assessment of quality of life. A prospective study.

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Pothula Rajendra, Vamsi Krishna; Sivanpillay Mahadevan, Sivaraj; Parvathareddy, Sivacharan Reddy; Nara, Bharat Kumar; Gorlagunta Ramachandra, Mallikarjuna; Tripuraneni Venkata, Aditya Chowdary; Bathalapalli, Jagan Mohan Reddy; Gudi, Vara Prasada Rao; Sampath, Thirunavukkarasu

2014-12-01

Tropical pancreatitis is a form of chronic pancreatitis originally described in the tropics. Prospective studies in Western countries have shown improved quality of life (QOL) following surgery in alcoholic chronic pancreatitis. In studies on Frey's pancreaticojejunostomy for tropical pancreatitis, improvement in pain was considered the endpoint, and there is a paucity of data in the literature with regard to QOL with tropical pancreatitis following surgery. Our objective was to prospectively analyze the outcome of Frey's pancreaticojejunostomy in tropical pancreatitis and health-related QOL following surgery by administering the Short Form 36-item health survey (SF-36). A total of 25 patients underwent Frey's pancreaticojejunostomy between 2010 and 2012 and were included in the study; data were collected prospectively. The visual analog scale (VAS) for pain and the SF-36 form were used to record health-related QOL preoperatively, and at 3 and 12 months post-surgery, comparing the same with the general population. Patients with tropical pancreatitis experience poor QOL (26.71 ± 15.95) compared with the general population (84.54 ± 12.42). Post-operative QOL scores (78.54 ± 15.84) were better than the pre-operative scores (26.71 ± 15.95) at 12-month post-surgery follow-up. The VAS score for pain improved at 12 months post-surgery (1.58 ± 1.41 vs. 8.21 ± 1.64). Two of the three patients (12.5 %) who had diabetes were free from anti-diabetes medication at 12 months post-surgery. Steatorrhea was seen in five patients (20.8 %) before surgery and increased to eight (33.3 %) at 12 months post-surgery. Mean body weight increased from 45.75 kg pre-operatively to 49.25 kg at 12 months post-operatively. Frey's pancreaticojejunostomy effectively reduces pain in tropical pancreatitis, with significant improvement in health-related QOL, which is comparable with the general population in most aspects.

Pancreatite necro-hemorrágica: atualização e momento de operar Necrotizing pancreatitis: update and when to operate

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Ricardo Antonio Refinetti

2010-06-01

Full Text Available INTRODUÇÃO: A pancreatite necro-hemorrágica representa a variante mais grave do espectro de apresentações clínicas que podem compor o quadro da pancreatite aguda. Embora já conhecida há muitos séculos, inúmeras questões permanecem em aberto acerca dessa entidade e o número de trabalhos sobre o assunto publicados nos últimos anos tem sido muito expressivo. MÉTODO: Foi realizada ampla pesquisa na literatura, com especial atenção aos artigos publicados nos últimos três anos e indexados ao PubMed. Foram utilizados os seguintes descritores de forma cruzada: pancreatitis, surgical procedures; necrosis. A pesquisa inicial evidenciou cerca de 13.000 artigos, sendo avaliados os mais relevantes dos últimos três anos além de artigos mais antigos, considerados "clássicos" sobre o assunto e que, portanto, não poderiam deixar de ser citados. CONCLUSÃO: O tratamento da pancreatite aguda envolve um grande número de questões, dentre as quais as mais importantes estão relacionadas ao manejo da antibioticoterapia, tipo de dieta empregada e as questões relacionadas ao manejo da necrose infectada. Em especial, mudanças radicais foram implementadas nos últimos anos sobre todos esses tópicos, e uma atualização constante deve ser obrigatoriamente buscada pelos profissionais envolvidos no tratamento dessa doença.BACKGROUND: Necrotizing pancreatitis represents the most severe form of presentation from the clinical spectra of acute pancreatitis. Although known for many centuries, many questions remain open about this entity and a great number of articles were published about this matter in the last few years. METHOD: A throughout research in the literature, with special attention to the articles published in the last three years and indexed to the PubMed was performed. The following headings were used: pancreatitis, surgical procedures, necrosis. The initial research rendered about 13 000 articles, and the ones published in the last three

Betatrophin: A liver-derived hormone for the pancreatic β-cell proliferation.

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Raghow, Rajendra

2013-12-15

The pancreatic β-cell failure which invariably accompanies insulin resistance in the liver and skeletal muscle is a hallmark of type-2 diabetes mellitus (T2DM). The persistent hyperglycemia of T2DM is often treated with anti-diabetic drugs with or without subcutaneous insulin injections, neither of which mimic the physiological glycemic control seen in individuals with fully functional pancreas. A sought after goal for the treatment of T2DM has been to harness the regenerative potential of pancreatic β-cells that might obviate a need for exogenous insulin injections. A new study towards attaining this aim was reported by Yi et al, who have characterized a liver-derived protein, named betatrophin, capable of inducing pancreatic β-cell proliferation in mice. Using a variety of in vitro and in vivo methods, Yi et al, have shown that betatrophin was expressed mainly in the liver and adipose tissue of mice. Exogenous expression of betatrophin in the liver led to dramatic increase in the pancreatic β-cell mass and higher output of insulin in mice that also concomitantly elicited improved glucose tolerance. The authors discovered that betatrophin was also present in the human plasma. Surprisingly, betatrophin has been previously described by three other names, i.e., re-feeding-induced fat and liver protein, lipasin and atypical angiopoeitin-like 8, by three independent laboratories, as nutritionally regulated liver-enriched factors that control serum triglyceride levels and lipid metabolism. Yi et al demonstration of betatrophin, as a circulating hormone that regulates β-cell proliferation, if successfully translated in the clinic, holds the potential to change the course of current therapies for diabetes.

Research on the relationships between pancreatic cancer and hyperglycemia in Chinese populations

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Huang, Shan; Ye, Hongying; Wu, Wei; Chen, Cheng; Li, Ji; Fu, Deliang; Li, Yiming

2012-01-01

Abstract Aims/Introduction Pancreatic cancer (PC) is related to diabetes. Long‐standing diabetes should be a prerequisite, whereas new‐onset hyperglycemia might be a result of PC. However, the association between diabetes and PC is still in dispute. Materials and Methods We investigated the relationship between glucose metabolism and other factors by retrospectively analyzing the clinical data of 331 PC patients. Any histopathological type was eligible. The patients were divided into three gr...

Inhibition of pancreatic lipase and amylase by extracts of different spices and plants.

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Sellami, Mohamed; Louati, Hanen; Kamoun, Jannet; Kchaou, Ali; Damak, Mohamed; Gargouri, Youssef

2017-05-01

The aim of this study is to search new anti-obesity and anti-diabetic agents from plant and spices crude extracts as alternative to synthetic drugs. The inhibitory effect of 72 extracts was evaluated, in vitro, on lipase and amylase activities. Aqueous extracts of cinnamon and black tea exhibited an appreciable inhibitory effect on pancreatic amylase with IC 50 values of 18 and 87 μg, respectively. Aqueous extracts of cinnamon and mint showed strong inhibitory effects against pancreatic lipase with IC 50 of 45 and 62 μg, respectively. The presence of bile salts and colipase or an excess of interface failed to restore the lipase activity. Therefore, the inhibition of pancreatic lipase, by extracts of spices and plants, belongs to an irreversible inhibition. Crude extract of cinnamon showed the strongest anti-lipase and anti-amylase activities which offer a prospective therapeutic approach for the management of diabetes and obesity.

Expansion and conversion of human pancreatic ductal cells into insulin-secreting endocrine cells.

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Lee, Jonghyeob; Sugiyama, Takuya; Liu, Yinghua; Wang, Jing; Gu, Xueying; Lei, Ji; Markmann, James F; Miyazaki, Satsuki; Miyazaki, Jun-Ichi; Szot, Gregory L; Bottino, Rita; Kim, Seung K

2013-11-19

Pancreatic islet β-cell insufficiency underlies pathogenesis of diabetes mellitus; thus, functional β-cell replacement from renewable sources is the focus of intensive worldwide effort. However, in vitro production of progeny that secrete insulin in response to physiological cues from primary human cells has proven elusive. Here we describe fractionation, expansion and conversion of primary adult human pancreatic ductal cells into progeny resembling native β-cells. FACS-sorted adult human ductal cells clonally expanded as spheres in culture, while retaining ductal characteristics. Expression of the cardinal islet developmental regulators Neurog3, MafA, Pdx1 and Pax6 converted exocrine duct cells into endocrine progeny with hallmark β-cell properties, including the ability to synthesize, process and store insulin, and secrete it in response to glucose or other depolarizing stimuli. These studies provide evidence that genetic reprogramming of expandable human pancreatic cells with defined factors may serve as a general strategy for islet replacement in diabetes. DOI: http://dx.doi.org/10.7554/eLife.00940.001.

Black Seed Thymoquinone Improved Insulin Secretion, Hepatic Glycogen Storage, and Oxidative Stress in Streptozotocin-Induced Diabetic Male Wistar Rats

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Heba M. A. Abdelrazek

2018-01-01

Full Text Available Diabetes mellitus is one of the metabolic diseases having several complications. Nigella sativa oil (NSO might have beneficial effects in the treatment of diabetic complications. Thirty-two mature male Wistar rats were equally divided into four experimental groups: control, control NSO 2 mL/kg, streptozotocin- (STZ- induced diabetic, and diabetic (STZ-induced treated with oral NSO 2 mg/kg for 30 days. Fasting blood glucose (FBG, insulin, and lipid profile levels were determined. Pancreatic and hepatic tissues were used for catalase and GSH. Histopathology, hepatic glycogen contents, insulin immunohistochemistry, and pancreatic islet morphometry were performed. NSO 2 mL/kg was noticed to decrease (P<0.05 FBG and increase (P<0.05 insulin levels in diabetic rats than in diabetic nontreated animals. Lipid profile showed significant (P<0.5 improvement in diabetic rats that received NSO 2 mL/kg than in the diabetic group. Both pancreatic and hepatic catalase and GSH activities revealed a significant (P<0.05 increment in the diabetic group treated with NSO than in the diabetic animals. NSO improved the histopathological picture and hepatic glycogen contents of the diabetic group as well as increased (P<0.05 insulin immunoreactive parts % and mean pancreatic islet diameter. NSO exerts ameliorative and therapeutic effects on the STZ-induced diabetic male Wistar rats.

Chronic pancreatitis. Diagnosis, therapy and follow-up results

International Nuclear Information System (INIS)

Moessner, J.

1996-01-01

The incidence of chronic pancreatitis is increasing in industrialized countries due to the steady increase of alcohol abuse. The pathogenesis of this disease is still incompletely understood. A cure is not possible. The knowledge of the patients history and a thorough clinical investigation together with the availability of a wide array of laboratory tests and imaging procedures enable the physician to characterize the stage of the disease. Exact knowledge of the present pancreatic morphology, potential complications of the disease, and knowledge about the present exocrine and endocrine function capacity are prerequisites for adequate therapeutic decision making. The therapeutic possibilities include termination of alcohol abuse, various options of treatment of pain according to the various pathogenetic possibilities leading to pain, pancreatic digestive enzyme supplementation, treatment of diabetes, and either endoscopic or surgical treatments of complications of the disease. (orig.) [de

Risk factors of exocrine and endocrine pancreatic insufficiency after pancreatic resection: A multi-center prospective study.

Science.gov (United States)

Maignan, A; Ouaïssi, M; Turrini, O; Regenet, N; Loundou, A; Louis, G; Moutardier, V; Dahan, L; Pirrò, N; Sastre, B; Delpero, J-R; Sielezneff, I

2018-01-26

Management of functional consequences after pancreatic resection has become a new therapeutic challenge. The goal of our study is to evaluate the risk factors for exocrine (ExoPI) and endocrine (EndoPI) pancreatic insufficiency after pancreatic surgery and to establish a predictive model for their onset. Between January 1, 2014 and June 19, 2015, 91 consecutive patients undergoing pancreatoduodenectomy (PD) or left pancreatectomy (LP) (72% and 28%, respectively) were followed prospectively. ExoPI was defined as fecal elastase content126mg/dL or aggravation of preexisting diabetes. The volume of residual pancreas was measured according to the same principles as liver volumetry. The ExoPI and EndoPI rates at 6 months were 75.9% and 30.8%, respectively. The rate of ExoPI after PD was statistically significantly higher than after LP (98% vs. 21%; Ppancreatic volume less than 39.5% was predictive of ExoPI. ExoPI occurs quasi-systematically after PD irrespective of the reconstruction scheme. The rate of EndoPI did not differ between PD and LP. Copyright © 2017. Published by Elsevier Masson SAS.

Reversible high blood CEA and CA19-9 concentrations in a diabetic ...

African Journals Online (AJOL)

dilatation of the main pancreatic duct. Positron emi- ... one of the benign diseases related to CA19-9 elevation. ... The histology of pancreatic islets from type 2 diabetic patients ... This is an Open Access article distributed under the terms of the Creative Commons Attribution- ... Attenuation of endocrine-exocrine pancreatic.

In Vivo Monitoring of Pancreatic β-Cells in a Transgenic Mouse Model

Directory of Open Access Journals (Sweden)

Steven J. Smith

2006-04-01

Full Text Available We generated a transgenic mouse model (RIP-luc for the in vivo monitoring of pancreatic islet mass and function in response to metabolic disease. Using the rat insulin promoter fused to firefly luciferase, and noninvasive technology to detect luciferase activity, we tracked changes in reporter signal during metabolic disease states and correlated the changes in luciferase signal with metabolic status of the mouse. Transgene expression was found to be specific to the pancreatic islets in this transgenic model. Basal transgene expression was tracked in male and female mice fed either a chow or a high-fat diet and in response to treatment with streptozotocin. Pancreatic bioluminescent signal increased in mice fed a high-fat diet compared with chow-fed animals. In a model of chemically induced diabetes, the bioluminescent signal decreased in accordance with the onset of diabetes and reduction of islet β-cell number. Preliminary studies using islets transplanted from this transgenic model suggest that in vivo image analysis can also be used to monitor transplanted islet viability and survival in the host. This transgenic model is a useful tool for in vivo studies of pancreatic β-cells and as a donor for islet transplantation studies.

Occurrence, clinical features and outcome of canine pancreatitis (80 cases).

Science.gov (United States)

Pápa, Kinga; Máthé, Akos; Abonyi-Tóth, Zsolt; Sterczer, Agnes; Psáder, Roland; Hetyey, Csaba; Vajdovich, Péter; Vörös, Károly

2011-03-01

Medical records of 80 dogs diagnosed with acute pancreatitis during a 4-year period were evaluated regarding history, breed predilection, clinical signs and additional examination findings. Cases were selected if compatible clinical symptoms, increased serum activity of amylase or lipase and morphologic evidence of pancreatitis by ultrasonography, laparotomy or necropsy were all present. Like in other studies, neutered dogs had an increased risk of developing acute pancreatitis. Although breed predilection was consistent with earlier reports, some notable differences were also observed. Apart from Dachshunds, Poodles, Cocker Spaniels and Fox Terriers, the sled dogs (Laikas, Alaskan Malamutes) also demonstrated a higher risk for pancreatitis according to our results. Concurrent diseases occurred in 56 dogs (70%), diabetes mellitus (n = 29, 36%) being the most common. Clinical signs of acute pancreatitis were similar to those observed in other studies. The study group represented a dog population with severe acute pancreatitis, having a relatively high mortality rate (40%) compared to data of the literature. Breed, age, gender, neutering and body condition had no significant association with the outcome. Hypothermia (p = 0.0413) and metabolic acidosis (p = 0.0063) correlated significantly with poor prognosis and may serve as valuable markers for severity assessment in canine acute pancreatitis.

Anti-diabetic effects of Sargassum oligocystum on Streptozotocin- induced diabetic rat

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Samad Akbarzadeh

2018-03-01

Full Text Available Objective(s: Diabetes is a metabolic syndrome which is associated with the worldwide major public health problems. There are many natural compounds from the sea-market, as a valuable aquatic source, along with the variety of health and therapeutic benefits. In the present research, with respect to the traditional and ethnic uses of Sargassum oligocystum algae for healing of some diseases which have similar metabolic mechanism to the diabetes, its anti-diabetic effects in animal model was proposed. Materials and Methods: The animals (rat were divided into the normal control, diabetic control, positive control and, the test groups. The test groups were gavaged with oral doses of 150 and 300 mg/kg of algae hydroalcoholic extracts. After 30 days of intervention the serum glucose, cholesterol, triglyceride, HDLC, LDLC, insulin, insulin resistance, β-cells function and, the histopathology of pancreatic tissue were evaluated. Results: In animals that were fed with algae extracts a significant decrease in the fasting blood glucose, triglyceride and HOMA-IR and an increase in the HOMA-B with no significant impacts on the insulin, cholesterol and HDL were observed. Also, the histopathology evaluations in the groups which were treated with algae extract revealed the regeneration and reconstitution of damaged pancreatic β-cells. Conclusion: The results give evidence that, the S. oligocystum algae extract has a healing effect on diabetes which can be considered as a new research prospect for the natural therapy of diabetes.

Altered volume, morphology and composition of the pancreas in type 2 diabetes.

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Mavin Macauley

Full Text Available Although impairment in pancreatic insulin secretion is known to precede the clinical diagnosis of type 2 diabetes by up to a decade, fasting blood glucose concentration only rises abnormally once the impairment reaches a critical threshold. Despite its centrality to the pathogenesis of type 2 diabetes, the pancreas is the least studied organ due to its inaccessible anatomical position. Previous ultrasound and CT studies have suggested a possible decrease in pancreatic volume in type 2 diabetes. However, ultrasound techniques are relatively insensitive while CT uses ionizing radiation, making these modalities unsuitable for precise, longitudinal studies designed to explore the underlying mechanisms of type 2 diabetes. Hence there is a need to develop a non-invasive, safe and precise method to quantitate pancreas volume.We developed and applied magnetic resonance imaging at 3.0T to obtain balanced turbo field echo (BTFE structural images of the pancreas, together with 3-point Dixon images to quantify pancreatic triglyceride content. Pancreas volume, morphology and triglyceride content was quantified in a group of 41 subjects with well-controlled type 2 diabetes (HbA1c ≤ 7.6% taking only metformin (duration of T2DM 5.7 ± 0.7 years, and a control group of 14 normal glucose tolerance subjects matched for age, weight and sex.The mean pancreatic volume was found to be 33% less in type 2 diabetes than in normal glucose tolerant subjects (55.5 ± 2.8 vs. 82.6 ± 4.8 cm3; p < 0.0001. Pancreas volume was positively correlated with HOMA-β in the type 2 diabetes subjects (r = 0.31; p = 0.03 and controls (r = 0.46; p = 0.05 considered separately; and in the whole population studied (r = 0.37; p = 0.003. In type 2 diabetes, the pancreas was typically involuted with a serrated border. Pancreatic triglyceride content was 23% greater (5.4 ± 0.3 vs. 4.4 ± 0.4%; p = 0.02 in the type 2 diabetes group.This study describes for the first time gross abnormalities

Altered Volume, Morphology and Composition of the Pancreas in Type 2 Diabetes

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Macauley, Mavin; Percival, Katie; Thelwall, Peter E.; Hollingsworth, Kieren G.; Taylor, Roy

2015-01-01

Objective Although impairment in pancreatic insulin secretion is known to precede the clinical diagnosis of type 2 diabetes by up to a decade, fasting blood glucose concentration only rises abnormally once the impairment reaches a critical threshold. Despite its centrality to the pathogenesis of type 2 diabetes, the pancreas is the least studied organ due to its inaccessible anatomical position. Previous ultrasound and CT studies have suggested a possible decrease in pancreatic volume in type 2 diabetes. However, ultrasound techniques are relatively insensitive while CT uses ionizing radiation, making these modalities unsuitable for precise, longitudinal studies designed to explore the underlying mechanisms of type 2 diabetes. Hence there is a need to develop a non-invasive, safe and precise method to quantitate pancreas volume. Methods We developed and applied magnetic resonance imaging at 3.0T to obtain balanced turbo field echo (BTFE) structural images of the pancreas, together with 3-point Dixon images to quantify pancreatic triglyceride content. Pancreas volume, morphology and triglyceride content was quantified in a group of 41 subjects with well-controlled type 2 diabetes (HbA1c ≤ 7.6%) taking only metformin (duration of T2DM 5.7±0.7years), and a control group of 14 normal glucose tolerance subjects matched for age, weight and sex. Results The mean pancreatic volume was found to be 33% less in type 2 diabetes than in normal glucose tolerant subjects (55.5±2.8 vs. 82.6±4.8cm3; pPancreas volume was positively correlated with HOMA-β in the type 2 diabetes subjects (r = 0.31; p = 0.03) and controls (r = 0.46; p = 0.05) considered separately; and in the whole population studied (r = 0.37; p = 0.003). In type 2 diabetes, the pancreas was typically involuted with a serrated border. Pancreatic triglyceride content was 23% greater (5.4±0.3 vs. 4.4±0.4%; p = 0.02) in the type 2 diabetes group. Conclusion This study describes for the first time gross