Impaired glucose-stimulated insulin secretion is coupled with exocrine pancreatic lesions in the cohen diabetic rat.

Impaired glucose-stimulated insulin secretion is coupled with exocrine pancreatic lesions in the cohen diabetic rat. Research Abstract Details 

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Impaired glucose-stimulated insulin secretion is coupled with exocrine pancreatic lesions in the cohen diabetic rat. Abstract Text:

Sarah Weksler-Zangen,Itamar Raz,Sigurd Lenzen,Anne ,Shira Ehrenfeld,Gail Amir,Andrei Oprescu,Yoram Yagil,Chana Yagil,David H Zangen,Nurit Kaiser,Sarah Weksler-Zangen,Itamar Raz,Sigurd Lenzen,Anne ,Shira Ehrenfeld,Gail Amir,Andrei Oprescu,Yoram Yagil,Chana Yagil,David H Zangen,Nurit Kaiser,

OBJECTIVE: The Cohen diabetes-sensitive rat develops postprandial hyperglycemia when fed a high-sucrose, copper-poor diet, whereas the Cohen diabetes-resistant rat maintains normoglycemia. The pathophysiological basis of diabetes was studied in the Cohen diabetic rat centering on the interplay between the exocrine and endocrine compartments of the pancreas. RESEARCH DESIGN AND METHODS: Studies used male Cohen diabetes-sensitive and Cohen diabetes-resistant rats fed 1-month high-sucrose, copper-poor diet. Serum insulin and glucose levels were measured during glucose and insulin tolerance tests. The pancreas was evaluated for weight, insulin content, macrophage, and fat infiltration. Glucose-stimulated insulin secretion (GSIS) was determined in isolated perfused pancreas and in islets. RESULTS: Hyperglycemic Cohen diabetes-sensitive rats exhibited reduced pancreatic weight with lipid deposits and interleukin-1beta-positive macrophage infiltration in the exocrine pancreas. Islet morphology was preserved, and total pancreatic insulin content did not differ from that of Cohen diabetes-resistant rats. Lipids did not accumulate in skeletal muscle, nor was insulin resistance observed in hyperglycemic Cohen diabetes-sensitive rats. Intravenous glucose-tolerance test revealed markedly elevated glucose levels associated with diminished insulin output. Insulin release was induced in vivo by the non-nutrient secretagogues arginine and tolbutamide, suggesting a selective unresponsiveness to glucose. Decreased GSIS was observed in the isolated perfused pancreas of the hyperglycemic Cohen diabetes-sensitive rat, whereas islets isolated from these rats exhibited glucose-dependent insulin secretion and proinsulin biosynthesis. CONCLUSIONS: The association of the in vivo insulin secretory defect with lipid accumulation and activated macrophage infiltration in the exocrine pancreas suggests that changes in the islet microenvironment are the culprit in the insulin secretory malfunction observed in vivo.

Impaired glucose-stimulated insulin secretion is coupled with exocrine pancreatic lesions in the cohen diabetic rat. Publishing Authors By Initials

S Weksler-Zangen,I Raz,S Lenzen,A ,S Ehrenfeld,G Amir,A Oprescu,Y Yagil,C Yagil,DH Zangen,N Kaiser,S Weksler-Zangen,I Raz,S Lenzen,A ,S Ehrenfeld,G Amir,A Oprescu,Y Yagil,C Yagil,DH Zangen,N Kaiser,

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Impaired glucose-stimulated insulin secretion is coupled with exocrine pancreatic lesions in the cohen diabetic rat. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Diabetes

VOLUME: 57

Page Numbers: 279-87

Journal Abbreviation: Diabetes

ISSN: 1939-327X

DAY: 31

MONTH: 10

YEAR: 2007

Impaired glucose-stimulated insulin secretion is coupled with exocrine pancreatic lesions in the cohen diabetic rat. Information

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LANGUAGE: eng

NlmUniqueID: 372763

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AFFILIATION: The Diabetes Unit, Hadassah-Hebrew University Medical Center, Jerusalem 1200, Israel. sarahz@hadassah.org.il

Country: United States

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MEDLINETA: Diabetes

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