期刊
PANCREATOLOGY
卷 12, 期 1, 页码 65-70出版社
KARGER
DOI: 10.1016/j.pan.2011.12.005
关键词
IFN gamma; Chronic pancreatitis; Diabetes
资金
- ICMR [5/4/3-10/09-NCD-II]
Background/aims: Although the role of cytokines in the etiopathology of chronic pancreatitis (CP) is well recognized, information on pancreatic tissue cytokines in CP with/without associated diabetes is unavailable. The aim of the present study was to identify the differences in pancreatic cytokines and observe their correlations with the glycemic status in CP. Methods: Pancreata were obtained from CP patients (n = 44), with/without associated diabetes and non-diabetic control subjects (n = 20). Patients with CP were classified into two groups after ascertaining their diabetic status. Pancreatic cytokines (IL 1 beta, IL 6, IL 8, IL 10, IL 12P70, TNF alpha, IFN gamma) were analyzed by flow cytometer. The influence of individual and cocktail of cytokines on glucose stimulated insulin release (GSIR) was examined by challenging the islets from control subjects. Results: The pancreatic IFN gamma levels in diabetic and non diabetic CP patients were significantly higher in comparison to controls. The glucose stimulated insulin release (GSIR) in response to high glucose concentration in control islets, islets from non-diabetic and diabetic CP patients was 8.2, 5.67 and 3.15 mu U x 10(-3)/min/islet equivalent respectively. IFN gamma resulted in 82.35% decrease in GSIR from the control islet cells at a concentration of >20 pg/ml which was reversed by epigallocatechin-3-gallate (EGCG). Conclusion: These results suggest that IFN gamma among other cytokines, play a major role in beta-cell dysfunction associated with CP. Copyright (C) 2012, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
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