The Studies of Rosiglitazone on Insulin Secretion in Glucosamine-Induced Desensitization Rat Pancreas

碩士 === 國立中興大學 === 獸醫學系 === 91 === Type 2 (non-insulin-dependent) diabetes mellitus is a metabolic disorder resulting from lowered pancreatic insulin secretion or insulin action. Recently, the evidence indicated that glucosamine was a product of glucose flux through hexosamine biosyntheti...

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Bibliographic Details
Main Authors: Wei-Cheng Ho, 何威成
Other Authors: Chi Yang
Format: Others
Language:zh-TW
Published: 2003
Online Access:http://ndltd.ncl.edu.tw/handle/94571256083269858838
Description
Summary:碩士 === 國立中興大學 === 獸醫學系 === 91 === Type 2 (non-insulin-dependent) diabetes mellitus is a metabolic disorder resulting from lowered pancreatic insulin secretion or insulin action. Recently, the evidence indicated that glucosamine was a product of glucose flux through hexosamine biosynthetic pathway. Glucosamine decreased glucose-induced insulin secreation and produced insulin resistance. In order to obtain a good diabetic animal model for the research of new antidiabetic agents. We perfused rat pancreas with glucosmine(5、10、20 mM). The perfusate collected from portal vein was assayed for deteriming insulin concentration by using radioimmunoassay. The data showed that glucosamine decreased basal insulin secretion and glucose-induced insulin secreation with a dose-dependent manner. The new potent antidiabetic agent rosiglitazone activated peroxisome proliferator-activated receptor γ(PPAR-γ), increased the sensitivity of skeletal muscle, liver and adipose tissue to insulin, and reduced plasma glucose levels. Our paper published in Diabetes showed that rosiglitazone stimulated insulin secretion and potentiated glucose-induced insulin secreation in normal Sprague-Dawley rats. In order to elucidate the direct effect of rosiglitazone on glucosamine-induced mimic type 2 diabetes. Glucosamine-induced type 2 mimic diabetic rats was perfused with 4.5 mM rosiglitazone. The data showed that rosiglitazone enhanced glucose- induced insulin secretion in glucosamine-induced desensitization rat pancreas.