Concurrently using rosiglitazone prevents glucosamine‐induced islet β‐Cell apoptosis and dysfunction |
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| Authors: | Xinxia Zhang Nanwei Tong Yao Li |
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| Institution: | 1. Division of Teaching & Research in Western Internal Medicine, Clinical College, Chengdu University of Traditional Chinese Medicine, China;2. Department of Endocrinology, Western China Hospital, Sichuan University, China;3. Department of Endocrinology, Chengdu Medical College Hospital, China |
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| Abstract: | Diabetes has merged as a significant health problem. This study aims to examine the effect of concurrently using rosiglitazone (RSG) on inhibiting glucosamine (GlcN)‐induced islet beta cell apoptosis and dysfunction. Using an islet beta cell line, HIT‐T15 cells, as a study platform, the inhibitory effect of RSG on GlcN‐induced pathophysiological changes in islet beta cells was examined. The results showed that treatment with GlcN induced HIT‐T15 cell death via apoptotic pathway, inhibited the expression of Bcl‐2 and Bcl‐xL, enhanced the expression of Bax, Bid and caspase‐3, reduced the production of ATP and decreased in insulin secretion. The changes were in a GlcN dose‐dependent manner. Concurrently using RSG with GlcN, the induced pathogenic changes in HIT‐T15 cells were abrogated. We conclude that concurrently using RSG can be useful in reducing the GlcN‐induced side effects on islet beta cells that has potential to prevent the complications caused by GlcN in the treatment of diabetes. Copyright © 2010 John Wiley & Sons, Ltd. |
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| Keywords: | Diabetes Islet beta cell Glucosamine Rosiglitazone Mitochondrion Apoptosis |
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