Concurrently using rosiglitazone prevents glucosamine-induced islet beta-cell apoptosis and dysfunction.

摘要

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.