Diazoxide Prevents Diabetes through Inhibiting Pancreatic β-Cells from Apoptosis via Bcl-2/Bax Rate and p38-β Mitogen-Activated Protein Kinase

• DOI: 10.1210/en.2006-0738
• Publication Date: 2006-10-20T00:53:30Z
• Authors: Qin Huang; Shizhong Bu; Yongwei Yu; Zhiyong Guo; Gautam Ghatnekar; Min Bu; Linhui Yang; Bin Lu; Zhengkang Feng; Shanrong Liu; Fengqi Wang
• Keywords: Diazoxide

Increased apoptosis of pancreatic β-cells plays an important role in the occurrence and development type 2 diabetes. We examined effect diazoxide on β-cell its potential mechanism Otsuka Long Evans Tokushima Fatty (OLETF) rats, established animal model human diabetes, at prediabetic diabetic stages. found a significant increase with age frequency apoptosis, sequential enlargement islets, proliferation connective tissue surrounding accompanied defective insulin secretory capacity increased blood glucose untreated OLETF rats. In contrast, treatment (25 mg·kg−1·d−1, administered ip) inhibited ameliorated changes islet morphology function, stores significantly whether was used or stage. Linear regression showed close correlation between hyperglycemia (r = 0.913; P < 0.0001). Further study demonstrated that up-regulated Bcl-2 expression p38β MAPK, which expressed very low levels due to high glucose, but not c-jun N-terminal kinase ERK. Hence, may play critical protection from apoptosis. this study, we demonstrate prevents onset diabetes rats by inhibiting via increasing elevating Bcl-2/Bax ratio, ameliorating action.