Reduction of pancreatic β-cell dedifferentiation after gastric bypass surgery in diabetic rats

• 来源期刊: 分子细胞生物学报（英文版）
• 年，卷（期）: 2014,（6）
• 页码范围: 531-534
• 页数: 4页
• 语种: 中文
• DOI: 10.1093/jmcb/mju042

摘要

Dear Editor, Type 2 diabetes mellitus (T2DM) develops only in insulin-resistant subjects when pancreatic β-cell compensation fails (Matveyenko and Butler,2006).Decreased insulin secretory function and reduced cell mass are traditionally viewed as major contributing factors in β-cell insufficiency.A recent study using a diabetic rodent model suggests that progressive β-cell dedifferentiation is an important underlying mechanism in β-cell failure (Talchai et al.,2012).β-cell dedifferentiation in diabetes refers to the loss by healthy β-cells of key components characteristic of the differentiated state (Dor and Glaser,2013),including insulin (for its secretory product),Glut2 (for glucose intake),and PDX-1 (for critical insulin transcription factor).β-cell dedifferentiation may be largely responsible for not only β-cell secretory dysfunction but also impaired β-cell identity,In view of findings that bariatric surgery in a rodent T2DM model led to increased β-cell mass and improved islet morphology (Strader et al.,2009),we investigated the effects of gastric bypass surgery on dedifferentiated β-cells.