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 ...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 de- differentiation 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 differen- tiated 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 respon- sible 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.展开更多
文摘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 de- differentiation 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 differen- tiated 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 respon- sible 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.
