Letter to the Editor

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Reduction of pancreatic β-cell dedifferentiation after gastric bypass surgery in diabetic rats Free
Bangguo Qian1,6,†, Xinrong Zhou2,†, Bing Li3,†, Bing Li1, Zhiyuan Liu1, Jiarui Wu1,4,5,*, and Huarong Zhou1,*
1Key Laboratory of Systems Biology, SIBS-Novo Nordisk Translational Research Centre for Prediabetes, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
2Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China
3The Armed Police General Hospital, Wuhan, China
4School of Life Science and Technology, ShanghaiTech University, Shanghai, China
5Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai, China
6Present address: Pathology Core Facility, Institute Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China *Correspondence to:Huarong Zhou, E-mail: hrzhou@sibs.ac.cn; Jiarui Wu, E-mail: wujr@sibs.ac.cn
J Mol Cell Biol, Volume 6, Issue 6, December 2014, 531-534,  https://doi.org/10.1093/jmcb/mju042

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.