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Comments on ‘Dietary intervention preserves β cell function in mice through CTCF-mediated transcriptional reprogramming’
Ruo-Ran Wang1,2,3 , Hongxing Fu4 , Jingya Li1,2,* , Zhuo-Xian Meng3,*
1School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310024, China
2State Key Laboratory of Drug Research, the National Center for Drug Screening, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
3Department of Pathology and Pathophysiology and Department of Cardiology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
4Department of Pharmacy, Shulan (Hangzhou) Hospital Affiliated to Zhejiang Shuren University Shulan International Medical College, Hangzhou 310000, China
*Correspondence to:Jingya Li , Email:jyli@simm.ac.cn Zhuo-Xian Meng , Email:zxmeng@zju.edu.cn
J Mol Cell Biol, Volume 14, Issue 7, July 2022, mjac043,  https://doi.org/10.1093/jmcb/mjac043

Type 2 diabetes (T2D) has become a common chronic disease worldwide. Pancreatic β cell dysfunction, together with insulin resistance, is among the main causes for the pathogenesis of T2D. However, the dynamic changes in the number and function of β cells and the molecular mechanism of irreversible damage in the pathogenesis of T2D are still unclear. A thorough analysis of the mechanism underlying β cell dysfunction will provide a theoretical basis and molecular targets for the development of new and more effective individualized therapies for diabetes.


Volume 14, Issue 7
July 2022