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Hereditas(Beijing) ›› 2022, Vol. 44 ›› Issue (10): 840-852.doi: 10.16288/j.yczz.22-265

• Review • Previous Articles     Next Articles

Molecular mechanism of islet β-cell functional alternations during type 2 diabetes

Chengan Lv1,2(), Ruoran Wang1,2, Zhuo-Xian Meng1,2()   

  1. 1. Department of Pathology and Pathophysiology, Zhejiang University School of Medicine, Hangzhou 310058, China
    2. Key Laboratory of Disease Proteomics of Zhejiang Province, Zhejiang University School of Medicine, Hangzhou 310058, China
  • Received:2022-08-04 Revised:2022-09-02 Online:2022-10-20 Published:2022-09-30
  • Contact: Meng Zhuo-Xian E-mail:3190100992@zju.edu.cn;zxmeng@zju.edu.cn
  • Supported by:
    the National Natural Science Foundation of China(91857110);the National Natural Science Foundation of China(81722012);the National Natural Science Foundation of China(81670740);the National Key R&D Program of the Ministry of Science and Technology(2018YFA0800403);the National Key R&D Program of the Ministry of Science and Technology(2021YFC20701903);the Zhejiang Provincial Natural Science Foundation of China(LZ21H070001);the Construction Fund of Medical Key Disciplines of Hangzhou(OO20200055)

Abstract:

In recent years, the incidence rate of type 2 diabetes (T2D) has risen rapidly and has become a global health crisis. Recent experimental and clinical studies have shown that islet β-cell dysfunction is an important cause of T2D and its related complications. β-cells undergo dynamic compensation and decompensation in the course of T2D. In this process, metabolic stress responses, such as ER stress, oxidative stress and inflammation, are key regulators of β-cell functional alternations. In this review, we summarize the research progress on the β-cell functional dynamics in the course of T2D, in order to deepen the understanding of the molecular mechanism of T2D, and provide reference for its precise diagnosis and clinical intervention.

Key words: β-cell, type 2 diabetes, molecular mechanism