Mitochondria as a target for exercise-mitigated type 2 diabetes

被引:7
作者
Tian, Jingjing [1 ,2 ]
Fan, Jingcheng [1 ,2 ]
Zhang, Tan [1 ,2 ]
机构
[1] Shanghai Univ Sport, Sch Exercise & Hlth, Shanghai, Peoples R China
[2] Shanghai Frontiers Sci Res Base Exercise & Metab, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
Exercise; Mitochondria; Insulin resistance; T2DM; Skeletal muscle; Liver; Adipose tissue; SKELETAL-MUSCLE; INSULIN-RESISTANCE; AUTOREGULATORY LOOP; OXIDATIVE STRESS; NITRIC-OXIDE; DYSFUNCTION; AUTOPHAGY; OBESITY; PGC-1-ALPHA; METABOLISM;
D O I
10.1007/s10735-023-10158-1
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Type 2 diabetes mellitus (T2DM) is one of most common metabolic diseases and continues to be a leading cause of death worldwide. Although great efforts have been made to elucidate the pathogenesis of diabetes, the underlying mechanism still remains unclear. Notably, overwhelming evidence has demonstrated that mitochondria are tightly correlated with the development of T2DM, and the defects of mitochondrial function in peripheral insulin-responsive tissues, such as skeletal muscle, liver and adipose tissue, are crucial drivers of T2DM. Furthermore, exercise training is considered as an effective stimulus for improving insulin sensitivity and hence is regarded as the best strategy to prevent and treat T2DM. Although the precise mechanisms by which exercise alleviates T2DM are not fully understood, mitochondria may be critical for the beneficial effects of exercise.
引用
收藏
页码:543 / 557
页数:15
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