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Published on: January 23, 2018
Mitochondria as a target for exercise-mitigated type 2 diabetes
Jingjing Tian1,2, Jingcheng Fan1,2, Tan Zhang3,4
1School of Exercise and Health, Shanghai University of Sport, Shanghai, China.
Abstract:
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.
Insights
Mitochondrial dysfunction in tissues like muscle and liver contributes to type 2 diabetes (T2DM). Exercise may improve insulin sensitivity by enhancing mitochondrial function, offering a key strategy for T2DM management.
Area of Science:
- Metabolic diseases
- Mitochondrial biology
- Exercise physiology
Background:
- Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disease and a major cause of mortality.
- The exact pathogenesis of T2DM remains incompletely understood despite extensive research.
- Mitochondrial dysfunction in key insulin-responsive tissues is strongly implicated in T2DM development.
Purpose of the Study:
- To explore the role of mitochondria in the development of T2DM.
- To investigate the potential mechanisms by which exercise training improves insulin sensitivity in T2DM.
Main Methods:
- Review of existing evidence linking mitochondrial function to T2DM pathogenesis.
- Analysis of studies investigating the effects of exercise training on insulin sensitivity and mitochondrial function.
Main Results:
- Defects in mitochondrial function in skeletal muscle, liver, and adipose tissue are identified as critical drivers of T2DM.
- Exercise training is a recognized effective intervention for enhancing insulin sensitivity.
- Mitochondria are hypothesized to play a central role in mediating the beneficial effects of exercise on T2DM.
Conclusions:
- Mitochondrial health is intrinsically linked to the development and progression of T2DM.
- Exercise-induced improvements in mitochondrial function are likely key to its therapeutic effects in T2DM.
- Further research is warranted to fully elucidate the precise molecular mechanisms involved.
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