Potential Mechanisms of Muscle Mitochondrial Dysfunction in Aging and Obesity and Cellular Consequences

被引:27
作者
Chanseaume, Emilie [1 ,2 ]
Morio, Beatrice [1 ,2 ]
机构
[1] INRA, UMR Nutr Huamine 1019, F-63120 St Genes Champanelle, France
[2] Univ Clermont 1, UFR Med, UMR Nutr Humaine 1019, F-63000 Clermont Ferrand, France
关键词
Mitochondrial dysfunction; skeletal muscle; metabolic disorders; obesity; insulin resistance; type; 2; diabetes; HUMAN SKELETAL-MUSCLE; TUMOR-NECROSIS-FACTOR; ACTIVATED-RECEPTOR-DELTA; TYPE-2 DIABETIC PARENTS; GAMMA COACTIVATOR 1-ALPHA; FACTOR-ALPHA EXPRESSION; SATURATED FATTY-ACIDS; NITRIC-OXIDE SYNTHASE; AGE-RELATED-CHANGES; KAPPA-B ACTIVATION;
D O I
10.3390/ijms10010306
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondria play a key role in the energy metabolism in skeletal muscle. A new concept has emerged suggesting that impaired mitochondrial oxidative capacity in skeletal muscle may be the underlying defect that causes insulin resistance. According to current knowledge, the causes and the underlying molecular mechanisms at the origin of decreased mitochondrial oxidative capacity in skeletal muscle still remain to be elucidated. The present review focuses on recent data investigating these issues in the area of metabolic disorders and describes the potential causes, mechanisms and consequences of mitochondrial dysfunction in the skeletal muscle.
引用
收藏
页码:306 / 324
页数:19
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