Abstract
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.
Highlights
Over the past decade, the list of publications suggesting an involvement of mitochondrial oxidative capacity in skeletal muscle in the aetiology of metabolic disorders such as obesity, insulin resistance or type 2 diabetes, has been growing steadily
Muscle oxidative capacity is mainly determined by the mitochondrial density that depends on mitochondrial biogenesis, and the mitochondrial oxidative capacity, which relies on the oxidative enzyme content and activity
When bound to their ligand, peroxisome proliferator-activated receptors (PPAR) form a heterodimeric complex with the retinoid X receptor (RXR) to regulate gene transcription involved in fatty acid metabolism
Summary
The list of publications suggesting an involvement of mitochondrial oxidative capacity in skeletal muscle in the aetiology of metabolic disorders such as obesity, insulin resistance or type 2 diabetes, has been growing steadily. By considering that lifestyle and physical activity, in addition to age, gender and genetic background, influence mitochondrial oxidative capacity in human muscle, it is clear that the understanding of the causes at the origin of oxidative phosphorylation (OXPHOS) activity impairment is far from being accomplished. In this context, the purpose of this review is to highlight recent knowledge regarding the potential causes, mechanisms and cellular consequences of muscle mitochondrial dysfunction
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