Purpose of review: Mitochondria are the site of oxidative substrate utilization to produce adenosine triphosphate for normal tissue function. Tissue substrate utilization is impaired in ageing and type 2 diabetes. Defects in mitochondrial gene expression, protein synthesis and function occur with ageing in various tissues including skeletal muscle, and are emerging in individuals with type 2 diabetes. The current review will discuss advances in the understanding of skeletal muscle mitochondrial alterations associated with age and type 2 diabetes.
Recent findings: Insulin acutely stimulates skeletal muscle mitochondrial protein synthesis and adenosine triphosphate production. These insulin effects are impaired in insulin-resistant patients with type 2 diabetes who also exhibit defective basal muscle mitochondrial function. The age-related reduction in mitochondrial adenosine triphosphate production has been confirmed in vivo in skeletal muscle in humans and rodents.
Summary: The emerging concept that insulin stimulates mitochondrial protein synthesis and function indicates potential novel molecular mechanisms of metabolic defects in type 2 diabetes, particularly in the post-prandial period characterized by acute increments of plasma insulin concentrations. The potential relationship between insulin resistance and basal post-absorptive muscle mitochondrial defects should be further investigated. As ageing is characterized by insulin resistance, the hypothesis that impaired insulin action could contribute to age-related muscle mitochondrial dysfunction, and metabolic alterations should be addressed.