Abstract
Mitochondrial abnormalities have been reported in both insulin-deficient and insulin-resistant states and in the related condition of obesity. The phrase ‘mitochondrial dysfunction’ is often used in this regard. However, beyond dysfunction, there is evidence for defects in mitochondrial biogenesis, number, morphology, and dynamics (fusion and fission). Diabetes and obesity are also associated with the overproduction of mitochondrial reactive oxygen species (ROS), leading to mitochondrial and cellular oxidative damage. This, in turn, contributes to the development and progression of diabetic complications and to worsening of the diabetic stateper se. Here we will review the evidence for mitochondrial abnormalities in type 2 diabetes and obesity and consider underlying mechanisms. We will also discuss potential therapeutic interventions targeted at mitochondria.
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