Purpose of review: Muscular mitochondrial dysfunction, leading to the accumulation of fat in skeletal muscle, has been proposed to be involved in the development of type 2 diabetes mellitus. Here, we review human studies that investigated various aspects of mitochondrial function in relation to muscular insulin sensitivity and/or diabetes.
Recent findings: In-vivo magnetic resonance spectroscopy allows assessment of mitochondrial functionality from adenosine triphosphate flux in the nonexercising state and from phosphocreatine recovery from (sub)maximal exercising. Application of both approaches revealed reduced mitochondrial oxidative capacity in insulin-resistant (pre)diabetic humans. Reductions in mitochondrial density may contribute to, or even underlie, these findings as well as intrinsic defects in mitochondrial respiration. So far, only two studies reported measurements of mitochondrial respiratory capacity in intact mitochondria in diabetic patients, with inconsistent findings.
Summary: Muscular mitochondrial aberrations in type 2 diabetes mellitus can be detected, but it is so far unclear if these aberrations are causally related to the development of the disease. Alternatively, mitochondrial dysfunction may simply be the consequence of elevated plasma fatty acids or glucose levels.