Mitochondrial dysfunction in type 2 diabetes and obesity

Endocrinol Metab Clin North Am. 2008 Sep;37(3):713-31, x. doi: 10.1016/j.ecl.2008.06.006.


Insulin resistance in skeletal muscle is a major hallmark of type 2 diabetes mellitus (T2D) and obesity that is characterized by impaired insulin-mediated glucose transport and glycogen synthesis and by increased intramyocellular content of lipid metabolites. Several studies have provided evidence for mitochondrial dysfunction in skeletal muscle of type 2 diabetic and prediabetic subjects, primarily due to a lower content of mitochondria (mitochondrial biogenesis) and possibly to a reduced functional capacity per mitochondrion. This article discusses the latest advances in the understanding of the molecular mechanisms underlying insulin resistance in human skeletal muscle in T2D and obesity, with a focus on possible links between insulin resistance and mitochondrial dysfunction.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Diabetes Mellitus, Type 2 / metabolism*
  • Humans
  • Insulin Resistance
  • Mitochondria / physiology*
  • Obesity / metabolism*
  • Organelle Biogenesis
  • Oxidation-Reduction
  • Proteomics