Respiratory chain dysfunction in skeletal muscle does not cause insulin resistance

  • Wredenberg A
  • Freyer C
  • Sandström M
 et al. 
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Abstract

Insulin resistance in skeletal muscle is a characteristic feature of diabetes mellitus type 2 (DM2). Several lines of circumstantial evidence suggest that reduced mitochondrial oxidative phosphorylation capacity in skeletal muscle is a primary defect causing insulin resistance and subsequent development of DM2. We have now experimentally tested this hypothesis by characterizing glucose homeostasis in tissue-specific knockout mice with progressive respiratory chain dysfunction selectively in skeletal muscle. Surprisingly, these knockout mice are not diabetic and have an increased peripheral glucose disposal when subjected to a glucose tolerance test. Studies of isolated skeletal muscle from knockout animals show an increased basal glucose uptake and a normal increase of glucose uptake in response to insulin. In summary, our findings indicate that mitochondrial dysfunction in skeletal muscle is not a primary etiological event in DM2. © 2006 Elsevier Inc. All rights reserved.

Author-supplied keywords

  • Diabetes
  • Insulin resistance
  • Mitochondria
  • Oxidative phosphorylation
  • Respiratory chain
  • mtDNA

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Authors

  • Anna Wredenberg

  • Christoph Freyer

  • Marie E. Sandström

  • Abram Katz

  • Håkan Westerblad

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