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Journal Article

Respiratory chain dysfunction in skeletal muscle does not cause insulin resistance


Larsson,  N.G.
Department Larsson - Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Max Planck Society;

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Wredenberg, A., Freyer, C., Sandstrom, M. E., Katz, A., Wibom, R., Westerblad, H., et al. (2006). Respiratory chain dysfunction in skeletal muscle does not cause insulin resistance. Biochem Biophys Res Commun, 350(1), 202-7. doi:10.1016/j.bbrc.2006.09.029.

Cite as: https://hdl.handle.net/21.11116/0000-000B-68F7-A
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.