Fluxing the mitochondria to insulin resistance
- PMID: 18177719
- DOI: 10.1016/j.cmet.2007.12.002
Fluxing the mitochondria to insulin resistance
Abstract
Elevated fatty acids promote inflammation and insulin resistance. In this issue of Cell Metabolism, Koves et al. (2008) explore a novel paradigm suggesting that beta-oxidation of fatty acids exceeding the capacity of the tricarboxylic acid cycle yields incomplete fat oxidation and mitochondrial distress, obligatory events in the pathogenesis of insulin resistance.
Comment on
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Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance.Cell Metab. 2008 Jan;7(1):45-56. doi: 10.1016/j.cmet.2007.10.013. Cell Metab. 2008. PMID: 18177724
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