Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance.

@article{Koves2008MitochondrialOA,
  title={Mitochondrial overload and incomplete fatty acid oxidation contribute to skeletal muscle insulin resistance.},
  author={Timothy R. Koves and John Reyes Ussher and Robert C. Noland and Dorothy H. Slentz and Merrie Mosedale and Olga Ilkayeva and James Bain and Robert Stevens and Jason R. B. Dyck and Christopher B. Newgard and Gary D Lopaschuk and Deborah M. Muoio},
  journal={Cell metabolism},
  year={2008},
  volume={7 1},
  pages={45-56}
}
Previous studies have suggested that insulin resistance develops secondary to diminished fat oxidation and resultant accumulation of cytosolic lipid molecules that impair insulin signaling. Contrary to this model, the present study used targeted metabolomics to find that obesity-related insulin resistance in skeletal muscle is characterized by excessive beta-oxidation, impaired switching to carbohydrate substrate during the fasted-to-fed transition, and coincident depletion of organic acid… CONTINUE READING
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