Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility.

@article{Muoio2012MusclespecificDO,
  title={Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility.},
  author={Deborah M. Muoio and Robert C. Noland and J P Kovalik and Sarah E. Seiler and Michael N Davies and Karen L. DeBalsi and Olga Ilkayeva and Robert A. Moffitt Johns Hopkins University David Stevens and Indu Kheterpal and Jingying Zhang and Jeffrey D Covington and Sudip Bajpeyi and Eric Ravussin and W. Kraus and Timothy R. Koves and Randall L. Mynatt},
  journal={Cell metabolism},
  year={2012},
  volume={15 5},
  pages={764-77}
}
The concept of "metabolic inflexibility" was first introduced to describe the failure of insulin-resistant human subjects to appropriately adjust mitochondrial fuel selection in response to nutritional cues. This phenomenon has since gained increasing recognition as a core component of the metabolic syndrome, but the underlying mechanisms have remained elusive. Here, we identify an essential role for the mitochondrial matrix enzyme, carnitine acetyltransferase (CrAT), in regulating substrate… CONTINUE READING
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Metabolic profiling ofmuscle contraction in lean compared with obese rodents

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