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Comment
. 2008 Jun 3;105(22):7627-8.
doi: 10.1073/pnas.0803901105. Epub 2008 May 28.

Muscle insulin resistance: a case of fat overconsumption, not mitochondrial dysfunction

Affiliations
Comment

Muscle insulin resistance: a case of fat overconsumption, not mitochondrial dysfunction

Edward W Kraegen et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
Interrelationship of energy metabolism and insulin action in skeletal muscle. Fatty acids and glucose are both substrates for energy metabolism in skeletal muscle. Cytosolic accumulation of lipid species such as diacylglycerol and ceramide are thought to decrease insulin action by inhibiting the insulin signaling pathway (blue shaded box). Metabolism of fatty acids by muscle cells is subject to regulation at the level of uptake and activation of fatty acids, the entry of activated fatty acids into the mitochondrion (CPT-1) and the capacity of the β-oxidation pathway, the tricarboxylic acid (TCA) cycle, electron transport chain (complex I–IV), and ATP synthesis (complex V) (red boxes). The balance between uptake and utilization of fatty acids will ultimately determine the magnitude of lipid accumulation in muscle cells.

Comment on

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