AMPK activation increases fatty acid oxidation in skeletal muscle by activating PPARα and PGC-1
WJ Lee, M Kim, HS Park, HS Kim, MJ Jeon… - Biochemical and …, 2006 - Elsevier
WJ Lee, M Kim, HS Park, HS Kim, MJ Jeon, KS Oh, EH Koh, JC Won, MS Kim, GT Oh…
Biochemical and biophysical research communications, 2006•ElsevierAMP-activated protein kinase (AMPK) activation increases fatty acid oxidation in skeletal
muscle by decreasing malonyl CoA concentrations. However, this may not explain the long-
term effects of AMPK activation. Here we show that AMPK activation by 5-aminoimidazole-4-
carboxamide ribonucleoside (AICAR) increases mRNA expression of PPARα target genes
and PGC-1 in cultured muscle cells and mouse skeletal muscle, and that inhibition of
PPARα and PGC-1 by siRNAs prevents AICAR-stimulated increase in fatty acid oxidation …
muscle by decreasing malonyl CoA concentrations. However, this may not explain the long-
term effects of AMPK activation. Here we show that AMPK activation by 5-aminoimidazole-4-
carboxamide ribonucleoside (AICAR) increases mRNA expression of PPARα target genes
and PGC-1 in cultured muscle cells and mouse skeletal muscle, and that inhibition of
PPARα and PGC-1 by siRNAs prevents AICAR-stimulated increase in fatty acid oxidation …
AMP-activated protein kinase (AMPK) activation increases fatty acid oxidation in skeletal muscle by decreasing malonyl CoA concentrations. However, this may not explain the long-term effects of AMPK activation. Here we show that AMPK activation by 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) increases mRNA expression of PPARα target genes and PGC-1 in cultured muscle cells and mouse skeletal muscle, and that inhibition of PPARα and PGC-1 by siRNAs prevents AICAR-stimulated increase in fatty acid oxidation. These data suggest that a novel transcriptional regulatory mechanism involving PPARα and PGC-1 exists that is responsible for long-term stimulation of fatty acid oxidation in skeletal muscle by AICAR.
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