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Biochem Biophys Res Commun. 2006 Feb 3;340(1):291-5. Epub 2005 Dec 12.

AMPK activation increases fatty acid oxidation in skeletal muscle by activating PPARalpha and PGC-1.

Author information

1
Department of Internal Medicine, University of Ulsan College of Medicine, Seoul, Republic of Korea.

Abstract

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 PPARalpha target genes and PGC-1 in cultured muscle cells and mouse skeletal muscle, and that inhibition of PPARalpha and PGC-1 by siRNAs prevents AICAR-stimulated increase in fatty acid oxidation. These data suggest that a novel transcriptional regulatory mechanism involving PPARalpha and PGC-1 exists that is responsible for long-term stimulation of fatty acid oxidation in skeletal muscle by AICAR.

PMID:
16364253
DOI:
10.1016/j.bbrc.2005.12.011
[Indexed for MEDLINE]

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