| First Author | Lee WJ | Year | 2006 |
| Journal | Biochem Biophys Res Commun | Volume | 340 |
| Issue | 1 | Pages | 291-5 |
| PubMed ID | 16364253 | Mgi Jnum | J:104210 |
| Mgi Id | MGI:3611518 | Doi | 10.1016/j.bbrc.2005.12.011 |
| Citation | Lee WJ, et al. (2006) AMPK activation increases fatty acid oxidation in skeletal muscle by activating PPARalpha and PGC-1. Biochem Biophys Res Commun 340(1):291-5 |
| abstractText | 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. |
