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.
|Number of pages||5|
|Journal||Biochemical and Biophysical Research Communications|
|State||Published - 3 Feb 2006|
Bibliographical noteFunding Information:
This study was supported by the National Research Laboratory Grant from the Ministry of Science and Technology (M1040000000804J000000810), Republic of Korea.
- Fatty acid oxidation