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

Woo Je Lee, Mina Kim, Hye-Sun Park, Hyoun Sik Kim, Min Jae Jeon, Ki Sook Oh, Eun Hee Koh, Jong Chul Won, Min-Seon Kim, Goo Taeg Oh, Michung Yoon, Ki-Up Lee, Joong-Yeol Park
Biochemical and Biophysical Research Communications 2006 February 3, 340 (1): 291-5
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.

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