AMPK activation increases fatty acid oxidation in skeletal muscle by activating PPARα 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

Research output: Contribution to journalArticlepeer-review

333 Scopus citations

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 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.

Original languageEnglish
Pages (from-to)291-295
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume340
Issue number1
DOIs
StatePublished - 3 Feb 2006

Bibliographical note

Funding Information:
This study was supported by the National Research Laboratory Grant from the Ministry of Science and Technology (M1040000000804J000000810), Republic of Korea.

Keywords

  • AICAR
  • AMPK
  • Fatty acid oxidation
  • Muscle
  • PGC-1
  • PPARα

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