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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

372 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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