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

doi:10.1016/j.bbrc.2005.12.011

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

Department of Life Science

Research output: Contribution to journal › Article › peer-review

337 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 language	English
Pages (from-to)	291-295
Number of pages	5
Journal	Biochemical and Biophysical Research Communications
Volume	340
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2005.12.011
State	Published - 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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Lee, W. J., Kim, M., Park, H. S., Kim, H. S., Jeon, M. J., Oh, K. S., Koh, E. H., Won, J. C., Kim, M. S., Oh, G. T., Yoon, M., Lee, K. U., & Park, J. Y. (2006). AMPK activation increases fatty acid oxidation in skeletal muscle by activating PPARα and PGC-1. Biochemical and Biophysical Research Communications, 340(1), 291-295. https://doi.org/10.1016/j.bbrc.2005.12.011

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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.",

keywords = "AICAR, AMPK, Fatty acid oxidation, Muscle, PGC-1, PPARα",

author = "Lee, {Woo Je} and Mina Kim and Park, {Hye Sun} and Kim, {Hyoun Sik} and Jeon, {Min Jae} and Oh, {Ki Sook} and Koh, {Eun Hee} and Won, {Jong Chul} and Kim, {Min Seon} and Oh, {Goo Taeg} and Michung Yoon and Lee, {Ki Up} and Park, {Joong Yeol}",

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

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AU - Lee, Woo Je

AU - Kim, Mina

AU - Park, Hye Sun

AU - Kim, Hyoun Sik

AU - Jeon, Min Jae

AU - Oh, Ki Sook

AU - Koh, Eun Hee

AU - Won, Jong Chul

AU - Kim, Min Seon

AU - Oh, Goo Taeg

AU - Yoon, Michung

AU - Lee, Ki Up

AU - Park, Joong Yeol

N1 - Funding Information: This study was supported by the National Research Laboratory Grant from the Ministry of Science and Technology (M1040000000804J000000810), Republic of Korea.

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N2 - 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.

AB - 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.

KW - AICAR

KW - AMPK

KW - Fatty acid oxidation

KW - Muscle

KW - PGC-1

KW - PPARα

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JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 1

ER -

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

Abstract

Bibliographical note

Keywords

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