Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase

Parkyong Song, Yonghoon Kwon, Kyungmoo Yea, Hyo Youl Moon, Jong Hyuk Yoon, Jaewang Ghim, Hyunjung Hyun, Dayea Kim, Ara Koh, Per Olof Berggren, Pann Ghill Suh, Sung Ho Ryu

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Apolipoprotein a1, which is a major lipoprotein component of high-density lipoprotein (HDL), was reported to decrease plasma glucose in type 2 diabetes. Although recent studies also have shown that apolipoprotein a1 is involved in triglyceride (TG) metabolism, the mechanisms by which apolipoprotein a1 modulates TG levels remain largely unexplored. Here we demonstrated that apolipoprotein a1 increased mitochondrial DNA and mitochondria contents through sustained AMPK activation in myotubes. This resulted in enhanced fatty acid oxidation and attenuation of free fatty acid-induced insulin resistance features in skeletal muscle. The increment of mitochondria was mediated through induction of transcription factors, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and nuclear transcription factor 1 (NRF-1). The inhibition of AMPK by a pharmacological agent inhibited the induction of mitochondrial biogenesis. Increase of AMPK phosphorylation by apolipoprotein a1 occurs through activation of upstream kinase LKB1. Finally, we confirmed that scavenger receptor Class B, type 1 (SR-B1) is an important receptor for apolipoprotein a1 in stimulating AMPK pathway and mitochondrial biogenesis. Our study suggests that apolipoprotein a1 can alleviate obesity related metabolic disease by inducing AMPK dependent mitochondrial biogenesis.

Original languageEnglish (US)
Pages (from-to)1873-1881
Number of pages9
JournalCellular Signalling
Volume27
Issue number9
DOIs
StatePublished - Sep 1 2015
Externally publishedYes

Fingerprint

AMP-Activated Protein Kinases
Apolipoprotein A-I
Organelle Biogenesis
Mitochondria
Triglycerides
Transcription Factors
NFI Transcription Factors
CD36 Antigens
Metabolic Diseases
Skeletal Muscle Fibers
HDL Lipoproteins
Mitochondrial DNA
Nonesterified Fatty Acids
Type 2 Diabetes Mellitus
Lipoproteins
Insulin Resistance
Skeletal Muscle
Phosphotransferases
Fatty Acids
Obesity

Keywords

  • AMPK
  • Apolipoprotein a1
  • Mitochondria
  • Skeletal muscle

ASJC Scopus subject areas

  • Cell Biology

Cite this

Song, P., Kwon, Y., Yea, K., Moon, H. Y., Yoon, J. H., Ghim, J., ... Ryu, S. H. (2015). Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase. Cellular Signalling, 27(9), 1873-1881. https://doi.org/10.1016/j.cellsig.2015.05.003

Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase. / Song, Parkyong; Kwon, Yonghoon; Yea, Kyungmoo; Moon, Hyo Youl; Yoon, Jong Hyuk; Ghim, Jaewang; Hyun, Hyunjung; Kim, Dayea; Koh, Ara; Berggren, Per Olof; Suh, Pann Ghill; Ryu, Sung Ho.

In: Cellular Signalling, Vol. 27, No. 9, 01.09.2015, p. 1873-1881.

Research output: Contribution to journalArticle

Song, P, Kwon, Y, Yea, K, Moon, HY, Yoon, JH, Ghim, J, Hyun, H, Kim, D, Koh, A, Berggren, PO, Suh, PG & Ryu, SH 2015, 'Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase', Cellular Signalling, vol. 27, no. 9, pp. 1873-1881. https://doi.org/10.1016/j.cellsig.2015.05.003
Song, Parkyong ; Kwon, Yonghoon ; Yea, Kyungmoo ; Moon, Hyo Youl ; Yoon, Jong Hyuk ; Ghim, Jaewang ; Hyun, Hyunjung ; Kim, Dayea ; Koh, Ara ; Berggren, Per Olof ; Suh, Pann Ghill ; Ryu, Sung Ho. / Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase. In: Cellular Signalling. 2015 ; Vol. 27, No. 9. pp. 1873-1881.
@article{000433a994c34ac39ae637c99a962b75,
title = "Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase",
abstract = "Apolipoprotein a1, which is a major lipoprotein component of high-density lipoprotein (HDL), was reported to decrease plasma glucose in type 2 diabetes. Although recent studies also have shown that apolipoprotein a1 is involved in triglyceride (TG) metabolism, the mechanisms by which apolipoprotein a1 modulates TG levels remain largely unexplored. Here we demonstrated that apolipoprotein a1 increased mitochondrial DNA and mitochondria contents through sustained AMPK activation in myotubes. This resulted in enhanced fatty acid oxidation and attenuation of free fatty acid-induced insulin resistance features in skeletal muscle. The increment of mitochondria was mediated through induction of transcription factors, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and nuclear transcription factor 1 (NRF-1). The inhibition of AMPK by a pharmacological agent inhibited the induction of mitochondrial biogenesis. Increase of AMPK phosphorylation by apolipoprotein a1 occurs through activation of upstream kinase LKB1. Finally, we confirmed that scavenger receptor Class B, type 1 (SR-B1) is an important receptor for apolipoprotein a1 in stimulating AMPK pathway and mitochondrial biogenesis. Our study suggests that apolipoprotein a1 can alleviate obesity related metabolic disease by inducing AMPK dependent mitochondrial biogenesis.",
keywords = "AMPK, Apolipoprotein a1, Mitochondria, Skeletal muscle",
author = "Parkyong Song and Yonghoon Kwon and Kyungmoo Yea and Moon, {Hyo Youl} and Yoon, {Jong Hyuk} and Jaewang Ghim and Hyunjung Hyun and Dayea Kim and Ara Koh and Berggren, {Per Olof} and Suh, {Pann Ghill} and Ryu, {Sung Ho}",
year = "2015",
month = "9",
day = "1",
doi = "10.1016/j.cellsig.2015.05.003",
language = "English (US)",
volume = "27",
pages = "1873--1881",
journal = "Cellular Signalling",
issn = "0898-6568",
publisher = "Elsevier Inc.",
number = "9",

}

TY - JOUR

T1 - Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase

AU - Song, Parkyong

AU - Kwon, Yonghoon

AU - Yea, Kyungmoo

AU - Moon, Hyo Youl

AU - Yoon, Jong Hyuk

AU - Ghim, Jaewang

AU - Hyun, Hyunjung

AU - Kim, Dayea

AU - Koh, Ara

AU - Berggren, Per Olof

AU - Suh, Pann Ghill

AU - Ryu, Sung Ho

PY - 2015/9/1

Y1 - 2015/9/1

N2 - Apolipoprotein a1, which is a major lipoprotein component of high-density lipoprotein (HDL), was reported to decrease plasma glucose in type 2 diabetes. Although recent studies also have shown that apolipoprotein a1 is involved in triglyceride (TG) metabolism, the mechanisms by which apolipoprotein a1 modulates TG levels remain largely unexplored. Here we demonstrated that apolipoprotein a1 increased mitochondrial DNA and mitochondria contents through sustained AMPK activation in myotubes. This resulted in enhanced fatty acid oxidation and attenuation of free fatty acid-induced insulin resistance features in skeletal muscle. The increment of mitochondria was mediated through induction of transcription factors, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and nuclear transcription factor 1 (NRF-1). The inhibition of AMPK by a pharmacological agent inhibited the induction of mitochondrial biogenesis. Increase of AMPK phosphorylation by apolipoprotein a1 occurs through activation of upstream kinase LKB1. Finally, we confirmed that scavenger receptor Class B, type 1 (SR-B1) is an important receptor for apolipoprotein a1 in stimulating AMPK pathway and mitochondrial biogenesis. Our study suggests that apolipoprotein a1 can alleviate obesity related metabolic disease by inducing AMPK dependent mitochondrial biogenesis.

AB - Apolipoprotein a1, which is a major lipoprotein component of high-density lipoprotein (HDL), was reported to decrease plasma glucose in type 2 diabetes. Although recent studies also have shown that apolipoprotein a1 is involved in triglyceride (TG) metabolism, the mechanisms by which apolipoprotein a1 modulates TG levels remain largely unexplored. Here we demonstrated that apolipoprotein a1 increased mitochondrial DNA and mitochondria contents through sustained AMPK activation in myotubes. This resulted in enhanced fatty acid oxidation and attenuation of free fatty acid-induced insulin resistance features in skeletal muscle. The increment of mitochondria was mediated through induction of transcription factors, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and nuclear transcription factor 1 (NRF-1). The inhibition of AMPK by a pharmacological agent inhibited the induction of mitochondrial biogenesis. Increase of AMPK phosphorylation by apolipoprotein a1 occurs through activation of upstream kinase LKB1. Finally, we confirmed that scavenger receptor Class B, type 1 (SR-B1) is an important receptor for apolipoprotein a1 in stimulating AMPK pathway and mitochondrial biogenesis. Our study suggests that apolipoprotein a1 can alleviate obesity related metabolic disease by inducing AMPK dependent mitochondrial biogenesis.

KW - AMPK

KW - Apolipoprotein a1

KW - Mitochondria

KW - Skeletal muscle

UR - http://www.scopus.com/inward/record.url?scp=84934443863&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84934443863&partnerID=8YFLogxK

U2 - 10.1016/j.cellsig.2015.05.003

DO - 10.1016/j.cellsig.2015.05.003

M3 - Article

AN - SCOPUS:84934443863

VL - 27

SP - 1873

EP - 1881

JO - Cellular Signalling

JF - Cellular Signalling

SN - 0898-6568

IS - 9

ER -