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 journalArticlepeer-review

15 Scopus citations


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
Issue number9
StatePublished - Sep 1 2015
Externally publishedYes


  • AMPK
  • Apolipoprotein a1
  • Mitochondria
  • Skeletal muscle

ASJC Scopus subject areas

  • Cell Biology


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