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Chronic AMPK activation via loss of FLCN induces functional beige adipose tissue through PGC-1α/ERRα

Ming Yan1, Étienne Audet-Walsh1, Sanaz Manteghi1

  • 1Goodman Cancer Research Centre, McGill University, Montréal, Quebec H3A 1A3, Canada; Department of Biochemistry, McGill University, Montréal, Quebec H3G 1Y6, Canada;

Genes & Development
|May 7, 2016
PubMed

Insights

Tumor suppressor folliculin (FLCN) loss reprograms fat metabolism, boosting energy expenditure and protecting against obesity. This involves chronic AMP-activated protein kinase (AMPK) activation, enhancing mitochondrial function.

Area of Science:

  • Metabolic regulation
  • Obesity research
  • Mitochondrial biology

Background:

  • The tumor suppressor folliculin (FLCN) interacts with AMP-activated protein kinase (AMPK), a key regulator of cellular energy.
  • Understanding FLCN's role in energy metabolism is crucial for metabolic disease research.

Purpose of the Study:

  • To investigate the function of FLCN in adipose tissue and its impact on energy metabolism.
  • To elucidate the molecular mechanisms by which FLCN influences metabolic reprogramming.

Main Methods:

  • Generation of an adipose-specific Flcn knockout mouse model (Adipoq-FLCN KO).
  • Analysis of metabolic parameters, energy expenditure, and response to high-fat diet (HFD).
  • Investigation of molecular pathways involving AMPK, PGC-1α, and ERRα in FLCN-deficient adipose tissue.

Main Results:

  • Loss of FLCN in adipose tissue leads to significant metabolic reprogramming and enhanced oxidative metabolism.
  • Adipoq-FLCN KO mice show increased energy expenditure and resistance to HFD-induced obesity.
  • FLCN ablation results in chronic AMPK hyperactivation, upregulating PGC-1α and ERRα, promoting mitochondrial biogenesis and activity.
  • Upregulation of mitochondrial uncoupling proteins and brown fat markers in FLCN-null adipose tissues enhances cold resistance.

Conclusions:

  • FLCN acts as a negative regulator of mitochondrial function in adipose tissue.
  • A novel AMPK/PGC-1α/ERRα pathway is identified, linking FLCN to the browning of white adipocytes and brown fat activity.
  • Targeting FLCN may offer therapeutic strategies for metabolic disorders and obesity.
Keywords:
brown fathigh-fat dietmetabolic reprogrammingnuclear receptorsobesitythermogenesis

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