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Cellular Feimin promotes cold-induced thermogenesis.

Ying Peng1, Xiaoliu Shi1, Yazhuo Wang1

  • 1State Key Laboratory of Membrane Biology, Ministry of Education Key Laboratory of Bioinformatics, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.

Proceedings of the National Academy of Sciences of the United States of America
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Scientists discovered Feimin, a protein crucial for adaptive thermogenesis (energy expenditure). It links AMPK signaling to gene control in fat tissue, offering a new target for obesity treatments.

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Area of Science:

  • Metabolic Regulation
  • Molecular Endocrinology
  • Obesity Research

Background:

  • Adaptive thermogenesis is vital for preventing obesity by dissipating energy.
  • Molecular links between energy sensing and gene expression in thermogenesis are not fully understood.

Purpose of the Study:

  • To identify key molecular players connecting energy sensing to transcriptional control in adaptive thermogenesis.
  • To elucidate the role of Feimin in regulating thermogenesis and its potential as an obesity therapeutic target.

Main Methods:

  • Investigated Feimin's role in adipose tissue using molecular biology techniques.
  • Utilized cold exposure and diet-induced obesity models in mice.
  • Examined protein interactions and subcellular localization via phosphorylation and nuclear translocation assays.
  • Performed adipose-specific Feimin knockout studies.

Main Results:

  • Feimin acts as a crucial activator of adaptive thermogenesis, linking AMP-activated protein kinase (AMPK) signaling to nuclear transcriptional regulation.
  • AMPK phosphorylates Feimin upon cold exposure, promoting its nuclear translocation and interaction with PGC1α to enhance thermogenic gene expression.
  • Obesity reduces Feimin phosphorylation and nuclear localization, impairing thermogenic capacity. Adipose-specific Feimin knockout exacerbates diet-induced obesity and abolishes cold-induced thermogenesis.

Conclusions:

  • Identified an AMPK-Feimin-PGC1α signaling axis essential for adaptive thermogenesis in adipose tissue.
  • Feimin's nuclear translocation, regulated by AMPK, is critical for thermogenic gene activation.
  • Feimin represents a promising therapeutic target for metabolic disorders like obesity.