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Related Experiment Video

Updated: Jun 23, 2025

Author Spotlight: Illuminating New Avenues for Adipose Tissue Metabolism and Disease Prevention
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Short-term cold exposure induces persistent epigenomic memory in brown fat.

Shin-Ichi Inoue1, Matthew J Emmett2, Hee-Woong Lim3

  • 1Institute for Diabetes, Obesity, and Metabolism, and Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.

Cell Metabolism
|June 18, 2024
PubMed
Summary

Short-term cold exposure protects mice lacking histone deacetylase 3 (HDAC3) in brown adipose tissue (BAT) from lethal hypothermia. This protection involves a C/EBPβ-dependent epigenetic memory, enhancing thermogenic gene expression.

Keywords:
C/EBPβERRαHDAC3PGC-1αUCP1brown adipose tissuecold memorymitochondriaoxidative phosphorylationthermogenesis

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Area of Science:

  • Metabolism and Endocrinology
  • Epigenetics
  • Thermoregulation

Background:

  • Histone deacetylase 3 (HDAC3) is crucial for brown adipose tissue (BAT) function.
  • HDAC3 deficiency in BAT impairs thermogenic responses and cold survival.
  • The mechanisms underlying cold adaptation and memory in BAT are not fully understood.

Purpose of the Study:

  • To investigate whether short-term mild cold exposure (STEMCT) can protect HDAC3-deficient BAT mice from hypothermia.
  • To elucidate the molecular mechanisms, including key transcription factors and epigenetic changes, involved in this cold adaptation.
  • To determine the duration and underlying basis of this protective effect.

Main Methods:

  • Utilized HDAC3 BAT knockout (KO) mice and wild-type littermates.
  • Exposed mice to short-term mild cold temperature (15°C for 24 h) followed by acute cold challenge (4°C).
  • Assessed thermogenic gene expression (PGC-1α, UCP1) and the role of transcription factor C/EBPβ using genetic deletion and viral-mediated knockdown.

Main Results:

  • STEMCT conferred significant protection against lethal hypothermia in HDAC3 BAT KO mice.
  • Protection was associated with restored induction of PGC-1α and UCP1, dependent on these factors.
  • A persistent increase in the transcriptional activator C/EBPβ was observed for up to 7 days, mediating this cold-adaptive memory independently of HDAC3.

Conclusions:

  • Short-term mild cold exposure can establish a lasting protective memory in brown adipose tissue.
  • This memory is mediated by a C/EBPβ-dependent epigenetic mechanism, enhancing thermogenesis.
  • This finding reveals a novel HDAC3-independent pathway for cold adaptation in brown adipose tissue.