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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

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HO-1 inhibits preadipocyte proliferation and differentiation at the onset of obesity via ROS dependent activation of

Gabriel Wagner1, Josefine Lindroos-Christensen1, Elisa Einwallner1

  • 1Department of Laboratory Medicine, Medical University of Vienna, 1090 Vienna, Austria.

Scientific Reports
|January 20, 2017
PubMed

Insights

Heme Oxygenase-1 (HO-1) inhibits white adipose tissue expansion by reducing precursor proliferation and differentiation. Deleting HO-1 in mice worsened obesity-related adipose tissue growth, highlighting HO-1

Area of Science:

  • Metabolism and Endocrinology
  • Molecular Biology
  • Obesity Research

Background:

  • Excessive white adipose tissue (WAT) accumulation is a key feature of obesity.
  • The molecular mechanisms driving WAT expansion, including adipose precursor proliferation and differentiation, are not fully understood.

Purpose of the Study:

  • To identify early molecular events in adipose precursors during high-fat diet (HFD) induced obesity.
  • To investigate the role of Heme Oxygenase-1 (HO-1) in regulating adipose precursor behavior and adipogenesis.

Main Methods:

  • Unbiased transcriptomics analysis of mouse adipose precursors after HFD.
  • Genetic deletion of HO-1 in adipose precursors (Hmox1fl/flPdgfraCre mice).
  • In vitro studies on human preadipocytes to assess HO-1 modulation effects.

Main Results:

  • Heme Oxygenase-1 (HO-1) was identified as upregulated in adipose precursors upon HFD.
  • Specific deletion of HO-1 enhanced HFD-induced visceral adipose precursor proliferation and differentiation.
  • HO-1 was found to reduce HFD-induced AKT2 phosphorylation via mitochondrial ROS, inhibiting adipogenesis upstream of Cebpα and PPARγ.

Conclusions:

  • HO-1 acts as a crucial inhibitor of adipogenesis by modulating ROS and AKT2 signaling.
  • HO-1 plays a cell-autonomous role in limiting adipose precursor proliferation and differentiation.
  • Modulating HO-1 offers a potential therapeutic target for managing obesity-related adipose tissue expansion.

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