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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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FABP4 attenuates PPARγ and adipogenesis and is inversely correlated with PPARγ in adipose tissues

Tali Garin-Shkolnik1, Assaf Rudich, Gökhan S Hotamisligil

  • 1Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.

Diabetes
|December 10, 2013
PubMed

Insights

Fatty acid binding protein 4 (FABP4) promotes the breakdown of a key protein, PPARγ, hindering fat cell development. This discovery sheds light on obesity-related diseases like insulin resistance and atherosclerosis.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Metabolic Diseases

Background:

  • Fatty acid binding protein 4 (FABP4) is a cytoplasmic protein found in adipocytes and myeloid cells.
  • FABP4 is linked to the development of insulin resistance and atherosclerosis.
  • Peroxisome proliferator-activated receptor γ (PPARγ) is a crucial regulator of adipogenesis and insulin sensitivity.

Purpose of the Study:

  • To investigate the molecular mechanism by which FABP4 influences PPARγ activity.
  • To determine the role of FABP4 in regulating adipogenesis and its implications in metabolic diseases.

Main Methods:

  • Utilized FABP4-null mouse preadipocytes and macrophages.
  • Performed complementation assays to restore FABP4 expression.
  • Analyzed PPARγ expression and ubiquitination.
  • Assessed adipogenesis in wild-type and FABP4-null cells.
  • Compared FABP4 and PPARγ levels in human and mouse adipose tissues from healthy and obese diabetic individuals.

Main Results:

  • FABP4 was found to trigger the ubiquitination and proteasomal degradation of PPARγ.
  • FABP4-null cells showed increased PPARγ expression and enhanced adipogenesis.
  • FABP4 levels were higher and PPARγ levels lower in visceral fat compared to subcutaneous fat.
  • Elevated FABP4 and reduced PPARγ were observed in adipose tissues of obese diabetic individuals.

Conclusions:

  • FABP4 negatively regulates adipogenesis by promoting PPARγ degradation.
  • FABP4-mediated suppression of PPARγ in visceral fat contributes to obesity-related morbidities.
  • Targeting FABP4 may offer a therapeutic strategy for insulin resistance, diabetes, and atherosclerosis.

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