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Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells
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Published on: March 28, 2013

Inhibiting adipose tissue lipogenesis reprograms thermogenesis and PPARγ activation to decrease diet-induced obesity.

Irfan J Lodhi1, Li Yin, Anne P L Jensen-Urstad

  • 1Division of Endocrinology, Metabolism & Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA.

Cell Metabolism
|August 7, 2012
PubMed
Summary
This summary is machine-generated.

Fatty acid synthase (FAS) and PexRAP regulate fat production in cells, impacting obesity. Inhibiting these lipogenic enzymes may offer new treatments for obesity and diabetes.

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Area of Science:

  • Biochemistry
  • Metabolism
  • Cell Biology

Background:

  • De novo lipogenesis in adipocytes is not fully understood, particularly under high-fat diets.
  • Adipocyte lipid metabolism plays a crucial role in energy balance and obesity development.

Purpose of the Study:

  • To investigate the role of fatty acid synthase (FAS) and PexRAP in adipocyte lipogenesis and PPARγ activation.
  • To determine the potential of targeting this pathway for obesity and diabetes treatment.

Main Methods:

  • Mice lacking FAS in adult adipose tissue were studied.
  • FAS and PexRAP knockdown experiments were performed in embryonic fibroblasts and 3T3-L1 cells.
  • Alkyl ether phosphatidylcholine species were analyzed for association with PPARγ.

Main Results:

  • Mice lacking adipose FAS showed increased energy expenditure and resistance to diet-induced obesity.
  • FAS knockdown reduced PPARγ activity and adipogenesis.
  • PexRAP knockdown decreased PPARγ activity, adipogenesis, and diet-induced adiposity in mice.

Conclusions:

  • The adipocyte lipogenic pathway involving FAS and PexRAP modulates PPARγ activation and adiposity.
  • Inhibiting PexRAP or related lipogenic enzymes presents a potential therapeutic strategy for obesity and diabetes.