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Dexras1 mediates glucocorticoid-associated adipogenesis and diet-induced obesity

Jiyoung Y Cha1, Hyo Jung Kim, Jung Hwan Yu

  • 1The Solomon H. Snyder Department of Neuroscience and Departments of Psychiatry and Behavioral Sciences and Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD 21205.

Proceedings of the National Academy of Sciences of the United States of America
|December 4, 2013
PubMed

Insights

Dexras1 protein mediates fat cell formation (adipogenesis) and diet-induced obesity. Its absence reduces adiposity and weight gain, highlighting its role in metabolic disease.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Metabolic Research

Background:

  • Adipogenesis, the process of fat cell development, is linked to obesity and influenced by glucocorticoids through unclear pathways.
  • Dexras1, a Ras family small G protein, is significantly induced by the synthetic glucocorticoid dexamethasone.

Purpose of the Study:

  • To investigate the role of Dexras1 in mediating adipogenesis and diet-induced obesity.
  • To elucidate the mechanism by which glucocorticoids regulate fat cell differentiation.

Main Methods:

  • Utilizing 3T3-L1 cells to study adipogenesis with Dexras1 depletion and overexpression.
  • Employing mouse embryonic fibroblasts from Dexras1-deleted mice.
  • Analyzing adiposity and diet-induced weight gain in wild-type and Dexras1-deleted mice.

Main Results:

  • Dexras1 depletion abolished adipogenic differentiation in 3T3-L1 cells.
  • Overexpression of Dexras1 promoted adipogenesis.
  • Adipogenesis was significantly reduced in Dexras1-deleted mouse embryonic fibroblasts.
  • Mutant mice exhibited diminished adiposity and reduced weight gain upon high-fat diet.

Conclusions:

  • Dexras1 is a key mediator of adipogenesis and diet-induced obesity.
  • Targeting Dexras1 may offer a therapeutic strategy for obesity and related metabolic disorders.
Keywords:
Cushing diseasecyclic AMPinsulinnitric oxide

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