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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

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

Published on: June 3, 2016

Adipogenesis and insulin sensitivity in obesity are regulated by retinoid-related orphan receptor gamma

Bettina Meissburger1, Jozef Ukropec, Eva Roeder

  • 1ETH Zürich, Institute of Food Nutrition and Health, Schwerzenbach, Switzerland.

EMBO Molecular Medicine
|August 20, 2011
PubMed

Insights

Retinoid-related orphan receptor gamma (RORγ) negatively regulates fat cell development. Blocking RORγ improves insulin sensitivity and protects against obesity-related metabolic disorders like type 2 diabetes.

Area of Science:

  • Metabolic disease research
  • Molecular endocrinology
  • Adipocyte biology

Background:

  • Obesity is a major risk factor for metabolic complications, including type 2 diabetes.
  • However, not all obese individuals develop metabolic disorders, suggesting underlying regulatory mechanisms.
  • Identifying factors that control adipocyte function is crucial for understanding metabolic health.

Purpose of the Study:

  • To investigate the role of retinoid-related orphan receptor gamma (RORγ) in regulating adipocyte differentiation and function.
  • To determine if RORγ influences insulin sensitivity and metabolic health in obesity.
  • To explore RORγ as a potential therapeutic target for obesity-associated insulin resistance.

Main Methods:

  • Investigated RORγ's role in adipocyte differentiation using mouse models (Rorγ-deficient mice).
  • Analyzed adipocyte size, insulin sensitivity, and metabolic parameters (hyperglycemia, insulin resistance) in obese Rorγ(-/-) mice.
  • Examined RORγ expression in adipose tissue from obese human subjects and correlated it with adipocyte size and insulin sensitivity.

Main Results:

  • RORγ acts as a negative regulator of adipocyte differentiation, partly via its target gene matrix metalloproteinase 3.
  • Rorγ-deficient mice exhibited enhanced adipocyte progenitor cell differentiation and smaller adipocytes when obese.
  • Obese Rorγ(-/-) mice showed improved insulin sensitivity, better free fatty acid control, and protection against hyperglycemia and insulin resistance.
  • In humans, RORγ expression in adipose tissue correlated with adipocyte size and inversely with adipogenesis and insulin sensitivity.

Conclusions:

  • RORγ controls adipogenesis and adipocyte size, thereby modulating insulin sensitivity in obesity.
  • RORγ is identified as a key factor linking obesity to insulin resistance.
  • RORγ represents a promising novel pharmaceutical target for treating obesity-associated insulin resistance.

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