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Critical roles of the p160 transcriptional coactivators p/CIP and SRC-1 in energy balance

Zhiyong Wang1, Chao Qi, Anna Krones

  • 1Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA. zwang@salk.edu

Cell Metabolism
|February 7, 2006
PubMed

Insights

Mice lacking SRC-1 and p/CIP coactivators show impaired brown fat development and thermogenesis. These mice are lean and resistant to obesity, highlighting the coactivators

Area of Science:

  • Molecular Endocrinology
  • Metabolic Regulation
  • Adipogenesis

Background:

  • Transcriptional coactivators modulate nuclear hormone receptor activity in vitro.
  • The physiological roles of coactivators like SRC-1 and p/CIP in energy homeostasis are largely unknown.

Purpose of the Study:

  • To investigate the in vivo function of SRC-1 and p/CIP in energy balance.
  • To determine the role of these coactivators in adaptive thermogenesis and diet-induced obesity.

Main Methods:

  • Generation and analysis of mice lacking both SRC-1 and p/CIP (p160 family coactivators).
  • Assessment of brown fat development, adaptive thermogenesis, energy intake, and metabolic rate.
  • Evaluation of PPARgamma target gene induction related to adipogenesis and mitochondrial uncoupling.

Main Results:

  • p160-deficient mice exhibit developmental arrest in brown fat and defective adaptive thermogenesis.
  • Absence of SRC-1 and p/CIP leads to increased food intake but prevents obesity due to reduced leptin levels.
  • These mice display increased basal metabolic rates and physical activity, conferring leanness and obesity resistance.

Conclusions:

  • SRC-1 and p/CIP are critical regulators of energy balance.
  • These coactivators control both energy intake and energy expenditure through PPARgamma target gene regulation.
  • Deficiency in SRC-1 and p/CIP impacts adipogenesis and mitochondrial uncoupling, affecting overall metabolic health.

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