C-C chemokine receptor type 5 activation stimulates adipocyte differentiation through ERK-dependent pathway

  • 0Institute of Physiology, College of Medicine, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.

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Summary

This summary is machine-generated.

CCR5 activation by RANTES promotes adipocyte differentiation and obesity through an ERK-dependent pathway. Blocking CCR5 inhibits these effects, highlighting its role in obesity development.

Area Of Science

  • Metabolism and Endocrinology
  • Immunology and Inflammation

Background

  • Obesity is linked to chronic inflammation, with elevated RANTES and CCR5 mRNA in visceral adipose tissue of obese individuals.
  • The specific role of CCR5 activation in obesity pathogenesis remains incompletely understood.

Purpose Of The Study

  • To investigate the impact of CCR5 activation on adipogenesis.
  • To elucidate the regulatory mechanisms underlying CCR5's role in obesity.

Main Methods

  • Utilized 3T3-F442A preadipocytes and primary preadipocytes from wild-type (WT) and CCR5 knockout (CCR5-/-) mice.
  • Administered RANTES, CCR5 inhibitor (maraviroc), and ERK inhibitor (PD98059) to assess adipocyte differentiation.
  • Fed WT and CCR5-/- mice normal chow or high-fat diets to evaluate in vivo effects on obesity.

Main Results

  • RANTES treatment increased triglyceride accumulation and adipogenic gene expression (PPARγ, C/EBPα, aP2) in differentiating adipocytes.
  • CCR5 inhibition and ERK pathway blockade attenuated RANTES-induced adipocyte differentiation.
  • WT mice on high-fat diets exhibited increased RANTES, adipose CCR5 expression, and obesity, unlike CCR5-/- mice.

Conclusions

  • CCR5 activation by RANTES enhances adipocyte differentiation via an ERK-dependent mechanism.
  • CCR5 plays a significant role in high-fat diet-induced obesity development.

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