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Novel phosphorylation of PPARγ ameliorates obesity-induced adipose tissue inflammation and improves insulin

Sunsil Choi1, Ji-Eun Jung1, Yong Ryoul Yang1

  • 1Department of Biological Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan 689-798, Korea.

Cellular Signalling
|September 20, 2015
PubMed

Insights

PPARγ phosphorylation in adipose tissue regulates inflammation and insulin resistance. Inhibiting c-Src kinase worsens insulin sensitivity, highlighting PPARγ modification as a therapeutic target for diabetes.

Area of Science:

  • Metabolism and Endocrinology
  • Molecular Biology
  • Immunology

Background:

  • Chronic inflammation in adipose tissue is linked to insulin resistance.
  • Peroxisome proliferator-activated receptor gamma (PPARγ) plays a role in metabolic regulation.

Purpose of the Study:

  • To investigate the role of PPARγ modification in adipose tissue inflammation and insulin resistance.
  • To elucidate the mechanism by which c-Src kinase and PTP-1B regulate PPARγ activity.

Main Methods:

  • Investigated PPARγ phosphorylation at Tyr78 by c-Src kinase and dephosphorylation by PTP-1B in adipocytes.
  • Assessed the impact of PPARγ phosphorylation on pro-inflammatory gene expression and chemokine/cytokine secretion.
  • Examined the effect of c-Src kinase inhibition on insulin resistance and adipose tissue inflammation in obese mice.

Main Results:

  • c-Src kinase phosphorylates PPARγ at Tyr78, a process reversed by PTP-1B.
  • PPARγ phosphorylation suppresses pro-inflammatory gene expression and reduces macrophage migration.
  • Inhibition of c-Src kinase exacerbates insulin resistance and increases adipose tissue inflammation in obese mice.

Conclusions:

  • PPARγ phosphorylation is a key regulator of adipose tissue inflammatory responses.
  • This mechanism is critically associated with glucose tolerance and insulin sensitivity.
  • Findings provide insights for developing novel anti-diabetic drugs targeting PPARγ phosphorylation.
Keywords:
InflammationMetabolic disordersPPARγPTP-1BPhosphorylationc-Src

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