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Increased apoptosis and browning of TAK1-deficient adipocytes protects against obesity

Antonia Sassmann-Schweda1, Pratibha Singh1, Cong Tang1

  • 1Department of Pharmacology and.

JCI Insight
|October 5, 2016
PubMed

Insights

Losing TGF-β-activated kinase 1 (TAK1) in fat cells reduces adipocyte numbers and increases energy expenditure. This finding suggests targeting TAK1 could be a novel obesity treatment strategy.

Area of Science:

  • Metabolic research
  • Cell biology
  • Obesity research

Background:

  • Obesity is a global health crisis with limited non-surgical treatment options.
  • Adipose tissue dysfunction plays a critical role in obesity and related metabolic disorders.

Purpose of the Study:

  • To investigate the role of TGF-β-activated kinase 1 (TAK1) in adipocytes regarding obesity.
  • To explore the therapeutic potential of targeting adipocyte TAK1 for obesity treatment.

Main Methods:

  • Generated mice with adipocyte-specific TAK1 deficiency.
  • Administered high-fat diets and leptin deficiency models to assess obesity resistance.
  • Analyzed adipocyte apoptosis, macrophage infiltration, and energy expenditure.

Main Results:

  • Loss of TAK1 in adipocytes increased adipocyte apoptosis and M2 macrophage infiltration.
  • Adipocyte-specific TAK1-deficient mice exhibited reduced adipocyte numbers and resistance to diet-induced obesity.
  • These mice showed increased energy expenditure, enhanced UCP1 expression, and improved glucose tolerance.

Conclusions:

  • Adipocyte TAK1 deficiency reduces adipocyte count and promotes white adipose tissue browning.
  • Targeting TAK1 in adipocytes presents a promising strategy for treating obesity and associated metabolic complications like diabetes.

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