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Adipocyte ALK7 links nutrient overload to catecholamine resistance in obesity

Tingqing Guo1, Patricia Marmol2, Annalena Moliner3

  • 1Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden Department of Physiology, National University of Singapore, Singapore, Singapore.

Elife
|August 28, 2014
PubMed

Insights

Targeted disruption of ALK7 alleviates diet-induced obesity by enhancing beta-adrenergic signaling in adipose tissue. This improves lipolysis and lipid oxidation, offering a potential therapeutic target for obesity.

Area of Science:

  • Metabolism and Endocrinology
  • Cell Biology
  • Obesity Research

Background:

  • Obesity is linked to reduced lipolysis and lipid oxidation in adipose tissue due to blunted beta-adrenoreceptor (β-AR) signaling.
  • The precise mechanisms connecting nutrient overload to catecholamine resistance in obesity remain unclear.

Purpose of the Study:

  • To investigate the role of TGF-β superfamily receptor ALK7 in diet-induced catecholamine resistance and obesity.
  • To explore ALK7 as a potential therapeutic target for obesity.

Main Methods:

  • Utilized global and fat-specific Alk7 knock-out mouse models.
  • Administered high-fat diets to induce obesity.
  • Employed chemical-genetic approaches for acute ALK7 inhibition in adult mice.
  • Assessed β-AR expression, β-adrenergic signaling, lipolysis, lipid oxidation, and mitochondrial biogenesis in adipose tissue.
  • Investigated ALK7 effects in both mouse and human adipocytes.

Main Results:

  • Targeted disruption of ALK7 in mice reduced diet-induced obesity.
  • Alk7 deficiency enhanced adipose β-AR expression, signaling, lipolysis, and lipid oxidation under high-fat diet conditions.
  • Activation of ALK7 inhibited β-AR signaling and lipolysis in adipocytes.
  • Acute ALK7 inhibition in adult mice decreased weight gain, fat accumulation, and adipocyte size while enhancing lipolysis and β-adrenergic signaling.

Conclusions:

  • ALK7 signaling contributes to diet-induced catecholamine resistance in adipose tissue.
  • Inhibition of ALK7 may represent a novel therapeutic strategy for managing human obesity.
Keywords:
TGF-betaadipose tissuebeta-adrenergicchemical-geneticlipolysisobesity

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