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Updated: Dec 8, 2025

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
07:46

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation

Published on: April 3, 2017

25.7K

Fgr kinase is required for proinflammatory macrophage activation during diet-induced obesity

Rebeca Acín-Pérez1,2, Salvador Iborra1,3, Yolanda Martí-Mateos1

  • 1Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.

Nature Metabolism
|September 18, 2020
PubMed

Insights

Mice lacking Fgr tyrosine kinase resist obesity by reducing proinflammatory macrophages. This discovery highlights a mitochondrial reactive oxygen species (ROS)-Fgr pathway crucial for obesity and related metabolic issues.

Area of Science:

  • Immunology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Proinflammatory macrophages and reactive oxygen species (ROS) are implicated in obesity development.
  • Fgr tyrosine kinase activation by ROS is a potential contributor to obesity.

Purpose of the Study:

  • To investigate the role of Fgr tyrosine kinase in high-fat diet (HFD)-induced obesity.
  • To elucidate the Fgr-ROS signaling pathway in metabolic regulation.

Main Methods:

  • Ablation of Fgr in mouse models.
  • Analysis of macrophage polarization, lipolysis, and liver fatty acid oxidation.
  • Bone marrow (BM)-derived cell transplantation experiments.
  • Mitochondrial peroxide scavenging.

Main Results:

  • Fgr ablation prevented HFD-induced obesity, insulin resistance, and liver steatosis in mice.
  • Systemic Fgr deficiency increased lipolysis and liver fatty acid oxidation.
  • Fgr knockout in BM cells conferred protection, and transfer of Fgr-expressing BM cells reversed protection.
  • Scavenging mitochondrial peroxides inhibited Fgr activation and prevented HFD-induced obesity.
  • Elevated Fgr expression in proinflammatory macrophages correlates with obesity in mice and humans.

Conclusions:

  • The mitochondrial ROS-Fgr kinase axis is a critical regulator of proinflammatory adipose tissue macrophage activation.
  • Targeting this pathway may offer therapeutic strategies for obesity, insulin resistance, and liver steatosis.

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