Macrophage-colony stimulating factor in obese adipose tissue: studies with heterozygous op/+ mice

Satoshi Sugita1, Yasutomi Kamei, Jun-Ichiro Oka

  • 1Department of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kanda-surugadai, Tokyo 101-0062, Japan.

Abstract

Insights

Macrophage-colony stimulating factor (M-CSF) gene expression remains unchanged in obese mice. Decreased M-CSF signaling did not significantly impact obesity or macrophage recruitment in adipose tissue.

Area of Science:

  • Immunology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Obesity is associated with chronic inflammation in adipose tissue, involving macrophage infiltration.
  • Macrophage-colony stimulating factor (M-CSF) is crucial for monocyte and macrophage development and function.

Purpose of the Study:

  • To investigate M-CSF gene expression in diet-induced and genetically obese mice.
  • To determine the role of M-CSF signaling in obesity susceptibility and adipose tissue macrophage recruitment.

Main Methods:

  • Quantitative real-time PCR and ELISA were used to measure M-CSF and MCP-1 levels in adipose tissue.
  • Mice with reduced M-CSF expression (op/+ heterozygotes) were subjected to high-fat diets or crossed with obese models (KKA(y)).
  • Macrophage marker gene expression (F4/80, CD68) in adipose tissue was analyzed.

Main Results:

  • M-CSF expression showed no significant alteration in diet-induced or genetically obese mice (KKA(y), ob/ob).
  • Mice with reduced M-CSF signaling (op/+) did not exhibit increased obesity or altered macrophage marker gene expression in adipose tissue.
  • Monocyte chemoattractant protein-1 (MCP-1) levels were also unchanged.

Conclusions:

  • M-CSF expression is not significantly altered in the adipose tissue of obese mice.
  • Reduced M-CSF signaling does not play a major role in macrophage recruitment into adipose tissue during obesity.
  • These findings suggest M-CSF is not a primary driver of adipose tissue inflammation in obesity.

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