Acute exercise induces a phenotypic switch in adipose tissue macrophage polarization in diet-induced obese rats

Obesity (Silver Spring). 2013 Dec;21(12):2545-56. doi: 10.1002/oby.20402. Epub 2013 Jun 11.

Abstract

Objective: It has become clear that exercise may be a useful therapy in the insulin resistance treatment, as it has anti-inflammatory effects and improves insulin sensitivity. However, it remains uncertain whether exercise affects the adipocytes or infiltrated macrophages. Thus, the aim was to investigate the effects of acute exercise on the inflammatory status and insulin signaling of the white adipose tissue (WAT) fractions (stromal-vascular fraction [SVF] and adipocytes).

Design and methods: The effect of acute swimming exercise was investigated on insulin sensitivity, insulin signaling, inflammatory pathways in the WAT fractions of high-fat fed Wistar rats. Additionally, macrophage infiltration and polarization were analyzed in the WAT.

Results: Acute exercise can improve insulin signaling in WAT fractions, along with a phenotypic switch from M1- to M2-macrophages in obese rats, as indicated by a marked increase in macrophage galactose-type C-type lectin 1-positive cells in WAT was observed. Additionally, exercise promoted a reduction in circulating levels of lipopolysaccharide, and toll-like receptor 4 activity along with TNF-alpha, IL-1-beta and MCP-1 mRNA levels in WAT fractions.

Conclusions: These data suggest that acute exercise improves insulin signaling in the WAT, at least in part by inducing macrophage polarization toward the M2-state.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / metabolism
  • Adipose Tissue, White / cytology*
  • Adipose Tissue, White / metabolism
  • Animals
  • Chemokine CCL2 / blood
  • Diet, High-Fat / adverse effects*
  • Insulin / blood
  • Insulin Resistance
  • Interleukin-1 / blood
  • Interleukin-10 / blood
  • Lipopolysaccharides / blood
  • Macrophages / metabolism*
  • Male
  • Obesity / metabolism*
  • Phenotype
  • Physical Conditioning, Animal*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Signal Transduction
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Ccl2 protein, rat
  • Chemokine CCL2
  • Insulin
  • Interleukin-1
  • Lipopolysaccharides
  • RNA, Messenger
  • Tlr4 protein, rat
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Interleukin-10