title: Acute exercise induces a phenotypic switch in adipose tissue macrophage polarization in diet-induced obese rats.
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).
  
  
  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.
authors.affiliation: Department of Internal Medicine, State University of Campinas, 13081-970, Campinas, SP, Brazil.
authors.forename: Alexandre G
authors.initials: AG
authors.lastname: Oliveira
authors.forename: Tiago G
authors.initials: TG
authors.lastname: Araujo
authors.forename: Bruno M
authors.initials: BM
authors.lastname: Carvalho
authors.forename: Dioze
authors.initials: D
authors.lastname: Guadagnini
authors.forename: Guilherme Z
authors.initials: GZ
authors.lastname: Rocha
authors.forename: Renata A
authors.initials: RA
authors.lastname: Bagarolli
authors.forename: Jose Barreto C
authors.initials: JB
authors.lastname: Carvalheira
authors.forename: Mario J A
authors.initials: MJ
authors.lastname: Saad
mesh_terms: D017667:Adipocytes / Q000378:metabolism; D052436:Adipose Tissue, White / Q000166:cytology* / Q000378:metabolism; D000818:Animals; D018932:Chemokine CCL2 / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007375:Interleukin-1 / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D008070:Lipopolysaccharides / Q000097:blood; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D009765:Obesity / Q000378:metabolism*; D010641:Phenotype; D010805:Physical Conditioning, Animal; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D007328:Insulin; D007375:Interleukin-1; D008070:Lipopolysaccharides; D012333:RNA, Messenger; C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10