title: Exercise attenuates M1 macrophages and CD8+ T cells in the adipose tissue of obese mice.
abstract: OBJECTIVE
  Obesity is associated with adipose tissue inflammation, which has been attributed to changes in the number and types of leukocytes in adipose tissue. Exercise training is thought to be important for the reduction of adipose tissue inflammation, but the mechanisms by which this may occur are incompletely understood. Here, we evaluated the effect of exercise training on several inflammation-associated changes in adipose tissue, including infiltration of inflammatory macrophages and T cells.
  
  
  METHODS
  Four-week-old male C57BL/6J mice were randomly assigned to four groups that received a normal diet (ND) plus sedentary (n = 8), an ND plus exercise training (n = 8), a high-fat diet (HFD) plus sedentary (n = 12), and an HFD plus exercise training (n = 12). Mice were fed the ND or the HFD from 4 to 20 wk of age. Mice in the exercise groups ran on a treadmill for 60 min·d, 5 d·wk over the same points.
  
  
  RESULTS
  Mice fed the HFD had increased numbers of macrophage clusters in adipose tissue, which were reduced by exercise training. Similarly, adipose tissue from the HFD sedentary mice contained higher levels of tumor necrosis factor α mRNA and increased numbers of CD11c inflammatory macrophages and CD8 T cells than adipose tissue from the ND mice, and those were also lowered by exercise training. The mRNA levels of monocyte chemoattractant proteins 1 and 2 and macrophage inflammatory proteins 1α and 1β in adipose tissue were lower in the HFD exercise mice than those in the HFD sedentary mice.
  
  
  CONCLUSIONS
  The results suggest that exercise training reduces adipose tissue inflammation by suppressing infiltration of inflammatory macrophages and CD8 T cells.
authors: Graduate School of Sport Sciences, Waseda University, Tokorozawa, Saitama, Japan. kawanishinoriaki@akane.waseda.jp
authors: Noriaki
authors: N
authors: Kawanishi
authors: Tsubasa
authors: T
authors: Mizokami
authors: Hiromi
authors: H
authors: Yano
authors: Katsuhiko
authors: K
authors: Suzuki
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology*; D000818:Animals; D039521:CD11c Antigen / Q000032:analysis; D018414:CD8-Positive T-Lymphocytes; D018932:Chemokine CCL2 / Q000235:genetics; D054405:Chemokine CCL3 / Q000235:genetics; D054407:Chemokine CCL4 / Q000235:genetics; D054412:Chemokine CCL8 / Q000235:genetics; D059305:Diet, High-Fat; D018655:Lymphocyte Count; D008264:Macrophages / Q000737:chemistry; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000378:metabolism* / Q000473:pathology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D057185:Sedentary Behavior; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D039521:CD11c Antigen; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054412:Chemokine CCL8; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha