title: Voluntary exercise ameliorates the progression of atherosclerotic lesion formation via anti-inflammatory effects in apolipoprotein E-deficient mice.
abstract: OBJECTIVE
  A sedentary lifestyle with insufficient exercise is associated with cardiovascular disease. Previous studies have demonstrated that endurance exercise benefits atherosclerosis and cardiovascular disorders; however, the mechanisms by which physical activity, such as voluntary exercise (Ex), produces these effects are not fully understood.
  
  
  RESULTS
  Eight-week-old male apolipoprotein (ApoE)-deficient mice were fed a standard diet (STD) or high fat diet (HFD) for 10 weeks. The HFD+Ex group mice performed Ex on a running wheel for 10 weeks. No significant differences in lipid profiles were observed between the HFD and HFD+Ex groups. Although changes in body and brown adipose tissue weights were comparable between the HFD and HFD+Ex groups, white adipose tissue weight was significantly lower in the HFD+Ex group than in the HFD group. The areas of atherosclerotic lesions in the aortic sinus and thoracoabdominal aorta were significantly reduced in the HFD+Ex group than in the HFD group (p<0.001). There was a strong negative correlation between atherosclerotic areas and the mean running distance per day in the HFD+Ex group (r=-0.90, p=0.01). Endothelial function was significantly preserved in the HFD+Ex group (p<0.05). Serum interleukin-6 and macrophage chemoattractant protein-1 levels were significantly lower and those of adiponectin were significantly higher in the HFD+Ex group than in the HFD group (p<0.05).
  
  
  CONCLUSIONS
  These results suggest that Ex ameliorates the progression of endothelial dysfunction and atherosclerotic lesion formation through anti-inflammatory effects, despite continued consumption of HFD.
authors.affiliation: Department of Cardiovascular Medicine, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: Kosuke
authors.initials: K
authors.lastname: Fukao
authors.forename: Kazunori
authors.initials: K
authors.lastname: Shimada
authors.forename: Hisashi
authors.initials: H
authors.lastname: Naito
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Sumiyoshi
authors.forename: Nao
authors.initials: N
authors.lastname: Inoue
authors.forename: Takafumi
authors.initials: T
authors.lastname: Iesaki
authors.forename: Atsumi
authors.initials: A
authors.lastname: Kume
authors.forename: Takashi
authors.initials: T
authors.lastname: Kiyanagi
authors.forename: Makoto
authors.initials: M
authors.lastname: Hiki
authors.forename: Kuniaki
authors.initials: K
authors.lastname: Hirose
authors.forename: Rie
authors.initials: R
authors.lastname: Matsumori
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Ohsaka
authors.forename: Yasue
authors.initials: Y
authors.lastname: Takahashi
authors.forename: Saori
authors.initials: S
authors.lastname: Toyoda
authors.forename: Seigo
authors.initials: S
authors.lastname: Itoh
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Miyazaki
authors.forename: Norihiro
authors.initials: N
authors.lastname: Tada
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Daida
mesh_terms: D052436:Adipose Tissue, White; D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency*; D050197:Atherosclerosis / Q000473:pathology* / Q000517:prevention & control; D016207:Cytokines; D004041:Dietary Fats / Q000494:pharmacology; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000503:physiopathology; D007249:Inflammation / Q000517:prevention & control*; D051379:Mice; D010805:Physical Conditioning, Animal
chemical_list: D001057:Apolipoproteins E; D016207:Cytokines; D004041:Dietary Fats