title: Obesity suppresses circulating level and function of endothelial progenitor cells and heart function.
abstract: OBJECTIVE
  This study tested the hypothesis that obesity suppresses circulating number as well as the function of endothelial progenitor cells (EPCs) and left ventricular ejection fraction (LVEF).
  
  
  METHODS
  High fat diet (45 Kcal% fat) was given to 8-week-old C57BL/6 J mice (n = 8) for 20 weeks to induce obesity (group 1). Another age-matched group (n = 8) were fed with control diet for 20 weeks as controls (group 2). The animals were sacrificed at the end of 20 weeks after obesity induction.
  
  
  RESULTS
  By the end of study period, the heart weight, body weight, abdominal fat weight, serum levels of total cholesterol and fasting blood sugar were remarkably higher in group 1 than in group 2 (all p<0.01). The circulating level of EPCs (C-kit/CD31, Sca-1/KDR, CXCR4/CD34) was significantly lower in group 1 than in group 2 (p<0.03) at 18 h after critical limb ischemia induction. The angiogenesis and migratory ability of bone marrow-derived EPCs was remarkably impaired in group 1 compared to that in group 2 (all p<0.01). The repair ability of aortic endothelium damage by lipopolysaccharide was notably attenuated in group 1 compared with that in group 2 (p<0.01). Collagen deposition (Sirius red staining) and fibrotic area (Masson's Trichrome staining) in LV myocardium were notably increased in group 1 compared with group 2 (p<0.001). LVEF was notably lower, whereas LV end-diastolic and end-systolic dimensions were remarkably higher in group 1 than in group 2 (all p<0.001).
  
  
  CONCLUSIONS
  Obesity diminished circulating EPC level, impaired the recovery of damaged endothelium, suppressed EPC angiogenesis ability and LVEF, and increased LV remodeling.
authors: Division of Cardiology, Department of Internal Medicine; Chang Gung Memorial Hospital- Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
authors: Tzu-Hsien
authors: TH
authors: Tsai
authors: Han-Tan
authors: HT
authors: Chai
authors: Cheuk-Kwan
authors: CK
authors: Sun
authors: Chia-Hung
authors: CH
authors: Yen
authors: Steve
authors: S
authors: Leu
authors: Yung-Lung
authors: YL
authors: Chen
authors: Sheng-Ying
authors: SY
authors: Chung
authors: Sheung-Fat
authors: SF
authors: Ko
authors: Hsueh-Wen
authors: HW
authors: Chang
authors: Chiung-Jen
authors: CJ
authors: Wu
authors: Hon-Kan
authors: HK
authors: Yip
mesh_terms: D000818:Animals; D001011:Aorta / Q000000981:diagnostic imaging / Q000473:pathology; D001391:Azo Compounds / Q000378:metabolism; D054443:Cell Migration Assays; D002465:Cell Movement; D049109:Cell Proliferation; D003094:Collagen / Q000378:metabolism; D004452:Echocardiography; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology*; D004801:Eosine Yellowish-(YS) / Q000378:metabolism; D005121:Extremities / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D005355:Fibrosis; D005455:Fluorescent Antibody Technique; D006321:Heart / Q000503:physiopathology*; D006334:Heart Function Tests; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D007511:Ischemia / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008739:Methyl Green / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000473:pathology; D018919:Neovascularization, Physiologic; D009569:Nitric Oxide / Q000378:metabolism; D009765:Obesity / Q000473:pathology* / Q000503:physiopathology*; D013194:Staining and Labeling; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology*; D014664:Vasodilation
chemical_list: D001391:Azo Compounds; C017768:trichrome stain; D009569:Nitric Oxide; D008739:Methyl Green; D003094:Collagen; D004801:Eosine Yellowish-(YS)