title: Elevated adiponectin expression promotes adipose tissue vascularity under conditions of diet-induced obesity.
abstract: OBJECTIVE
  Despite the clinical prevalence of obesity, only recently has the importance of adipose tissue microenvironment been addressed at a molecular level. Here, I focused on the fat-derived cytokine adiponectin as a model system to understand the mechanism underlying adipose tissue vascularity, perfusion, inflammation, and systemic metabolic function.
  
  
  METHODS
  Wild type, adiponectin-deficient, and adiponectin transgenic-overexpressing mice were maintained on chow diet or high fat/high sucrose diet for 32weeks. Vascularization of adipose tissue was examined by confocal microscopy and perfusion was determined by recovery of injected microspheres. Adipose tissue inflammation and systemic metabolic function were also assessed.
  
  
  RESULTS
  Modest over-expression of adiponectin led to a marked increase in adipose tissue vascularity and perfusion, and this was associated with diminished hypoxia and an increase in vascular endothelial growth factor-A (VEGF-A) expression in the obese mice. Adiponectin over-expression in diet-induced obese mice also led to the virtual absence of macrophage infiltration and the elimination of crown-like structures. Adiponectin transgenic mice also displayed a remarkable sensitivity to insulin and diminished hepatic steatosis. Under the conditions of these experiments, adiponectin deficiency did not diminish adipose tissue perfusion or worsen metabolic function compared to wild type mice fed the high fat/high sucrose diet.
  
  
  CONCLUSIONS
  These data demonstrate that increased circulating adiponectin levels, and the obese environment, are associated with increased adipose tissue vascularization and perfusion, and improved metabolic function under conditions of long term diet-induced obesity.
authors.affiliation: Department of Medicine-Renal Section, Boston University School of Medicine, 650 Albany Street, X536, Boston, MA 02118, USA. Electronic address: aprahami@bu.edu.
authors.forename: Tamar R
authors.initials: TR
authors.lastname: Aprahamian
mesh_terms: D052242:Adiponectin / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D000273:Adipose Tissue / Q000033:anatomy & histology / Q000098:blood supply*; D052436:Adipose Tissue, White / Q000098:blood supply / Q000473:pathology; D000818:Animals; D004032:Diet; D000860:Hypoxia / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008833:Microcirculation / Q000502:physiology; D018613:Microscopy, Confocal; D008863:Microspheres; D018919:Neovascularization, Physiologic / Q000502:physiology; D009765:Obesity / Q000503:physiopathology*; D060888:Real-Time Polymerase Chain Reaction; D012039:Regional Blood Flow / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
chemical_list: D052242:Adiponectin; D042461:Vascular Endothelial Growth Factor A
keywords: Angiogenesis; Animal model; Apn-KO; Apn-TG; CLS; HFHS; IL-6; Metabolic dysfunction; Shh; Sonic Hedgehog; TNFα; VEGF-A; adiponectin knockout mouse; adiponectin transgenic/overexpressing mouse; crown-like structure; high fat/high sucrose diet; interleukin 6; tumor necrosis factor alpha; vascular endothelial growth factor-A