title: Functional dilator capacity is independently associated with insulin sensitivity and age in central obesity and is not improved by high dose statin treatment.
abstract: OBJECTIVE
  To test the hypothesis that: (i) functional microvascular dilator capacity is independently associated with insulin sensitivity and age in individuals with central adiposity at risk of cardiovascular disease (CVD); and (ii) functional microvascular dilator capacity is improved by high dose statin treatment.
  
  
  METHODS
  Functional dilator capacity (measured as change in laser Doppler blood flux from baseline during post occlusive reactive hyperemia [peak flux%resting flux; PF%RF] and flowmotion (power spectral density [PSD] analysis)) were assessed in 40 people with central adiposity and one or more other CVD risk factors. Measurements were made at rest and during acute hyperinsulinaemia before and six months after high dose atorvastatin (40 mg daily) or placebo.
  
  
  RESULTS
  Insulin-induced change in PF%RF was independently associated with insulin sensitivity (M/I) (r = 0.46 p = 0.02) and age (r = -0.46 p = 0.02), which together explained almost half of the variance in PF%RF (adjusted r² = 0.37, p = 0.008). Whilst atorvastatin decreased LDL cholesterol by 51% (p < 0.001), PF%RF and flowmotion remained unchanged.
  
  
  CONCLUSIONS
  Insulin sensitivity and age are independently associated with an insulin-induced change in functional microvascular dilator capacity in individuals with central adiposity at risk of CVD. Dilator capacity is not improved by six months high dose statin treatment.
authors.affiliation: Institute of Developmental Sciences, School of Medicine, University of Southampton, Southampton General Hospital (MP 887), Southampton, UK. g.f.clough@soton.ac.uk
authors.forename: Geraldine F
authors.initials: GF
authors.lastname: Clough
authors.forename: Veline
authors.initials: V
authors.lastname: L'Esperance
authors.forename: Magdalena
authors.initials: M
authors.lastname: Turzyniecka
authors.forename: Lara
authors.initials: L
authors.lastname: Walter
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Chipperfield
authors.forename: John
authors.initials: J
authors.lastname: Gamble
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Krentz
authors.forename: Christopher D
authors.initials: CD
authors.lastname: Byrne
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D000069059:Atorvastatin; D001783:Blood Flow Velocity / Q000187:drug effects; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D006940:Hyperemia / Q000188:drug therapy / Q000503:physiopathology; D006946:Hyperinsulinism / Q000188:drug therapy / Q000503:physiopathology; D007333:Insulin Resistance; D008297:Male; D008833:Microcirculation / Q000187:drug effects*; D008875:Middle Aged; D056128:Obesity, Abdominal / Q000188:drug therapy / Q000503:physiopathology; D011758:Pyrroles / Q000008:administration & dosage*; D012307:Risk Factors; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D011758:Pyrroles; D000069059:Atorvastatin