title: Endothelial function varies according to insulin resistance disease type.
abstract: OBJECTIVE
  We examined the relationship between insulin resistance and vascular function in three insulin-resistant states (type 2 diabetes, non-HIV lipodystrophic diabetes, and nondiabetic polycystic ovary syndrome [PCOS]) and in healthy control subjects.
  
  
  METHODS
  The population included 12 women with type 2 diabetes, 6 with lipodystrophic diabetes, 10 with PCOS, and 19 healthy female subjects. Metabolic measures included insulin sensitivity by the homeostasis model assessment, lipids, free fatty acids, and adiponectin. High-resolution B-mode ultrasound was used to determine endothelium-dependent and -independent vasodilation.
  
  
  RESULTS
  Type 2 diabetic, liposdystrophic, and PCOS subjects were insulin resistant compared with control subjects (P = 0.001). Flow-mediated vasodilation was reduced in diabetic (3.4 +/- 1.3%) compared with control (7.3 +/- 1.1%) subjects but not in lipodystrophic (7.7 +/- 1.2%) or PCOS (9.9 +/- 0.7%) subjects (P = 0.005). Nitroglycerin-mediated vasodilation was attenuated in both diabetic (15.2 +/- 2.0%) and lipodystrophic (16.7 +/- 3.6%) subjects compared with healthy control (24.6 +/- 2.4%) and PCOS (23.2 +/- 1.8%) subjects (P = 0.019). Insulin resistance, free fatty acids, adiponectin, or C-reactive protein did not associate with vascular dysfunction.
  
  
  CONCLUSIONS
  Among these different types of patients with insulin resistance, we found abnormal endothelium-dependent vasodilation only in the patients with type 2 diabetes. We postulate that variations in the mechanism of insulin resistance may affect endothelial function differently than glucose homeostasis.
authors.affiliation: Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St., Boston, MA 02115, USA. jbeckman@partners.org
authors.forename: Joshua A
authors.initials: JA
authors.lastname: Beckman
authors.forename: Allison B
authors.initials: AB
authors.lastname: Goldfine
authors.forename: Andrea
authors.initials: A
authors.lastname: Dunaif
authors.forename: Marie
authors.initials: M
authors.lastname: Gerhard-Herman
authors.forename: Mark A
authors.initials: MA
authors.lastname: Creager
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D001916:Brachial Artery / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000453:epidemiology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008875:Middle Aged; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000453:epidemiology*; D012016:Reference Values
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008055:Lipids