title: Skin microvascular vasodilatory capacity in offspring of two parents with Type 2 diabetes.
abstract: OBJECTIVE
  Microvascular dysfunction occurs in Type 2 diabetes and in subjects with fasting hyperglycaemia. It is unclear whether this dysfunction relates to dysglycaemia. This study investigated in normogylcaemic individuals whether a genetic predisposition to diabetes, or indices of insulin resistance including endothelial markers, were associated with impaired microvascular function.
  
  
  METHODS
  Maximum microvascular hyperaemia to local heating of the skin was measured using laser Doppler flowmetry in 21 normoglycaemic subjects with no family history of diabetes (Group 1) and 21 normoglycaemic age, sex and body mass index-matched offspring of two parents with Type 2 diabetes (Group 2).
  
  
  RESULTS
  Although Group 2 had normal fasting plasma glucose and glucose tolerance tests, the 120-min glucose values were significantly higher at 6.4 (5.3-6.6) mmol/l (median (25th - 75th centile)) than the control group at 4.9 (4.6-5.9) mmol/l (P = 0.005) and the insulinogenic index was lower at 97.1 (60.9-130.8) vs. 124.0 (97.2-177.7) (P = 0.027). Skin maximum microvascular hyperaemia (Group 1: 1.56 (1.39-1.80) vs. Group 2: 1.53 (1.30-1.98) V, P = 0.99) and minimum microvascular resistance which normalizes the hyperaemia data for blood pressure (Group 1: 52.0 (43.2-67.4) vs. Group 2: 56.0 (43.7-69.6) mmHg/V, P = 0.70) did not differ in the two groups. Significant positive associations occurred between minimum microvascular resistance and indices of the insulin resistance syndrome; plasminogen activator inhibitor type 1 (R(s) = 0.46, P = 0.003), t-PA (R(s) = 0.36, P = 0.03), total cholesterol (R(s) = 0.35, P = 0.02), and triglyceride concentration (R(s) = 0.35, P = 0.02), and an inverse association with insulin sensitivity (R(s) = -0.33, P = 0.03).
  
  
  CONCLUSIONS
  In normoglycaemic adults cutaneous microvascular vasodilatory capacity is associated with features of insulin resistance syndrome, particularly with plasminogen activator inhibitor type 1. A strong family history of Type 2 diabetes alone does not result in impairment in the maximum hyperaemic response. Diabet. Med. 18, 541-545 (2001)
authors.affiliation: Department of Diabetes and Vascular Medicine, School of Postgraduate Medicine and Health Sciences, University of Exeter, Exeter, UK.
authors.forename: B C
authors.initials: BC
authors.lastname: Lee
authors.forename: A C
authors.initials: AC
authors.lastname: Shore
authors.forename: J M
authors.initials: JM
authors.lastname: Humphreys
authors.forename: G D
authors.initials: GD
authors.lastname: Lowe
authors.forename: A
authors.initials: A
authors.lastname: Rumley
authors.forename: P M
authors.initials: PM
authors.lastname: Clark
authors.forename: A T
authors.initials: AT
authors.lastname: Hattersley
authors.forename: J E
authors.initials: JE
authors.lastname: Tooke
mesh_terms: D000328:Adult; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics* / Q000503:physiopathology*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008833:Microcirculation / Q000502:physiology*; D008875:Middle Aged; D009679:Nuclear Family; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012016:Reference Values; D012867:Skin / Q000098:blood supply*; D014280:Triglycerides / Q000097:blood; D014655:Vascular Resistance; D014664:Vasodilation / Q000502:physiology*
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D002784:Cholesterol