Skin microvascular vasodilatory capacity in offspring of two parents with Type 2 diabetes

Aims Microvascular dysfunction occurs in Type 2 diabetes and in subjects wi th fasting hyperglycaemia. It is unclear whether this dysfunction relates t o dysglycaemia. This study investigated in normogylcaemic individuals wheth er a genetic predisposition to diabetes, or indices of insulin resistance i ncluding endothelial markers, were associated with impaired microvascular f unction. Methods Maximum microvascular hyperaemia to local heating of the skin was m easured using laser Doppler flowmetry in 21 normoglycaemic subjects with no family history of diabetes (Group 1) and 21 normoglycaemic age, sex and bo dy mass index-matched offspring of two parents with Type 2 diabetes (Group 2). Results Although Group 2 had normal fasting plasma glucose and glucose tole rance 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 hype raemia (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 f or blood pressure (Group 1: 52.0 (43.2-67.4) vs. Group 2: 56.0 (43.7-69.6) mmHgN, P=0.70) did not differ in the two groups. Significant positive assoc iations occurred between minimum microvascular resistance and indices of th e 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=0.0 2), and triglyceride concentration (R-s=0.35, P=0.02), and an inverse assoc iation with insulin sensitivity (R-s=-0.33, P=0.03). Conclusions In normoglycaemic adults cutaneous microvascular vasodilatory c apacity is associated with features of insulin resistance syndrome, particu larly with plasminogen activator inhibitor type 1. A strong family history of Type 2 diabetes alone does not result in impairment in the maximum hyper aemic response.