Endothelial vasodilator function in normal-weight adults with metabolic syndrome

Metabolic syndrome (MetS) typically presents with obesity; however, obesity is not a requisite characteristic for MetS classification and related vascular risk. We tested the hypothesis that MetS, independent of excess adiposity, is associated with impaired endothelial vasodilator dysfunction. Thirty-two sedentary, middle-aged adults were studied: 11 normal weight (9 male and 2 female; body mass index (BMI), 24.0 ± 0.3 kg/m²); 11 normal weight with MetS (9 male and 2 female; BMI, 24.7 ± 0.3 kg/m²); and 10 obese without MetS (8 male and 2 female; BMI, 31.4 ± 0.5 kg/m²). MetS was established according to National Cholesterol Education Program Adult Treatment Panel III criteria. Forearm blood flow (FBF) responses to intra-arterial infusions of acetylcholine and sodium nitroprusside were measured via strain-gauge plethysmography. FBF responses to acetylcholine were ∼20% lower (P < 0.05) in the normal-weight subjects with MetS (from 4.0 ± 0.3 to 13.0 ± 1.0 mL/(100 mL tissue·min)) and obese subjects (from 4.8 ± 0.2 to 12.2 ± 1.1 mL/(100 mL tissue·min)) compared with the normal-weight subjects (from 4.6 ± 0.4 to 15.8 ± 0.7 mL/(100 mL tissue·min)). Of note, FBF responses to acetylcholine were similar between the normal-weight adults with MetS and the obese adults. There were no differences among groups in FBF response to sodium nitroprusside. These data indicate that the presence of MetS, independent of obesity, is associated with diminished endothelium-dependent vasodilation. Endothelial vasodilator dysfunction may underlie the increased cardiovascular risk in normal-weight adults with MetS.