Effect of short-term weight loss on the metabolic syndrome and conduit vascular endothelial function in overweight adults.

Impaired vascular endothelial function may be an important mechanism linking obesity to increased cardiovascular risk. We investigated whether short-term weight loss improves conduit artery endothelial dysfunction in overweight adults. Forty-three otherwise healthy overweight patients with a body mass index > or =27 kg/m(2) completed an open-label 3-month trial consisting of a calorie-restricted diet and 120 mg of orlistat taken 3 times daily with meals. Endothelial function and parameters of the metabolic syndrome were measured before and after intervention. Subjects lost 6.6 +/- 3.4% of their body weight. Low-density lipoprotein cholesterol, low-density lipoprotein concentration, fasting insulin, and leptin decreased significantly (all p <0.009), and C-reactive protein decreased (p = 0.22). Conduit vascular function did not change as assessed by flow-mediated dilation (3.86 +/- 3.54 vs 3.74 +/- 3.78%, p = 0.86) and nitroglycerin-mediated dilation (17.18 +/- 5.89 vs 18.87 +/- 7.11%, p = 0.13) of the brachial artery. A moderate degree of weight reduction over 3 months improved the metabolic syndrome profile but not the vascular dysfunction associated with uncomplicated obesity.

Hypertension and triglyceride catabolism: implications for the hemodynamic model of the metabolic syndrome.

OBJECTIVE: We sought to determine if hypertensive adults have a blunted triglyceride catabolic rate (TG K(2)) and if related hemodynamic and vascular alterations are determinants of TG K(2). METHODS: Fasting levels of insulin, glucose, lipoproteins and plasma catecholamines were measured in 10 normotensive and 10 hypertensive adults. TG K(2) was determined by an intravenous fat tolerance test. Forearm blood flow, maximum forearm blood flow and minimal forearm vascular resistance were determined by strain gauge plethysmography. Vascular compliance and systemic hemodynamics were measured by computerized arterial pulse waveform analysis. RESULTS: Compared to normotensives, hypertensives had a significantly elevated blood pressure (145 +/- 8/94 +/- 11 versus 111 +/- 15/74 +/- 14 mm Hg, p < 0.001), systemic vascular resistance (1695 +/- 441 versus 1172 +/- 430 dynes x sec x cm(-5), p = 0.02) and reduced large vessel compliance (11.7 +/- 3.6 versus 15.1 +/- 3.1 ml/mm Hg x 100, p = 0.04). There were no significant group differences in TG K(2) (3.07 +/- 2.01 versus 2.88 +/- 2.12 mg/dL/min, p = 0.85) or other metabolic and anthropometric variables. TG K(2) was not predicted by the forearm vascular measures or the hemodynamic variables, but was correlated to waist/hip ratio (r = -0.71, p = 0.001), fasting triglycerides (r = -0.64, p = 0.003), and male gender (r = 0.56, p = 0.012). An enhanced TG K(2) was independently predicted by a reduced small vessel compliance (r = -0.61, p = 0.006). CONCLUSIONS: Elevated blood pressure per se and hypertension-related hemodynamic and vascular alterations are not associated with reduced TG K(2) or other metabolic abnormalities. Rather, aspects of the insulin resistance syndrome are closely related to abdominal adiposity. The independent association between small vessel compliance and TG K(2) deserves further investigation.