Early Upregulation of Endothelial Adhesion Molecules in Obese Hypertensive Men

<jats:p> <jats:italic>Abstract</jats:italic> —Upregulation of endothelial adhesion molecules is the earliest step of atherogenesis. Whether obesity induces endothelial adhesin upregulation is unknown. To address this topic, circulating vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and von Willebrand factor (vWF) concentrations were evaluated in 22 obese hypertensive (51.4±4.6 years [mean±SD age]), 19 obese normotensive (50.6±3.8 years), 18 nonobese hypertensive (52.3±3.9 years), and 16 nonobese normotensive (52.4±3.5 years) men without other risk factors or overt atherosclerosis. All measurements were repeated in the obese subgroups after weight loss induced by 12 weeks of caloric restriction. Basal circulating VCAM-1 levels were similar between the 2 obese groups but were higher ( <jats:italic>P</jats:italic> <0.0001) than in the 2 nonobese groups. No differences were found between nonobese hypertensives and normotensives. Serum low density lipoprotein cholesterol was weakly correlated with plasma soluble VCAM-1 levels in pooled, obese subjects ( <jats:italic>r</jats:italic> =0.362, <jats:italic>P</jats:italic> =0.02). Plasma soluble adhesin and vWF concentrations decreased significantly after weight loss in obese hypertensives (VCAM-1 <jats:italic>P</jats:italic> =0.03, ICAM-1 <jats:italic>P</jats:italic> =0.004, E-selectin <jats:italic>P</jats:italic> <0.0001, and vWF <jats:italic>P</jats:italic> =0.003) and normotensives (VCAM-1 <jats:italic>P</jats:italic> =0.04, ICAM-1 <jats:italic>P</jats:italic> =0.003, E-selectin <jats:italic>P</jats:italic> <0.0001, and vWF <jats:italic>P</jats:italic> <0.0001). Body mass index was correlated with plasma E-selectin concentrations at baseline and after weight loss in obese hypertensives ( <jats:italic>r</jats:italic> =0.501, <jats:italic>P</jats:italic> =0.018 and <jats:italic>r</jats:italic> =0.466, <jats:italic>P</jats:italic> =0.03, respectively) and obese normotensives ( <jats:italic>r</jats:italic> =0.523, <jats:italic>P</jats:italic> =0.021 and <jats:italic>r</jats:italic> =0.460, <jats:italic>P</jats:italic> =0.05, respectively). In conclusion, our data show that obesity per se induces early endothelial activation in hypertensive and normotensive men. Weight loss counteracted endothelial activation in both obese hypertensive and normotensive men. </jats:p>