Early upregulation of endothelial adhesion molecules in obese hypertensivemen

Upregulation of endothelial adhesion molecules is the earliest step of athe rogenesis. Whether obesity induces endothelial adhesin upregulation is unkn own. To address this topic, circulating vascular cell adhesion molecule-1 ( VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and von Wi llebrand factor (vWF) concentrations were evaluated in 22 obese hypertensiv e (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 n ormotensive (52.4 +/- 3.5 years) men without other risk factors or overt at herosclerosis, All measurements were repeated in the obese subgroups after weight loss induced by 12 weeks of caloric restriction. Basal circulating V CAM-1 levels were similar between the 2 obese groups but were higher (P<0.0 001) than in the 2 nonobese groups. No differences were found between nonob ese hypertensives and normotensives. Serum low density lipoprotein choleste rol was weakly correlated with plasma soluble VCAM-1 levels in pooled, obes e subjects (r=0.362, P=0.02). Plasma soluble adhesin and vWF concentrations decreased significantly after weight loss in obese hypertensives (VCAM-1 P =0.03, ICAM-1 P=0.004, E-selectin P<0.0001, and vWF P=0.003) and normotensi ves (VCAM-1 P=0.04, ICAM-1 P=0.003, E-selectin P<0.0001, and vWF P<0.0001). Body mass index was correlated with plasma E-selectin concentrations at ba seline and after weight loss in obese hypertensives (r=0.501, P=0.018 and r =0.466, P=0.03, respectively) and obese normotensives (r=0.523, P=0.021 and r=0.460, P=0.05, respectively). In conclusion, our data show that obesity per se induces early endothelial activation in hypertensive and normotensiv e men. Weight loss counteracted endothelial activation in both obese hypert ensive and normotensive men.