Ferri C, Desideri G, Valenti M, Bellini C, Pasin M, Santucci A, De Mattia G
University "La Sapienza," Cattedra di I Clinica Medica, Andrea Cesalpino Foundation, Rome.
Hypertension. 1999 Oct;34(4 Pt 1):568-73. doi: 10.1161/01.hyp.34.4.568.
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 (P<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 (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 normotensives (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 baseline 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 normotensive men. Weight loss counteracted endothelial activation in both obese hypertensive and normotensive men.
内皮黏附分子的上调是动脉粥样硬化发生的最早步骤。肥胖是否会诱导内皮黏附分子上调尚不清楚。为了探讨这一问题，我们评估了22名肥胖高血压患者（平均年龄51.4±4.6岁[均值±标准差]）、19名肥胖血压正常者（50.6±3.8岁）、18名非肥胖高血压患者（52.3±3.9岁）和16名非肥胖血压正常者（52.4±3.5岁）男性的循环血管细胞黏附分子-1（VCAM-1）、细胞间黏附分子-1（ICAM-1）、E-选择素和血管性血友病因子（vWF）浓度，这些男性无其他危险因素或明显的动脉粥样硬化。在通过12周热量限制诱导体重减轻后，对肥胖亚组的所有测量值进行了重复测量。两个肥胖组的基础循环VCAM-1水平相似，但高于两个非肥胖组（P<0.0001）。非肥胖高血压患者和血压正常者之间未发现差异。在合并的肥胖受试者中，血清低密度脂蛋白胆固醇与血浆可溶性VCAM-1水平呈弱相关（r=0.362，P=0.02）。肥胖高血压患者（VCAM-1 P=0.03，ICAM-1 P=0.004，E-选择素P<0.0001，vWF P=0.003）和血压正常者（VCAM-1 P=0.04，ICAM-1 P=0.003，E-选择素P<0.0001，vWF P<0.0001）体重减轻后，血浆可溶性黏附分子和vWF浓度显著降低。在肥胖高血压患者（分别为r=0.501，P=0.018和r=0.466，P=0.03）和肥胖血压正常者（分别为r=0.523，P=0.021和r=0.460，P=0.05）中，体重指数与基线时和体重减轻后的血浆E-选择素浓度相关。总之，我们的数据表明，肥胖本身会在高血压和血压正常的男性中诱导早期内皮激活。体重减轻可抵消肥胖高血压和血压正常男性的内皮激活。
