Bahia Luciana, Aguiar Luiz Guilherme, Villela Nivaldo, Bottino Daniel, Godoy-Matos Amelio F, Geloneze Bruno, Tambascia Marcos, Bouskela Eliete
Department of Physiological Sciences, Institute of Biology Roberto Alcântara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Clinics (Sao Paulo). 2006 Oct;61(5):433-40. doi: 10.1590/s1807-59322006000500010.
Metabolic syndrome is an important risk factor for cardiovascular disease. Adipokines interfere with insulin action and endothelial cell function. We investigated the relationship among adipokines, metabolic factors, inflammatory markers, and vascular reactivity in obese subjects with metabolic syndrome and lean controls.
Cross-sectional study of 19 obese subjects with metabolic syndrome and 8 lean volunteers evaluated as controls. Vascular reactivity was assessed by venous occlusion pletysmography measuring braquial forearm blood flow (FBF) and vascular resistance (VR) responses to intra-arterial infusions of endothelium-dependent (acetylcholine-Ach) and independent (sodium nitroprusside-SNP) vasodilators. Blood samples were obtained to evaluate C reactive protein (CRP), plasminogen activator inhibitor 1 (PAI-1), fibrinogen, adiponectin, resistin, and lipid profile. Patients were classified with regard to insulin resistance through the HOMA-IR index.
PAI-1, CRP and fibrinogen were higher and adiponectin was lower in metabolic syndrome subjects compared to controls. Metabolic syndrome subjects had impaired vascular reactivity. Adiponectin and PAI-1 were associated with insulin, HOMA-IR, triglycerides, and HDLc; and resistin with CRP. Adiponectin was associated with VR after Ach in the pooled group and resistin with D FBF after Ach in the metabolic syndrome group.
Metabolic syndrome subjects exhibited low levels of adiponectin and high levels of CRP, fibrinogen, and PAI-1. Adiponectin and PAI-1 correlated with insulin resistance markers. Adiponectin and resistin correlated with vascular reactivity parameters. An adipocyte-endothelium interaction might be an important mechanism of inflammation and vascular dysfunction.
代谢综合征是心血管疾病的重要危险因素。脂肪因子会干扰胰岛素作用和内皮细胞功能。我们研究了患有代谢综合征的肥胖受试者和瘦对照组中脂肪因子、代谢因素、炎症标志物与血管反应性之间的关系。
对19名患有代谢综合征的肥胖受试者和8名作为对照的瘦志愿者进行横断面研究。通过静脉阻塞体积描记法评估血管反应性，测量肱动脉前臂血流量（FBF）和血管阻力（VR）对动脉内输注内皮依赖性（乙酰胆碱 - Ach）和非内皮依赖性（硝普钠 - SNP）血管扩张剂的反应。采集血样以评估C反应蛋白（CRP）、纤溶酶原激活物抑制剂1（PAI - 1）、纤维蛋白原、脂联素、抵抗素和血脂谱。通过HOMA - IR指数对患者的胰岛素抵抗进行分类。
与对照组相比，代谢综合征受试者的PAI - 1、CRP和纤维蛋白原水平较高，脂联素水平较低。代谢综合征受试者的血管反应性受损。脂联素和PAI - 1与胰岛素、HOMA - IR、甘油三酯和高密度脂蛋白胆固醇相关；抵抗素与CRP相关。在合并组中，脂联素与Ach刺激后的VR相关，在代谢综合征组中，抵抗素与Ach刺激后的ΔFBF相关。
代谢综合征受试者表现出低水平的脂联素和高水平的CRP、纤维蛋白原和PAI - 1。脂联素和PAI - 1与胰岛素抵抗标志物相关。脂联素和抵抗素与血管反应性参数相关。脂肪细胞 - 内皮相互作用可能是炎症和血管功能障碍的重要机制。
