Skilton M R, Sieveking D P, Harmer J A, Franklin J, Loughnan G, Nakhla S, Sullivan D R, Caterson I D, Celermajer D S
Department of Medicine, University of Sydney, Sydney, Australia.
Diabetes Obes Metab. 2008 Sep;10(10):874-84. doi: 10.1111/j.1463-1326.2007.00817.x. Epub 2007 Nov 22.
The mechanisms by which obesity confers increased cardiovascular risk and the effects of moderate weight loss on cardiovascular health are incompletely understood. We sought to characterize the preclinical changes in cardiac and vascular health that accompany obesity and the influence of lifestyle modification on these parameters.
Preclinical markers of vasculopathy in resistance vessels and conduit arteries and left ventricular structure and function were assessed in 39 obese subjects (BMI > 30 kg/m(2)) and 11 healthy weight controls. The influence of serum on cellular adhesion molecule (CAM) expression on human endothelial cells was studied ex vivo in a subgroup of 13 obese and nine healthy weight subjects. These analyses were repeated in all 17 of the obese subjects who complied with 4-9 months of lifestyle modification treatment (six with weight loss >5% and 11 with weight loss <5%).
Compared with healthy weight controls, obese subjects had decreased peak hyperaemic forearm blood flow (p = 0.015), increased carotid intima-media thickness (p = 0.009), increased left ventricular wall thickness and volume and evidence of systolic and diastolic dysfunction as assessed using tissue Doppler imaging (S', p = 0.09; E'/A', p = 0.02), and serum from obese subjects increased the intercellular CAM-1 expression on human endothelial cells (p = 0.009). However, arterial endothelial function assessed by flow-mediated dilatation was not altered (p = 0.99). Lifestyle modification treatment resulted in potentially beneficial changes in fibrinogen (p = 0.003), HDL cholesterol (p = 0.05) and soluble vascular CAM-1 (p = 0.06). In subjects with weight loss greater than 5% of body weight, there was also a decrease in low-level inflammation (high-sensitivity C-reactive protein, p = 0.05), lipid peroxidation (thiobarbituric acid-reactive substances, p = 0.05) and triglycerides (p = 0.07).
Obesity is associated with widespread alterations in cardiac and vascular structure and function. Moderate short-term weight loss by lifestyle modification results in some beneficial changes in serum profile; however, these are not accompanied by significant alterations to either cardiac or vascular structure and function.
肥胖增加心血管疾病风险的机制以及适度体重减轻对心血管健康的影响尚未完全明确。我们试图明确肥胖伴随的心脏和血管健康的临床前变化以及生活方式改变对这些参数的影响。
在39名肥胖受试者(BMI>30kg/m²)和11名健康体重对照者中评估阻力血管和传导动脉血管病变的临床前标志物以及左心室结构和功能。在13名肥胖和9名健康体重受试者的亚组中,体外研究血清对人内皮细胞上细胞粘附分子(CAM)表达的影响。在所有17名遵守4-9个月生活方式改变治疗的肥胖受试者中重复这些分析(6名体重减轻>5%,11名体重减轻<5%)。
与健康体重对照者相比,肥胖受试者的充血前臂血流峰值降低(p=0.015),颈动脉内膜中层厚度增加(p=0.009),左心室壁厚度和容积增加,并且使用组织多普勒成像评估有收缩和舒张功能障碍的证据(S',p=0.09;E'/A',p=0.02),肥胖受试者的血清增加了人内皮细胞上细胞间CAM-1的表达(p=0.009)。然而,通过血流介导的扩张评估的动脉内皮功能未改变(p=0.99)。生活方式改变治疗导致纤维蛋白原(p=0.003)、高密度脂蛋白胆固醇(p=0.05)和可溶性血管CAM-1(p=0.06)出现潜在的有益变化。在体重减轻超过体重5%的受试者中,低水平炎症(高敏C反应蛋白,p=0.05)、脂质过氧化(硫代巴比妥酸反应物质,p=0.05)和甘油三酯(p=0.07)也有所降低。
肥胖与心脏和血管结构及功能的广泛改变有关。通过生活方式改变进行适度的短期体重减轻会使血清指标产生一些有益变化;然而,这些变化并未伴随心脏或血管结构及功能的显著改变。