Vogel R A, Corretti M C, Plotnick G D
Department of Medicine, University of Maryland School of Medicine, Baltimore 21201-2595, USA.
Am J Cardiol. 1997 Feb 1;79(3):350-4. doi: 10.1016/s0002-9149(96)00760-6.
Although there is a well-established relation between serum cholesterol and coronary artery disease risk, individual and national variations in this association suggest that other factors are involved in atherogenesis. High-fat diet associated triglyceride-rich lipoproteins have also been suggested to be atherogenic. To assess the direct effect of postprandial triglyceride-rich lipoproteins on endothelial function, an early factor in atherogenesis--10 healthy, normocholesterolemic volunteers--were studied before and for 6 hours after single isocaloric high- and low-fat meals (900 calorie; 50 and 0 g fat, respectively). Endothelial function, in the form of flow-mediated vasoactivity, was assessed in the brachial artery using 7.5-MHz ultrasound as percent arterial diameter change 1 minute after 5 minutes of upper-arm arterial occlusion. Serum lipoproteins and glucose were determined before eating and 2 and 4 hours postprandially. Serum triglycerides increased from 94 +/- 55 mg/dl preprandially to 147 +/- 80 mg/dl 2 hours after the high-fat meal (p = 0.05). Flow-dependent vasoactivity decreased from 21 +/- 5% preprandially to 11 +/- 4%, 11 +/- 6%, and 10 +/- 3% at 2, 3, and 4 hours after the high-fat meal, respectively (all p <0.05 compared with low-fat meal data). No changes in lipoproteins or flow-mediated vasoactivity were observed after the low-fat meal. Fasting low-density lipoprotein cholesterol correlated inversely (r = -0.47, p = 0.04) with preprandial flow-mediated vasoactivity, but triglyceride level did not. Mean change in postprandial flow-mediated vasoactivity at 2, 3, and 4 hours correlated with change in 2-hour serum triglycerides (r = -0.51, p = 0.02). These results demonstrate that a single high-fat meal transiently impairs endothelial function. These findings identify a potential process by which a high-fat diet may be atherogenic independent of induced changes in cholesterol.
尽管血清胆固醇与冠状动脉疾病风险之间存在既定关系,但这种关联在个体和国家层面上的差异表明,动脉粥样硬化的发生还涉及其他因素。富含甘油三酯的脂蛋白与高脂饮食有关,也被认为具有致动脉粥样硬化作用。为了评估餐后富含甘油三酯的脂蛋白对内皮功能(动脉粥样硬化发生的早期因素)的直接影响,我们对10名健康的、胆固醇水平正常的志愿者进行了研究,在他们分别摄入等热量的高脂和低脂餐(900卡路里;分别含50克和0克脂肪)之前及之后6小时进行观察。使用7.5兆赫超声,以上臂动脉闭塞5分钟后1分钟时动脉直径变化百分比的形式,评估肱动脉的内皮功能,即血流介导的血管活性。在进食前以及餐后2小时和4小时测定血清脂蛋白和血糖。高脂餐后,血清甘油三酯从餐前的94±55毫克/分升升至餐后2小时的147±80毫克/分升(p = 0.05)。高脂餐后2小时、3小时和4小时,血流依赖性血管活性分别从餐前的21±5%降至11±4%、11±6%和10±3%(与低脂餐数据相比,所有p<0.05)。低脂餐后未观察到脂蛋白或血流介导的血管活性有变化。空腹低密度脂蛋白胆固醇与餐前血流介导的血管活性呈负相关(r = -0.47,p = 0.04),但甘油三酯水平与之无关。餐后2小时、3小时和4小时血流介导的血管活性的平均变化与2小时血清甘油三酯的变化相关(r = -0.51,p = 0.02)。这些结果表明,单次高脂餐会短暂损害内皮功能。这些发现确定了一个潜在过程,通过这个过程,高脂饮食可能在不依赖于胆固醇诱导变化的情况下具有致动脉粥样硬化作用。