Association of postprandial triglyceride and retinyl palmitate responses with asymptomatic carotid artery atherosclerosis in middle-aged men and women. The Atherosclerosis Risk in Communities (ARIC) Study.
Association of postprandial triglyceride and retinyl palmitate responses with asymptomatic carotid artery atherosclerosis in middle-aged men and women. The Atherosclerosis Risk in Communities (ARIC) Study.
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DOI：
10.1161/01.atv.15.12.2122
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发表时间：
1995-12
期刊：
影响因子：
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通讯作者：
A. Sharrett;L. Chambless;G. Heiss;C. Paton;W. Patsch
中科院分区：
文献类型：
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作者：
A. Sharrett;L. Chambless;G. Heiss;C. Paton;W. Patsch
脂肪餐后血脂改变可能是动脉粥样硬化的原因，但很少有关于其与疾病的关联独立于空腹血脂的信息。无症状的动脉粥样硬化病例（n = 229）和373例对照受试者无动脉粥样硬化（根据超声图像上的颈动脉内膜中层厚度定义），给予含维生素A的脂肪餐，然后测量3.5小时和8小时的甘油三酯（TG）、富TG脂蛋白TG、载脂蛋白B48和棕榈酸视黄酯。在白色男性和女性中，病例状态与TG和富含TG的脂蛋白TG的更大餐后反应相关，但仅在非肥胖人群中（体重指数< 30 kg/m2）。在控制冠状动脉危险因素（比值比，约2.0）和空腹TG（比值比，1.5）后，相关性强且显著。在控制了空腹血脂后，与其他餐后血脂测量的相关性并不持续。餐后TG升高似乎是非肥胖白人颈动脉内膜增厚的独立危险因素。在肥胖受试者中缺乏这样的关系和他们表现出的脂质谱表明，餐后TG必须伴随着富含TG的脂蛋白残余物的积累才能致动脉粥样硬化。
Blood lipid alterations after a fatty meal may be atherogenic, but there is little information regarding their associations with disease independent of fasting lipids. Asymptomatic atherosclerosis cases (n = 229) and 373 control subjects free of atherosclerosis, as defined by carotid intima-media thickness on ultrasound images, were given a fatty meal with vitamin A, followed by 3.5- and 8-hour measurements of triglycerides (TGs), TG-rich lipoprotein TGs, apoproteinB48, and retinyl palmitate. Among white men and women but not among blacks, case status was associated with greater postprandial responses of TGs and TG-rich lipoprotein TGs, but only in nonobese persons (body mass index < 30 kg/m2). The associations were strong and significant after controlling for coronary risk factors (odds ratio, approximately 2.0) and fasting TGs (odds ratio, 1.5). Associations with other postprandial lipid measurements did not persist after controlling for fasting lipids. Elevated postprandial TGs appear to be an independent risk factor for carotid intimal thickening in nonobese whites. The lack of such a relation in obese subjects and the lipid profile they manifest suggest that postprandial TGs must be accompanied by accumulation of TG-rich lipoprotein remnants to be atherogenic.