Groot P H, van Stiphout W A, Krauss X H, Jansen H, van Tol A, van Ramshorst E, Chin-On S, Hofman A, Cresswell S R, Havekes L
Department of Biochemistry, Erasmus University Rotterdam, The Netherlands.
Arterioscler Thromb. 1991 May-Jun;11(3):653-62. doi: 10.1161/01.atv.11.3.653.
A delayed clearance of postprandial lipoproteins from the plasma may play a role in the etiology of premature coronary atherosclerosis. To address this hypothesis, we studied chylomicron (remnant) metabolism in two groups of 20 selected normolipidemic men aged 35-65 years, a group of coronary artery disease (CAD) patients, and a matched control group with documented minimal coronary atherosclerosis. Subjects received an oral fat load supplemented with cholesterol and retinyl palmitate. Plasma samples obtained during the next 24-hour period were analyzed for total as well as d less than 1.019 g/ml and d greater than 1.019 g/ml triacylglycerol, cholesterol, and retinyl ester concentrations. Although both groups of patients responded identically in terms of the appearance of gut-derived lipids in the plasma, CAD patients showed a marked delay in the clearance of retinyl esters as well as in the normalization of plasma triacylglycerol concentrations. Postheparin plasma hepatic lipase activity was significantly lower in the CAD group. Apolipoprotein E phenotype measurements did not reveal marked differences in frequency between both groups. The frequency distribution was not unusual in comparison with the normal Dutch population. The magnitude of the postprandial responses of triacylglycerol and retinyl esters was correlated positively with the fasting levels of plasma triacylglycerol and negatively with high density lipoprotein subfraction 2 cholesterol concentrations. These data indicate that the clearance of postprandial lipoproteins in normolipidemic CAD patients as selected in the present study is delayed as compared with that of controls without coronary atherosclerosis and suggest that postprandial lipoproteins may play a role in the etiology of their disease.
餐后脂蛋白从血浆中清除延迟可能在早发性冠状动脉粥样硬化的病因中起作用。为了验证这一假设,我们研究了两组各20名年龄在35 - 65岁的血脂正常男性、一组冠状动脉疾病(CAD)患者以及一组经记录冠状动脉粥样硬化程度极低的匹配对照组的乳糜微粒(残余物)代谢情况。受试者口服补充了胆固醇和视黄醇棕榈酸酯的脂肪负荷。对接下来24小时内采集的血浆样本分析了总甘油三酯、密度小于1.019 g/ml和密度大于1.019 g/ml的甘油三酯、胆固醇以及视黄醇酯的浓度。尽管两组患者在血浆中出现源自肠道的脂质方面反应相同,但CAD患者在视黄醇酯清除以及血浆甘油三酯浓度恢复正常方面明显延迟。CAD组肝素后血浆肝脂酶活性显著降低。载脂蛋白E表型测量未显示两组之间频率有明显差异。与正常荷兰人群相比,频率分布并无异常。餐后甘油三酯和视黄醇酯反应的幅度与空腹血浆甘油三酯水平呈正相关,与高密度脂蛋白亚组分2胆固醇浓度呈负相关。这些数据表明,与无冠状动脉粥样硬化的对照组相比,本研究中所选血脂正常的CAD患者餐后脂蛋白的清除延迟,提示餐后脂蛋白可能在其疾病病因中起作用。