Sentí M, Pedro-Botet J, Rubiés-Prat J, Marrugat J
Unitat de Lípids i Epidemíologia Cardiovascular, Institut Municipal d'Investigació Mèdica, IMIM, Barcelona, Spain.
Scand J Clin Lab Invest. 1996 Jul;56(4):311-8. doi: 10.3109/00365519609090582.
At present, the biochemical mechanisms underlying lipoprotein(a) (Lp(a)) metabolism are not fully understood. We analysed sera from 202 patients with atherosclerotic disease and 109 healthy subjects as a control group to investigate the possible relationship between triglyceride-rich lipoproteins (TRL) and serum lipoprotein(a) levels. To assess the influence of apolipoprotein (apo) (a) isoforms on the Lp(a)-TRL association, the apo(a) phenotypes of 177 patients and 95 controls were included in the analysis. Patients with atherosclerotic disease showed triglyceride levels almost within the normal range. There was no significant correlation between serum Lp(a) levels and triglyceride concentrations, or between Lp(a) and TRL levels in either group. When a subset of subjects from each group with serum triglycerides above 1.7 mmol l-1 was considered, a significant negative correlation between lipid concentration of very low density lipoproteins (VLDL) and serum Lp(a) levels was found only in patients. Control subjects with triglyceride levels under or over 1.7 mmol l-1 showed similar median Lp(a) levels (0.06 gl-1), in contrast to atherosclerotic patients, in whom median Lp(a) concentration was higher in the subset with serum triglycerides under 1.7 mmol l-1 than in those with triglyceride concentration above this value (0.16 vs. 0.13 gl-1). When patients with triglyceride concentrations above 1.7 mmol l-1 were classified into quartiles according to VLDL lipid concentration, subjects with the highest quartiles showed the lowest Lp(a) median levels. Despite the dependence of the Lp(a) concentration on apo(a) size isoforms, we found no effect of apo(a) genetic polymorphism on triglyceride levels or on TRL concentrations. We conclude that the variation in TRL metabolism may constitute a source of variation in serum Lp(a) concentrations that is independent of the genetically determined apo(a) molecule size.
目前，脂蛋白(a) [Lp(a)] 代谢的生化机制尚未完全明确。我们分析了202例动脉粥样硬化疾病患者的血清，并将109名健康受试者作为对照组，以研究富含甘油三酯的脂蛋白（TRL）与血清脂蛋白(a) 水平之间的可能关系。为评估载脂蛋白（apo）(a) 异构体对Lp(a)-TRL关联的影响，分析纳入了177例患者和95名对照的apo(a) 表型。动脉粥样硬化疾病患者的甘油三酯水平几乎在正常范围内。两组中血清Lp(a) 水平与甘油三酯浓度之间，或Lp(a) 与TRL水平之间均无显著相关性。当考虑每组中血清甘油三酯高于1.7 mmol/L的受试者亚组时，仅在患者中发现极低密度脂蛋白（VLDL）脂质浓度与血清Lp(a) 水平之间存在显著负相关。甘油三酯水平低于或高于1.7 mmol/L的对照受试者显示出相似的Lp(a) 中位数水平（0.06 g/L），与之形成对比的是，动脉粥样硬化患者中，血清甘油三酯低于1.7 mmol/L的亚组的Lp(a) 中位数浓度高于甘油三酯浓度高于此值的亚组（0.16 vs. 0.13 g/L）。当根据VLDL脂质浓度将甘油三酯浓度高于1.7 mmol/L的患者分为四分位数时，四分位数最高的受试者显示出最低的Lp(a) 中位数水平。尽管Lp(a) 浓度依赖于apo(a) 大小异构体，但我们发现apo(a) 基因多态性对甘油三酯水平或TRL浓度没有影响。我们得出结论，TRL代谢的变化可能构成血清Lp(a) 浓度变化的一个来源，该来源独立于基因决定的apo(a) 分子大小。
