Cohn J S, Lam C W, Sullivan D R, Hensley W J
Department of Clinical Biochemistry, Royal Prince Alfred Hospital, Sydney, Australia.
Atherosclerosis. 1991 Sep;90(1):59-66. doi: 10.1016/0021-9150(91)90244-w.
In order to quantitate the contribution of triglyceride-rich lipoprotein (TRL) apolipoprotein(a) to total plasma apo(a) concentration in the fed and fasted states, we have studied a group of 20 male subjects (age 49 +/- 3 years) with fasting apo(a) concentrations varying from 39 to 1385 U/l. After a 12-h overnight fast, each subject was given a fat-rich meal (1 g fat/kg body weight) and venous blood samples were obtained at hourly intervals for 10 h. TRL were isolated from bihourly plasma samples by ultracentrifugation (d less than 1.006 g/ml) and apo(a) was measured by radioimmunoassay. Total plasma apo(a) concentration did not change after the meal. However, TRL apo(a) increased significantly (0 h: 3 +/- 1, 4 h: 30 +/- 7 U/l; p less than 0.001) and 'd greater than 1.006' apo(a) decreased (0 h: 267 +/- 56, 4 h: 231 +/- 50 U/l; P less than 0.05). Similar postprandial changes were observed in apoB concentration (TRL apo B at 0 h: 10.3 +/- 1.5, 4 h: 13.6 +/- 1.7 g/l, P less than 0.001, 'd greater than 1.006' apoB at 0 h: 118 +/- 7, 4 h: 110 +/- 7 g/l, P less than 0.001). In the fasted state 2.0 +/- 1.0% and in the fed state (4 h postprandially) 16.0 +/- 4.6% of total plasma apo(a) was found in the TRL fraction. Eleven subjects had less than 10% of total apo(a) in TRL, 5 had 25% or more apo(a) in TRL in the fed state. Postprandial increase in TRL apo(a) was significantly correlated (r = 0.75, P less than 0.001) with increase in plasma triglycerides. TRL apo(a) concentration in the fed state was not correlated with total fasting cholesterol, triglyceride, apo(a) or HDL cholesterol concentration. We conclude that in some individuals, TRL apo(a) makes a significant contribution to total plasma apo(a) concentration in the fed state.
为了定量富含甘油三酯的脂蛋白（TRL）载脂蛋白（a）在进食和空腹状态下对血浆总载脂蛋白（a）浓度的贡献，我们研究了一组20名男性受试者（年龄49±3岁），其空腹载脂蛋白（a）浓度在39至1385 U/l之间。经过12小时的夜间禁食后，给每位受试者提供一顿富含脂肪的餐食（1 g脂肪/千克体重），并在10小时内每隔1小时采集静脉血样。通过超速离心（密度小于1.006 g/ml）从每两小时的血浆样本中分离出TRL，并通过放射免疫测定法测量载脂蛋白（a）。餐后血浆总载脂蛋白（a）浓度没有变化。然而，TRL载脂蛋白（a）显著增加（0小时：3±1，4小时：30±7 U/l；p＜0.001），而“密度大于1.006”的载脂蛋白（a）减少（0小时：267±56，4小时：231±50 U/l；P＜0.05）。在载脂蛋白B浓度方面也观察到类似的餐后变化（0小时TRL载脂蛋白B：10.3±1.5，4小时：13.6±1.7 g/l，P＜0.001，0小时“密度大于1.006”的载脂蛋白B：118±7，4小时：110±7 g/l，P＜0.001）。在空腹状态下，TRL部分中血浆总载脂蛋白（a）的比例为2.0±1.0%，在进食状态下（餐后4小时）为16.0±4.6%。11名受试者的TRL中总载脂蛋白（a）的比例低于10%，5名受试者在进食状态下TRL中载脂蛋白（a）的比例达到25%或更高。餐后TRL载脂蛋白（a）的增加与血浆甘油三酯的增加显著相关（r = 0.75，P＜0.001）。进食状态下TRL载脂蛋白（a）浓度与空腹总胆固醇、甘油三酯、载脂蛋白（a）或高密度脂蛋白胆固醇浓度无关。我们得出结论，在某些个体中，TRL载脂蛋白（a）在进食状态下对血浆总载脂蛋白（a）浓度有显著贡献。
