Metabolism of apolipoproteins B-48 and B-100 of triglyceride-rich lipoproteins in normal and lipoprotein lipase-deficient humans.
Metabolism of apolipoproteins B-48 and B-100 of triglyceride-rich lipoproteins in normal and lipoprotein lipase-deficient humans.
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正常人和脂蛋白脂肪酶缺陷人群中富含甘油三酯的脂蛋白的载脂蛋白 B-48 和 B-100 的代谢。
DOI：
10.1073/pnas.81.6.1839
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发表时间：
1984
影响因子：
11.1
通讯作者：
Havel,RJ
中科院分区：
文献类型：
--
作者：
Stalenhoef,AF;Malloy,MJ;Kane,JP;Havel,RJ
在3名正常受试者和2名遗传性脂蛋白脂酶缺乏症受试者中，比较了大的富含甘油三酯脂蛋白（直径300 - 1500）中载脂蛋白B-48和B-100（apo B-48和B-100）的代谢。富含甘油三酯的脂蛋白是从脂蛋白脂肪酶缺乏的供体在富含脂肪的膳食后4小时获得的，以获得乳糜微粒（含有apo B-48）和极低密度脂蛋白（VLDL）（含有apo B-100），其性质未被该酶的作用改变。富含磷脂酰肌醇的脂蛋白用125 I标记，并静脉注射到禁食过夜的受体中。在正常受体中，大多数载脂蛋白B-48在15分钟内从血液中去除，大多数载脂蛋白B-100在30分钟内去除。在脂蛋白脂肪酶缺乏受体中，大多数注射的载脂蛋白B-100在血液中保留超过8小时;载脂蛋白B-48的去除仅略快。在所有受试者中，在密度大于1.006 g/ml的脂蛋白中仅发现痕量的蛋白质。结果表明：（i）乳糜微粒和大VLDL的apo B从血液中的去除依赖于脂蛋白脂肪酶对其组分甘油三酯的水解，和（ii）乳糜微粒的apo B-48或大VLDL的apo B-100很少或没有明显转化为低密度脂蛋白（LDL）。我们的研究结果表明，所报道的VLDL转化为LDL的变异性可能与肝脏分泌的颗粒的大小和组成有关。残余颗粒的快速产生可以被肝脏有效地去除，这可以最大限度地减少导致LDL形成的进一步反应的机会。
The metabolism of apolipoproteins B-48 and B-100 (apo B-48 and B-100) in large triglyceride-rich lipoproteins (300 to 1500 A in diameter) has been compared in three normal subjects and two subjects with genetically determined deficiency of lipoprotein lipase. The triglyceride-rich lipoproteins were obtained from a lipoprotein lipase-deficient donor 4 hr after a fat-rich meal in order to obtain chylomicrons (containing apo B-48) and very low density lipoproteins (VLDL) (containing apo B-100), whose properties had not been modified by the action of this enzyme. The triglyceride-rich lipoproteins were labeled with 125I and injected intravenously into recipients who had fasted overnight. In normal recipients, most of the apo B-48 was removed from the blood within 15 min, and most of the apo B-100 was removed within 30 min. In the lipoprotein lipase-deficient recipients, most of the injected apo B-100 remained in the blood for more than 8 hr; removal of apo B-48 was only slightly more rapid. In all subjects, only trace amounts of either protein were found in lipoproteins more dense than 1.006 g/ml. The results indicate that (i) the removal of the apo B of both chylomicrons and large VLDL from the blood is dependent upon the hydrolysis of their component triglycerides by lipoprotein lipase, and (ii) little or no apo B-48 of chylomicrons or apo B-100 of large VLDL is converted appreciably to low density lipoproteins (LDL). Our results suggest that the reported variability of the conversion of VLDL to LDL may be related to the size and composition of the particles secreted from the liver. The rapid production of remnant particles that are removed efficiently by the liver may minimize the opportunity for further reactions leading to the formation of LDL.