Metabolsim of apoB and apoC lipoproteins in man: kinetic studies in normal and hyperlipoproteininemic subjects.
Metabolsim of apoB and apoC lipoproteins in man: kinetic studies in normal and hyperlipoproteininemic subjects.
复制标题
人类 apoB 和 apoC 脂蛋白的代谢：正常和高脂蛋白血症受试者的动力学研究。
作者：
M. Berman;M. Hall;R. Levy;S. Eisenberg;D. Bilheimer;R. Phair;R. Goebel
在 14 名正常和高脂蛋白血症受试者注射外源 (125)I 标记的极低密度脂蛋白 (VLDL) 颗粒后，研究了载脂蛋白 B 和 C 的动力学。在 4 天的时间内测定 VLDL (d < 1.006) 中 apoB 和 apoC 的血浆放射性，以及中 (IDL) (1.006 < d < 1.019)、低 (LDL) (1.019 < d < 1.063) 和高 (HDL) (1.063 < d < 1.21) 密度脂蛋白的总放射性。使用主要根据这些数据开发的模型对数据进行分析，得到以下结果。 VLDL 颗粒经历一系列增量密度变化，很可能是由于许多脱脂步骤，在此期间 apoB 与颗粒保持在一起，直到密度达到 IDL 范围。然而，这些脱脂步骤会导致 apoC 损失。在我们的正常受试者中，所有 IDL apoB 最终都会变成 LDL。在我们的高脂血症受试者中，IDL 上的一些 apoB 也被直接降解。 VLDL和IDL损失的apoC回收为HDL，其中大部分又被新合成的VLDL重新拾取。所有研究的高脂血症个体的逐步脱脂过程均减慢。 III 类受试者中另外三个特征也变得明显。首先，通过 VLDL，apoB 合成率显着增加（与正常相比增加 2 倍）；其次，存在通过IDL（和/或LDL）诱导的直接apoB合成途径；第三，诱导绕过常规逐步VLDL脱脂途径，VLDL颗粒失去apoC但不失去apoB，从而形成代谢特性与LDL相似的新颗粒，但密度仍处于VLDL密度范围内。两名接受烟酸和安妥明治疗的 III 型患者的 VLDL apoB 合成率急剧下降。 IDL apoB 合成率的增加在一定程度上补偿了这一点。接受中链甘油三酯饮食的 I 型患者也表现出许多代谢变化，包括 VLDL apoB 合成减少以及诱导大量 IDL 和/或 LDL apoB 合成。
The kinetics of apolipoproteins B and C were studied in 14 normal and hyperlipoproteinemic subjects after injection of exogenously (125)I-labeled very low density lipoprotein (VLDL) particles. Plasma radioactivities of apoB and apoC were determined over a period of 4 days in VLDL (d < 1.006) and total radioactivity in intermediate (IDL) (1.006 < d < 1.019), low (LDL) (1.019 < d < 1.063), and high (HDL) (1.063 < d < 1.21) density lipoproteins. The data were analyzed by the use of a model, developed mostly from these data, with the following results. The VLDL particle undergoes a series of incremental density changes, most likely due to a number of delipidation steps, during which apoB stays with the particle until the density reaches the IDL range. There is, however, a loss of apoC associated with these delipidation steps. In our normal subjects, all IDL apoB eventually becomes LDL. In our hyperlipemic subjects some of the apoB on IDL is also degraded directly. The apoC lost by VLDL and IDL recycles to HDL, and most of it is picked up again by newly synthesized VLDL. There is a slowdown of the stepwise delipidation process in all hyperlipemic individuals studied. Three additional features became apparent in the type III subjects. First, there is a significant increase (a factor of 2 compared to normal) in the apoB synthesis rate by way of VLDL; second, there is an induced direct apoB synthesis pathway by way of IDL (and/or LDL); third, a bypass of the regular stepwise VLDL delipidation pathway is induced by which VLDL particles lose apoC but none of their apoB, thereby forming a new particle with metabolic properties similar to LDL, but with a density still in the VLDL density range. Two type III patients treated with nicotinic acid and clofibrate showed a sharp decrease in their VLDL apoB synthesis rates. This was somewhat compensated by an increased IDL apoB synthesis rate. A type I patient on a medium chain triglyceride diet also showed a number of metabolic changes, including reduced VLDL apoB synthesis and the induction of considerable IDL and/or LDL apoB synthesis.