Differential metabolism of human VLDL according to content of ApoE and ApoC-III.
Differential metabolism of human VLDL according to content of ApoE and ApoC-III.
复制标题
根据 ApoE 和 ApoC-III 的含量，人 VLDL 的差异代谢。
DOI：
10.1161/hq0901.094489
复制
发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Sacks,FM
中科院分区：
文献类型：
--
作者：
Tomiyasu,K;Walsh,BW;Ikewaki,K;Judge,H;Sacks,FM
我们通过内源标记血浆载脂蛋白 B，研究了 12 名血脂正常女性中含有或不含载脂蛋白 E (apoE) 的极低密度脂蛋白 (VLDL) 和中密度脂蛋白 (IDL) 颗粒的代谢。使用单克隆抗体 (1D7) 将血浆分为结合 (E+) 和未结合 (E−) 级分，并对级分进行超速离心，得到 E+ 和 E− 亚级分轻质和密质 VLDL 和 IDL。 VLDL E+和IDL E+主要由肝脏产生。与相应的 E− 颗粒相比，VLDL E+ 和 IDL E+ 的分解代谢率较低，载脂蛋白 C-III (apoC-III) 含量则高得多。大多数轻质 VLDL apoE+ 经历脂解作用，变成稠密 VLDL E+，其中 apoC-III 含量减少，从循环中去除，而不转化为 IDL。相比之下，大多数轻质 VLDL apoE−（apoC-III 含量较低）被从循环中去除，而一小部分则经历脂肪分解，形成致密 VLDL E−。大多数密集的 VLDL E− 经历脂肪分解为 IDL E−。 E- 的致密 VLDL 脂肪分解为 IDL 的速率常数大于 E+，并且致密 VLDL E+ 的血浆清除速率常数大于 E-。总之，人 VLDL 颗粒的代谢受到 apoE 含量的影响，并进一步受到 apoC-III 共存的调节。
We studied the metabolism of very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) particles that did or did not have apolipoprotein E (apoE) in 12 normolipidemic women by endogenously labeling plasma apolipoprotein B. The plasma was separated into bound (E+) and unbound (E−) fractions by use of a monoclonal antibody (1D7), and the fractions were ultracentrifuged to yield E+ and E− subfractions of light and dense VLDL and IDL. VLDL E+ and IDL E+ were produced mainly by the liver. VLDL E+ and IDL E+ had lower fractional catabolic rates and much higher apolipoprotein C-III (apoC-III) content than did the corresponding E− particles. Most light VLDL apoE+ underwent lipolysis to dense VLDL E+ with reduced apoC-III content, which was removed from the circulation without conversion to IDL. In contrast, most light VLDL apoE−, poor in apoC-III, was removed from the circulation, and a smaller proportion underwent lipolysis to dense VLDL E−. Most dense VLDL E− underwent lipolysis to IDL E−. The rate constant for lipolysis of dense VLDL to IDL was greater for E− than for E+, and the rate constant for clearance from plasma was greater for dense VLDL E+ than for E−. In conclusion, metabolism of human VLDL particles is influenced by their content of apoE, further modulated by the coexistence of apoC-III.