The crucial roles of apolipoproteins E and C-III in apoB lipoprotein metabolism in normolipidemia and hypertriglyceridemia.
The crucial roles of apolipoproteins E and C-III in apoB lipoprotein metabolism in normolipidemia and hypertriglyceridemia.
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DOI：
10.1097/mol.0000000000000146
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发表时间：
2015-02
影响因子：
4.4
通讯作者：
Sacks FM
中科院分区：
文献类型：
--
作者：
Sacks FM
为了描述载脂蛋白C-III（apoC-III）和apoE在VLDL和LDL代谢中的作用，ApoC-III可阻断载脂蛋白B（apoB）脂蛋白从循环中的清除，而apoE介导其清除。正常血脂通过肝脏分泌VLDL和IDL亚种（包含apoE和apoC-III（VLDL E+C-III+））维持。大多数VLDL E+C-III+迅速脂解，apoC-III含量减少，并作为含有致密VLDL、IDL和轻LDL的apoE从循环中清除。相反，在高脂血症中，大多数VLDL与apoC-III一起分泌，但不含apoE，因此直到在脂解成致密LDL期间失去apoC-III才被清除。在血脂正常的情况下，肝脏也分泌IDL和大中型LDL，而在高血脂症中，肝脏分泌更致密的LDL（含和不含apoC-III）。这些途径建立了高脂血症表型，并将其代谢连接到致密LDL。与不饱和脂肪相比，膳食碳水化合物抑制了由apoE介导的代谢途径，这与高脂血症中抑制的代谢途径在性质上相似。apoC-III和apoE对VLDL和LDL亚种的相反作用，以及LDL以几种大小的直接分泌，建立了正常和高脂血症人类中人类apoB脂蛋白代谢的大部分基本结构。
To describe the roles of apolipoprotein C-III (apoC-III) and apoE in VLDL and LDL metabolism ApoC-III can block clearance from the circulation of apolipoprotein B (apoB) lipoproteins, whereas apoE mediates their clearance. Normolipidemia is sustained by hepatic secretion of VLDL and IDL subspecies that contain both apoE and apoC-III (VLDL E+C-III+). Most of this VLDL E+C-III+ is speedily lipolyzed, reduced in apoC-III content, and cleared from the circulation as apoE containing dense VLDL, IDL, and light LDL. In contrast, in hypertriglyceridemia, most VLDL is secreted with apoC-III but without apoE, and so it is not cleared until it loses apoC-III during lipolysis to dense LDL. In normolipidemia, the liver also secretes IDL and large and medium-size LDL, whereas in hypertriglyceridemia, the liver secretes more dense LDL with and without apoC-III. These pathways establish the hypertriglyceridemic phenotype and link it metabolically to dense LDL. Dietary carbohydrate compared with unsaturated fat suppresses metabolic pathways mediated by apoE that are qualitatively similar to those suppressed in hypertriglyceridemia. The opposing actions of apoC-III and apoE on subspecies of VLDL and LDL, and the direct secretion of LDL in several sizes, establish much of the basic structure of human apoB lipoprotein metabolism in normal and hypertriglyceridemic humans.