Dietschy J M
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-8887, USA.
Am J Clin Nutr. 1997 May;65(5 Suppl):1581S-1589S. doi: 10.1093/ajcn/65.5.1581S.
The concentration of cholesterol carried in low-density-lipoprotein cholesterol (LDL-C) is predominantly dictated by metabolic events occurring in liver. LDL-C is derived from the intravascular metabolism of very-low-density lipoproteins, and, in every species, this lipoprotein particle is predominantly cleared by liver through receptor-dependent mechanisms. In addition to cholesterol absorbed from the diet, sterol is also synthesized within the body and this synthesis occurs predominantly in extrahepatic organs. When the amount of cholesterol input into the body is increased, there is expansion of the pools of sterol within liver cells and down-regulation of the receptors responsible for clearing LDL-C from the bloodstream. As a consequence, the concentration of LDL-C in plasma increases. When dietary cholesterol intake is kept constant, some long-chain saturated fatty acids further suppress hepatic LDL receptor activity whereas several unsaturated fatty acids have the opposite effect. These regulatory events are apparently articulated through the ability of these fatty acids to shift intracellular cholesterol between a regulatory and a storage pool. High-density lipoproteins, in contrast, function primarily to move excess cholesterol from the extrahepatic organs to liver for excretion. Although the concentration of high-density-lipoprotein cholesterol in the plasma may be influenced by the rate of apolipoprotein A-I production or the activity of cholesterol ester transfer protein, it is less clear whether dietary long-chain fatty acids have any effect on these processes. The regulatory effects of the saturated and unsaturated long-chain fatty acids on LDL-C concentrations can be shown in a variety of experimental animals and also in humans.
低密度脂蛋白胆固醇（LDL-C）所携带的胆固醇浓度主要由肝脏中发生的代谢事件决定。LDL-C源自极低密度脂蛋白的血管内代谢，并且在每个物种中，这种脂蛋白颗粒主要通过受体依赖性机制由肝脏清除。除了从饮食中吸收的胆固醇外，体内也会合成固醇，且这种合成主要发生在肝外器官。当进入体内的胆固醇量增加时，肝细胞内的固醇池会扩大，负责从血液中清除LDL-C的受体下调。结果，血浆中LDL-C的浓度增加。当饮食中的胆固醇摄入量保持恒定时，一些长链饱和脂肪酸会进一步抑制肝脏LDL受体活性，而几种不饱和脂肪酸则有相反的作用。这些调节事件显然是通过这些脂肪酸在调节池和储存池之间转移细胞内胆固醇的能力来实现的。相比之下，高密度脂蛋白的主要功能是将多余的胆固醇从肝外器官转运到肝脏进行排泄。虽然血浆中高密度脂蛋白胆固醇的浓度可能受载脂蛋白A-I产生速率或胆固醇酯转移蛋白活性的影响，但饮食中的长链脂肪酸是否对这些过程有任何影响尚不清楚。饱和和不饱和长链脂肪酸对LDL-C浓度的调节作用在多种实验动物和人类中都有体现。
