低密度脂蛋白在兔体内实质和非实质肝细胞中的摄取。在喂食胆固醇的兔子中，内皮细胞的低密度脂蛋白摄取增加。

Uptake of LDL in parenchymal and non-parenchymal rabbit liver cells in vivo. LDL uptake is increased in endothelial cells in cholesterol-fed rabbits.

作者信息

Nenseter M S, Blomhoff R, Drevon C A, Kindberg G M, Norum K R, Berg T

机构信息

Institute for Nutrition Research, University of Oslo, Norway.

出版信息

Biochem J. 1988 Sep 1;254(2):443-8. doi: 10.1042/bj2540443.

DOI:10.1042/bj2540443

PMID:2845951

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1135097/

Abstract

Hepatic uptake of low-density lipoprotein (LDL) in parenchymal cells and non-parenchymal cells was studied in control-fed and cholesterol-fed rabbits after intravenous injection of radioiodinated native LDL (125I-TC-LDL) and methylated LDL (131I-TC-MetLDL). 2. LDL was taken up by rabbit liver parenchymal cells, as well as by endothelial and Kupffer cells. Parenchymal cells, however, were responsible for 92% of the hepatic LDL uptake. 3. Of LDL in the hepatocytes, 89% was taken up via the B,E receptor, whereas 16% and 32% of the uptake of LDL in liver endothelial cells and Kupffer cells, respectively, was B,E receptor-dependent. 4. Cholesterol feeding markedly reduced B,E receptor-mediated uptake of LDL in parenchymal liver cells and in Kupffer cells, to 19% and 29% of controls, respectively. Total uptake of LDL in liver endothelial cells was increased about 2-fold. This increased uptake is probably mediated via the scavenger receptor. The B,E receptor-independent association of LDL with parenchymal cells was not affected by the cholesterol feeding. 5. It is concluded that the B,E receptor is located in parenchymal as well as in the non-parenchymal rabbit liver cells, and that this receptor is down-regulated by cholesterol feeding. Parenchymal cells are the main site of hepatic uptake of LDL, both under normal conditions and when the number of B,E receptors is down-regulated by cholesterol feeding. In addition, LDL is taken up by B,E receptor-independent mechanism(s) in rabbit liver parenchymal, endothelial and Kupffer cells. The non-parenchymal liver cells may play a quantitatively important role when the concentration of circulating LDL is maintained at a high level in plasma, being responsible for 26% of hepatic uptake of LDL in cholesterol-fed rabbits as compared with 8% in control-fed rabbits. The proportion of hepatic LDL uptake in endothelial cells was greater than 5-fold higher in the diet-induced hypercholesterolaemic rabbits than in controls.

摘要

在给对照饮食和胆固醇饮食的兔子静脉注射放射性碘化天然低密度脂蛋白（125I-TC-LDL）和甲基化低密度脂蛋白（131I-TC-MetLDL）后，研究了实质细胞和非实质细胞对低密度脂蛋白（LDL）的肝摄取情况。2. 兔肝实质细胞以及内皮细胞和库普弗细胞均可摄取LDL。然而，实质细胞占肝脏LDL摄取量的92%。3. 肝细胞内LDL的摄取，89%是通过B、E受体进行的，而肝内皮细胞和库普弗细胞摄取LDL的过程中，分别有16%和32%依赖B、E受体。4. 给予胆固醇饮食显著降低了实质肝细胞和库普弗细胞中B、E受体介导的LDL摄取，分别降至对照的19%和29%。肝内皮细胞中LDL的总摄取量增加了约2倍。这种摄取增加可能是通过清道夫受体介导的。LDL与实质细胞的非B、E受体依赖性结合不受胆固醇饮食的影响。5. 得出的结论是，B、E受体存在于兔肝的实质细胞和非实质细胞中，且该受体可被胆固醇饮食下调。无论是在正常情况下，还是当B、E受体数量因胆固醇饮食而下调时，实质细胞都是肝脏摄取LDL的主要部位。此外，兔肝实质细胞、内皮细胞和库普弗细胞可通过非B、E受体依赖性机制摄取LDL。当血浆中循环LDL浓度维持在高水平时，非实质肝细胞可能在数量上发挥重要作用，在给予胆固醇饮食的兔子中，其占肝脏LDL摄取量的26%，而在对照饮食的兔子中为8%。饮食诱导的高胆固醇血症兔子的肝内皮细胞中LDL摄取比例比对照高5倍以上。