Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metaboli

1982

DOI: 10.1016/0005-2760(82)90263-6

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Receptor-mediated catabolism and tissue uptake of human low density lipoprotein in the cholesterol-fed, atherosclerotic rabbit

Howard R. Slater

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Christopher J. Packard

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Cited by 30 publications

(6 citation statements)

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“…This pathway is also available for native LDL, and by determining total and B,E receptor-independent uptake, the B,E receptordependent removal can be estimated. Previous studies have shown that plasma decay curves for native and cyclohexanedione-modified LDL were superimposable in cholesterol fed rabbits [7]. All LDL was removed from the blood via a B,E receptor-independent pathway in these animals.…”

Section: Introductionmentioning

confidence: 79%

“…By feeding rabbits a cholesterol-enriched diet, the hepatic uptake of LDL is markedly reduced, due to a decrease in the number of LDL receptors [4]. By chemical modification of lysine and arginine residues of LDL, the lipoprotein particles do not bind to the LDL receptor; the modified LDL is instead taken up via a B,E receptorindependent mechanism [5][6][7]. This pathway is also available for native LDL, and by determining total and B,E receptor-independent uptake, the B,E receptordependent removal can be estimated.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

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et al. 1988

Biochemical Journal

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1. 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.

“…This pathway is also available for native LDL, and by determining total and B,E receptor-independent uptake, the B,E receptordependent removal can be estimated. Previous studies have shown that plasma decay curves for native and cyclohexanedione-modified LDL were superimposable in cholesterol fed rabbits [7]. All LDL was removed from the blood via a B,E receptor-independent pathway in these animals.…”

Section: Introductionmentioning

confidence: 79%

“…By feeding rabbits a cholesterol-enriched diet, the hepatic uptake of LDL is markedly reduced, due to a decrease in the number of LDL receptors [4]. By chemical modification of lysine and arginine residues of LDL, the lipoprotein particles do not bind to the LDL receptor; the modified LDL is instead taken up via a B,E receptorindependent mechanism [5][6][7]. This pathway is also available for native LDL, and by determining total and B,E receptor-independent uptake, the B,E receptordependent removal can be estimated.…”

Section: Introductionmentioning

confidence: 99%

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

¹

,

²

,

³

et al. 1988

Biochemical Journal

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1. 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.

“…in perfusate per g of liver) of native and modified LDLs was also measured in each perfusion experiment. Slater et al [44] have shown that tissue uptake of LDL reflects the immediate binding to membranes rather than the cumulative uptake of LDL, since internalization and degradation occurs very rapidly. We found that about 85 % of the radioactivity associated with the liver was in the TCA pellet.…”

Section: Resultsmentioning

confidence: 99%

Altered hepatic catabolism of low-density lipoprotein subjected to lipid peroxidation in vitro

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et al. 1994

Biochemical Journal

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Recent evidence suggests that oxidatively modified forms of low-density lipoprotein (LDL) may be particularly atherogenic. In this investigation, the catabolism of human LDL modified by lipid peroxidation in vitro was studied with a recirculating rat liver perfusion system. A dual-labelling technique was used that permitted native LDL and modified LDL to be studied simultaneously in the liver perfusion system. Native human LDL was found to have a fractional catabolic rate (FCR) of 1.00 +/- 0.21%/h, in agreement with other investigators. Subjecting LDL to oxidation for 12 h in the presence of 30 microM FeEDTA did not significantly affect its FCR. LDL treated with a superoxide-generating system (xanthine oxidase, hypoxanthine, O2) in the presence of 30 microM FeEDTA did, however, show a significant increase in FCR (3.23 +/- 0.19%/h). The hepatic uptakes of native LDL and LDL oxidized with FeEDTA+O2 were similar, but both were significantly lower than the hepatic uptake of LDL treated with the superoxide-radical-generating system. The proteolysis of LDL with pancreatin did not influence either its susceptibility to oxidation or its FCR. LDL oxidation resulted in the preferential loss of alpha-tocopherol rather than gamma-tocopherol. These data indicate that the rat liver effectively catabolizes LDL oxidatively modified by treatment with the superoxide-generating system. Furthermore, our results suggest that only very low plasma levels of highly oxidized LDL could be found under conditions in vivo. The liver may therefore play a major role in protecting the arterial vasculature from highly atherogenic forms of LDL.

“…CETP transgenic/ LDLr knockout mice showed 1.8-fold more atherosclerosis than LDLr knockout mice (35). A more indirect indication that CETP may promote atherosclerosis is the finding that a CETP inhibitor attenuated atherosclerosis in rabbits fed an atherogenic diet (36), and this diet would have suppressed LDLr function (37). These studies indicate that high CETP activity is proatherogenic when LDLr function is strongly suppressed.…”

Section: Discussionmentioning

confidence: 99%

Influence of dietary fatty acid composition on the relationship between CETP activity and plasma lipoproteins in monkeys

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et al. 2001

Journal of Lipid Research

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CETP activity, measured as transfer of cholesteryl ester from exogenous HDL to exogenous VLDL and LDL, reflecting CETP mass as determined by ELISA, was documented in three groups of St. Kitts vervet monkeys fed diets enriched in saturated (Sat), monounsaturated (Mono), or n-6 polyunsaturated (Poly) fatty acids. CETP activity was not different when comparing the three dietary fats. However, CETP activity was significantly higher when cholesterol was added to each of the diets. Significant positive associations between CETP activity and VLDL and LDL cholesterol concentrations were found whereas significant negative associations were seen between CETP activity and HDL cholesterol in each of the diet groups. The strength of these associations was highest in the Sat group. Cholesteryl ester (CE) fatty acid composition of lipoproteins varied widely among diet groups, with the more polyunsaturated CE of the Poly group being associated with a higher rate of CE transfer to endogenous acceptor apolipoprotein B-containing lipoproteins.Finally, only the Sat diet group showed significant positive correlations of CETP activity with LDL particle diameter ( r ‫؍‬ 0.76), cholesteryl ester percentage ( r ‫؍‬ 0.67), and a strong negative correlation ( r ‫؍‬ ؊ 0.86) with LDL receptor function, estimated as the difference between native and methylated LDL turnover rates. We speculate that strong associations between CETP and LDL metabolism may explain, at least in part, the increased atherogenicity of dietary saturated fat. -Fusegawa, Y.

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