scholarly journals Morphological characterization of the cholesteryl ester cycle in cultured mouse macrophage foam cells.

1983 ◽  
Vol 97 (4) ◽  
pp. 1156-1168 ◽  
Author(s):  
D J McGookey ◽  
R G Anderson
Keyword(s):  
Cholesteryl Ester ◽  
Lipase Activity ◽  
Lipid Droplets ◽  
Free Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
The Body ◽  
Cyclic Process ◽  
Low Density ◽  
Cholesteryl Esters

Mouse peritoneal macrophages can be induced to accumulate cholesteryl esters by incubating them in the presence of acetylated low density lipoprotein. The cholesteryl esters are sequestered in neutral lipid droplets that remain in the cell even when the acetylated low density lipoprotein is removed from the culture media. Previous biochemical studies have determined that the cholesterol component of cholesteryl ester droplets constantly turns over with a half time of 24 h by a cyclic process of de-esterification and re-esterification. We have used morphologic techniques to determine the spatial relationship of cholesteryl ester, free cholesterol, and lipase activity during normal turnover and when turnover is disrupted. Lipid droplets were surrounded by numerous 7.5-10.0-nm filaments; moreover, at focal sites on the margin of each droplet there were whorles of concentrically arranged membrane that penetrated the matrix. Histochemically detectable lipase activity was associated with these stacks of membrane. Using filipin as a light and electron microscopic probe for free cholesterol, we determined that a pool of free cholesterol was associated with each lipid droplet. Following incubation in the presence of the exogenous cholesterol acceptor, high density lipoprotein, the cholesteryl ester droplets disappeared and were replaced with lipid droplets of a different lipid composition. Inhibition of cholesterol esterification caused cholesteryl ester droplets to disappear and free cholesterol to accumulate in numerous myelin-like structures in the body of the cell.

scholarly journals Cholesterol is required for secretion of very-low-density lipoprotein by rat liver

1989 ◽  
Vol 258 (3) ◽  
pp. 807-816 ◽  
Author(s):  
B Khan ◽  
H G Wilcox ◽  
M Heimberg
Keyword(s):  
Free Cholesterol ◽  
Low Density Lipoprotein ◽  
Specific Radioactivity ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Cholesterol Concentration ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Cholesteryl Esters ◽  
Metabolic Pool

To study potential effects of hepatic cholesterol concentration on secretion of very-low-density lipoprotein (VLDL) by the liver, male rats were fed on unsupplemented chow, chow with lovastatin (0.1%), or chow with lovastatin (0.1%) and cholesterol (0.1%) for 1 week. Livers were isolated from these animals and perfused in vitro, with a medium containing [2-14C]acetate, bovine serum albumin and glucose in Krebs-Henseleit buffer, and with an oleate-albumin complex. With lovastatin feeding, the hepatic concentrations of cholesteryl esters and triacylglycerols before perfusion were decreased, although free cholesterol was unchanged. However, hepatic secretion of all the VLDL lipids was decreased dramatically by treatment with lovastatin. Although total secretion of VLDL triacylglycerol, phospholipid, cholesterol and cholesteryl esters was decreased, the decrease in triacylglycerol was greater than that in free cholesterol or cholesteryl esters, resulting in secretion of a VLDL particle enriched in sterols relative to triacylglycerol. In separate studies, the uptake of VLDL by livers from control animals or animals treated with lovastatin was measured. Uptake of VLDL was estimated by disappearance of VLDL labelled with [1-14C]oleate in the triacylglycerol moiety, and was observed to be similar in both groups. During perfusion, triacylglycerol accumulated to a greater extent in livers from lovastatin-fed rats than in control animals. The depressed output of VLDL triacylglycerols and the increase in triacylglycerol in the livers from lovastatin-treated animals was indicative of a limitation in the rate of VLDL secretion. Addition of cholesterol (either free cholesterol or human low-density lipoprotein) to the medium perfusing livers from lovastatin-fed rats, or addition of cholesterol to the diet of lovastatin-fed rats, increased the hepatic concentration of cholesteryl esters and the output of VLDL lipids. The concentration of cholesteryl esters in the liver was correlated with the secretion of VLDL by the liver. These data suggest that cholesterol is an obligate component of the VLDL required for its secretion. It is additionally suggested that cholesteryl esters are in rapid equilibrium with a small pool of free cholesterol which comprises a putative metabolic pool available and necessary for the formation and secretion of the VLDL. Furthermore, the specific radioactivity (d.p.m./mumol) of the secreted VLDL free cholesterol was much greater than that of hepatic free cholesterol, suggesting that the putative hepatic metabolic pool is only a minor fraction of total hepatic free cholesterol.

scholarly journals Hydrolysis of cholesteryl ester in low density lipoprotein converts this lipoprotein to a liposome.

1992 ◽  
Vol 267 (7) ◽  
pp. 4992-4998
Author(s):  
F.F. Chao ◽  
E.J. Blanchette-Mackie ◽  
V.V. Tertov ◽  
S.I. Skarlatos ◽  
Y.J. Chen ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Hydrolysis Of

Plasma lipoprotein profiles of normocholesterolemic and hypercholesterolemic homozygotes for apolipoprotein E2(Arg158-->Cys) compared

1994 ◽  
Vol 40 (8) ◽  
pp. 1559-1566 ◽  
Author(s):  
S P Zhao ◽  
A H Smelt ◽  
A M Van den Maagdenberg ◽  
A Van Tol ◽  
T F Vroom ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoprotein ◽  
Cholesterol Concentration ◽  
Low Density ◽  
Plasma Cholesteryl Ester ◽  
Familial Dysbetalipoproteinemia ◽  
Lipoprotein Profiles

Abstract We compared plasma lipoprotein profiles of 15 individuals with normocholesterolemic (plasma cholesterol 4.81 +/- 0.90 mmol/L) familial dysbetalipoproteinemia (NFD) and 15 patients with hypercholesterolemic (plasma cholesterol 10.61 +/- 2.32 mmol/L) familial dysbetalipoproteinemia (HFD), matched for age and sex. All subjects were homozygous for apoE2(Arg158-->Cys). Compared with 15 normolipidemic controls (plasma cholesterol 5.47 +/- 0.92 mmol/L), subjects with NFD and HFD had greater cholesterol concentrations of large very-low-density lipoprotein (VLDL1), small VLDL (VLDL2), and intermediate-density lipoprotein, each of which was correlated to their plasma total cholesterol concentration. VLDL1 and VLDL2 subfractions were enriched in cholesteryl ester, and plasma cholesteryl ester transfer protein activities were increased in both NFD and HFD; however, absolute changes were larger in HFD than in NFD. Concentrations of low-density lipoprotein cholesterol were lower in HFD (1.89 +/- 0.48 mmol/L) and NFD (1.56 +/- 0.36 mmol/L) than in normolipidemic controls (3.35 +/- 0.73 mmol/L). We conclude that all subjects homozygous for apoE2(Arg158-->Cys) show features of dysbetalipoproteinemia.

scholarly journals The preferential uptake of very-low-density lipoprotein cholesteryl ester by rat liver in vivo

1990 ◽  
Vol 272 (3) ◽  
pp. 735-741 ◽  
Author(s):  
J C Holder ◽  
V A Zammit ◽  
D S Robinson
Keyword(s):  
Fatty Acid ◽  
Cholesteryl Ester ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Apoprotein B ◽  
Preferential Uptake ◽  
Triacylglycerol Fraction

The removal from the blood and the uptake by the liver of injected very-low-density lipoprotein (VLDL) preparations that had been radiolabelled in their apoprotein and cholesteryl ester moieties was studied in lactating rats. Radiolabelled cholesteryl ester was removed from the blood and taken up by the liver more rapidly than sucrose-radiolabelled apoprotein. Near-maximum cholesteryl ester uptake by the liver occurred within 5 min of the injection of the VLDL. At this time, apoprotein B uptake by the liver was only about 25% of the maximum. Maximum uptake of the injected VLDL apoprotein B label was not achieved until at least 15 min after injection, by which time the total uptakes of cholesteryl ester and apoprotein B label were very similar. The results suggest that preferential uptake of the lipoprotein cholesteryl ester by the liver occurred before endocytosis of the entire lipoprotein complex. The fate of the injected VLDL cholesteryl ester after its uptake by the liver was also monitored. Radiolabel associated with the hepatic cholesteryl ester fraction fell steadily from its early maximum level, the rate of fall being faster and more extensive when the fatty acid, rather than the cholesterol, moiety of the ester was labelled. By 30 min after the injection of VLDL containing [3H]cholesteryl ester, over one-third of the injected label was already present as [3H]cholesterol in the liver. When VLDL containing cholesteryl [14C]oleate was injected, a substantial proportion (about 25%) of the injected radiolabelled fatty acid appeared in the hepatic triacylglycerol fraction within 60 min: very little was present in the plasma triacylglycerol fraction at this time.

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