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.

Effect of Turmeric and Ginger on Lipid Profile in Male Rats Exposed to Oxidative Stress

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Eman A. Al-Rekabi ◽  
Dheyaa K. Alomer ◽  
Rana Talib Al-Muswie ◽  
Khalid G. Al-Fartosi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Drinking Water ◽  
Lipid Profile ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Control Group ◽  
Very Low Density Lipoprotein ◽  
Low Density

The present study aimed to investigate the effect of turmeric and ginger on lipid profile of male rats exposed to oxidative stress induced by hydrogen peroxide H2O2 at a concentration of 1% given with consumed drinking water to male rats. Methods: 200 mg/kg from turmeric and ginger were used, and the animals were treatment for 30 days. Results: the results showed a significant increase in cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), whereas it explained a significant decrease in high density lipoprotein (HDL) of male rats exposed to oxidative stress when compared with control group. the results showed a significant decrease in cholesterol, triglycerides, (LDL), (VLDL), whereas it explained a significant increase in (HDL) of rats treated with turmeric and ginger at dose 200 mg/kg when compared with male rats exposed to oxidative stress.

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.

Tracking of Serum Cholesterol and Lipoprotein Levels From the First Year of Life

PEDIATRICS ◽  
1993 ◽  
Vol 91 (5) ◽  
pp. 949-954
Author(s):  
Markku J. T. Kallio ◽  
Leena Salmenperä ◽  
Martti A. Siimes ◽  
Jaakko Perheentupa ◽  
Tatu A. Miettinen
Keyword(s):  
Serum Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cholesterol Concentration ◽  
Total Serum ◽  
Total Serum Cholesterol ◽  
First Year ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
First Year Of Life

Objective. To examine the development of tracking of serum cholesterol concentration from birth to childhood. Design. In a longitudinal study of healthy children, concentrations of total serum cholesterol and triglyceride were determined at birth (n = 193); at 2 (n = 192), 4 (n = 192), 6 (n = 190), 7.5 (n = 118), 9 (n = 188), and 12 months (n = 196); and at 5 years of age (n = 162). Concentrations of cholesterol—very-low-density lipoprotein, low-density lipoprotein, high-density lipoprotein-2 (HDL2), and HDL3—were determined at 2, 6, 9, and 12 months (n = 36) and at 5 years (n = 162). Results. The correlation coefficients of total cholesterol levels during the first year of life with the level at 5 years of age were as follows: at birth .04, at 2 months .36 (P < .001), at 4 months .26 (P < .001), at 6 months .28 (P < .001), at 7.5 months .25 (P < .001), at 9 months .35 (P < .001), and at 12 months .48 (P < .001). The correlation for exclusively breast-fed children between 6 months and 5 years of age was r = .37, P < .001, while that for children receiving partially breast milk, formula, or solid foods was r = .12, P = not significant (NS), and between 9 months and 5 years r = .38, P < .01, and r = .28, P < .05, respectively. The correlation coefficients of the lipoprotein levels between ages 12 months and 5 years were as follows: low-density lipoprotein cholesterol .58 (P < .001), total HDL cholesterol .30 (P < .05), HDL2 cholesterol .34 (P < .05), HDL3 cholesterol .17 (P = NS), very-low-density lipoprotein cholesterol .24 (P = NS), total triglyceride .37 (P < .05), and triglyceride-very-low-density lipoprotein .37 (P < .05). Of the children whose total serum cholesterol level was above the 90th percentile at birth, or at 2, 4, 6, 7.5, 9, or 12 months, 6%, 35%, 29%, 30%, 31%, 33%, and 45%, respectively, were above the 90th percentile at 5 years of age. In retrospect, 45% of the children whose serum cholesterol level was above the 90th percentile at 5 years were above the 90th percentile at the age of 12 months and 80% were in the highest quartile. Conclusions. The results indicate that tracking of serum cholesterol concentration during the first year of life is stronger when examining children who are receiving a relatively homogenous diet, such as exclusive breast-feeding, and weaker as children are weaned to formula and solid foods. After the weaning process is completed, children's relative serum cholesterol levels have become established and the tracking of serum cholesterol is of the same magnitude as for older children and adolescents.

Physiological and Histological Study to the Effects of Monosodium Glutamate in Laboratory male Rats and the protective role of vitamin E

2019 ◽  
Vol 10 (02) ◽  
Author(s):  
Genan Musheer Ghaib AL-Khatawi ◽  
Mohammed R S AL-Attabi ◽  
Ali Fayadh Bargooth
Keyword(s):  
Body Weight ◽  
Vitamin E ◽  
Low Density Lipoprotein ◽  
Monosodium Glutamate ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Liver And Kidney

The current study was conducted at the Department of Biology, College of Science, Wasit University to investigate physiological and histological effect monosodium glutamate in laboratory male rats, preventive role of vitamin E. This study was carried out in Laboratories of College of Science, Wasit University, AL- Shaheed Dr. Fairooz Hospitals, from November 2017 to April 2018.The study included twenty-four and divided into four groups (six rats per group). the first group severe as a control group orally dosed with distilled water, and treated the second group (100 mg/kg b.w. Monosodium glutamate for 30 days, and the third group were dosed orally 200 mg/kg of b.w. for 30 days, either The fourth group were dosed with a mixture of Monosodium glutamate 200mg/kg and vitamin E 100 mg/kg of body weight for 30 days. after the trial period has been sacrificing animals for testing and chemical standards physiological and histological. As are result of by exposure to Monosodium glutamate in blood serum are negatively biochemical whole height of the level of serum cholesterol, triglycerides, Low-density lipoprotein, very- low density lipoprotein, liver enzymes, AST, ALT, ALP, creatinine level, urea serum, further more we noticed a decrease in high density lipoprotein. The preventive treatment resulted in vitamin E 100mg/kg b.w. with Monosodium glutamate 200 mg/kg b.w. (p≤ 0.05) in body weight and relative weights of organs (liver and kidney). We noticed a higher moral when treatment with vitamin E with Monosodium glutamate 100 mg/kg in high- density lipoprotein, while serum cholesterol level decrease, triglycerides, Low-density lipoprotein, very- low density lipoprotein. And liver and kidney functions have improved by low Enzyme AST, ALT, ALP, creatinine and urea serum level. Histological examination revealed that the liver and kidneys, of rats exposed 100, 200 mg/kg of Monosodium glutamate has been adversely affected by exposure to Monosodium glutamate. Whereas, the histological of the liver of animals treated with vitamin E with Monosodium glutamate natural pictures showed improvement. These results demonstrate that MSG toxic effects on the liver and kidney tissue. The more toxic than salt rate too. The study recommends to avoid using MSG as food additives and food for animals because of the toxic effects of this salt.

Effect of storage at 4 degrees C and -20 degrees C on lipid, lipoprotein, and apolipoprotein concentrations

1995 ◽  
Vol 41 (3) ◽  
pp. 392-396 ◽  
Author(s):  
K Evans ◽  
J Mitcheson ◽  
M F Laker
Keyword(s):  
High Density Lipoprotein ◽  
Apolipoprotein B ◽  
Free Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Total Serum ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Serum Concentrations ◽  
Vldl Triglyceride

Abstract We have investigated the effects on lipid, apolipoprotein, and lipoprotein measurements of storing unfractionated serum at 4 degrees C for 10 days and at -20 degrees C for 10 days or 3 months. Total serum concentrations of lipids were stable, although apolipoprotein B showed a 5.3% increase after 3 months at -20 degrees C (P < 0.001). Increases in low-density (LDL) and high-density lipoprotein (HDL) triglyceride and very-low-density lipoprotein (VLDL) esterified cholesterol concentrations and decreases in free cholesterol concentrations in LDL and HDL after storage of serum for 10 days at 4 degrees C were verified by fractionation of lipoproteins by sequential flotation ultracentrifugation. Ten days' storage of serum at -20 degrees C resulted in increases in VLDL triglyceride and phospholipid concentrations, with decreases in HDL concentrations in triglycerides and phospholipids; changes were more extensive after 3 months at -20 degrees C. We conclude that ultracentrifugation of serum for lipoprotein analysis should be performed as soon as possible after collection.

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