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At least 19 recordsLinked to original sources
PubMedDate not supplied

Relation of diet to LDL cholesterol, VLDL cholesterol, and plasma total cholesterol and triglycerides in white adults. The Lipid Research Clinics Prevalence Study.

The association of diet with low density lipoprotein cholesterol (LDL-C) and total triglycerides, as well as with total and very low density lipoprotein cholesterol (VLDL-C), was investigated in a random sample of 4374 white participants aged 20 to 59 years seen by the Lipid Research Clinic Prevalence Study. Carbohydrate and total calories were negatively associated with LDL-C. There was also a statistically significant positive association of LDL-C with the percentage of total calories from fat. These three findings are generally consistent with what other cross-sectional studies have reported for the relation of diet with total cholesterol levels. The only diet variables significantly related to triglyceride levels in both men and women were the percentage of calories from fats, particularly polyunsaturated fatty acids (PFA), the P/S ratio, and the number of grams of PFA per day, all of which were inversely associated with the level of this lipid.

Adult↗
PubMed1987

VLDL cholesterol and VLDL apolipoprotein B. Preliminary cross-sectional data of the prospective epidemiological study of company employees in Westphalia.

VLDL cholesterol concentrations were determined in 1641 male and 608 female and VLDL apolipoprotein B concentrations in 505 male and 211 female company employees in Westphalia aged 17-70 years. VLDL cholesterol and VLDL apolipoprotein B values were found to be distributed with positive skew in both sexes but were higher in men than in women (median in men: VLDL cholesterol 0.30 mmol/l, VLDL apolipoprotein B 0.066 g/l, median in women: VLDL cholesterol 0.18 mmol/l, VLDL apolipoprotein B 0.047 g/l). In males VLDL cholesterol and VLDL apolipoprotein B were closely correlated to each other (r = 0.757) as well as to triacylglycerols (VLDL cholesterol: r = 0.673, VLDL apolipoprotein B: r = -0.419). In females these observed correlations were weaker. The VLDL cholesterol/VLDL apolipoprotein B ratio was also higher in men (median 4.28 mmol/g) than in women (median 3.15 mmol/g). The ratio correlated to triacylglycerols (men: r = 0.591, women: r = 0.321). The results suggest that the composition of VLDL may be related to triacylglycerols in serum.

Adolescent↗
PubMed1992

Evidence for a common biliary cholesterol and VLDL cholesterol precursor pool in rat liver.

Hepatic free cholesterol levels are influenced by cholesterol synthesis and ester formation, which, in turn, might regulate cholesterol secretion into bile and plasma. We manipulated the rates of hepatic cholesterol synthesis and esterification and measured biliary and very low density lipoprotein (VLDL) cholesterol secretion, and bile acid synthesis. Mevalonate decreased HMG CoA reductase by 80%, increased acyl coenzyme A: cholesterol acyltransferase (ACAT) by 60% and increased [3H]oleate incorporation into microsomal and VLDL cholesteryl esters by 174% and 122%, respectively. Microsomal and biliary free cholesterol remained constant at the expense of increased microsomal and VLDL cholesteryl ester content. Mevalonate did not change bile acid synthesis. 25-OH cholesterol decreased HMG-CoA reductase by 39%, increased ACAT by 24%, but did not effect 7 alpha-hydroxylase. 25-OH cholesterol increased [3H]oleate in microsomal and VLDL cholesterol esters by 71% and 120%. Biliary cholesterol decreased by 40% and VLDL cholesteryl esters increased by 83%. A small and unsustained decrease in bile acid synthesis (14CO2 release) occurred after 25-OH cholesterol. After orotic acid feeding, HMG-CoA reductase increased 352%, and [3H]oleate in microsomal and VLDL cholesteryl esters decreased by 43% and 89%. Orotic acid decreased all VLDL components including free cholesterol (68%) and cholesteryl esters (55%), and increased biliary cholesterol by 160%. No change in bile acid synthesis occurred. Hepatic cholesterol synthesis and esterification appear to regulate a cholesterol pool available for both biliary and VLDL secretion. Changing cholesterol synthesis and esterification did not alter bile acid synthesis, suggesting that either this common bile/VLDL secretory pool is functionally distinct from the cholesterol pool used for bile salt synthesis, or that free cholesterol availability in this precursor pool is not a major determinant of bile acid synthesis.

Animals↗
PubMed1980

[Comparative study of total cholesterol, HDL cholesterol, LDL + VLDL cholesterol. Two methods: precipitation by concanavalin A and ultra centrifugation (author's transl)].

The authors determined in 3 populations (37 controls, 59 asymptomatic hyperlipemias, and 20 cases of arterial hyperlipemia) the total cholesterol, the HDL cholesterol and the LDL + VLDL cholesterol and their ratio by two methods : precipitation by concanavalin A and ultracentrifugation (AirFuge). These various lipid parameters were compared between 3 populations in order to determine their more or less discriminant character; furthermore, was established the degree of correlation between the results obtained by precipitation with concanavalin A and by ultracentrifugation. The results show : firstly, that the LDL + VLDL was significantly higher and the ratio HDL/LDL + VLDL significantly lower in hyperlipemia and in arterial disease compared with controls ; the HDL was significantly lower in arterial disease than in controls. No lipid parameter permitted one to differentiate between asymptomatic hyperlipemia and arterial disease. Furthermore, the correlation determined by the chi square method was very strong between the results obtained by precipitation with concanavalin A and ultracentrifugation as the coefficient of simple linear regression is very little different from the value + 1. They emphasize the interest of the method of precipitation by concanavalin A which is simple, rapid and very reliable.

Adult↗
PubMed1984

Effect of human high density lipoproteins, anti-apolipoproteins CII and CIII, and hydrolysis of very low density lipoprotein (VLDL) cholesterol ester on VLDL catabolism in vitro.

Lipolysis of human very low density lipoproteins (VLDL) by lipoprotein lipase (LPL) was inhibited in the presence of high density lipoproteins (HDL), anti-apolipoprotein (apo) CII, and by increasing the VLDL free cholesterol content but not with anti-apo CIII or lipoprotein-free plasma. The experiments lend direct evidence that the composition of VLDL and their milieu are important determinants of lipolysis by LPL. Apo CIII may not be critical in LPL mediated VLDL catabolism.

Antibodies↗
PubMed1989

Triglycerides, cholesterol, HDL, LDL, and VLDL cholesterol in serum of phenylketonuric children under dietary control.

Phenylketonuria is currently treated by a special diet to avoid elevated blood concentration of the essential amino acid phenylalanine. The authors examined 20 phenylketonuric children in the Inborn Error of Metabolism Department of Institute of Child Health in Athens. The children had simultaneous clinical and laboratory investigations. Blood cholesterol levels of these children were low in comparison with the levels of healthy children of the same age, but the triglyceride levels were higher as a result of a special diet containing a large amount of carbohydrates. Because of the triglyceride elevation the authors recommend supplementary vegetable fat intake, such as in olive oil, for their patients' dietary control.

Child↗
PubMed2001

Compared with saturated fatty acids, dietary monounsaturated fatty acids and carbohydrates increase atherosclerosis and VLDL cholesterol levels in LDL receptor-deficient, but not apolipoprotein E-deficient, mice.

Heart-healthy dietary recommendations include decreasing the intake of saturated fatty acids (SFA). However, the relative benefit of replacing SFA with monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), or carbohydrates (CARB) is still being debated. We have used two mouse models of atherosclerosis, low density lipoprotein receptor-deficient (LDLRKO) and apolipoprotein E-deficient (apoEKO) mice to measure the effects of four isocaloric diets enriched with either SFA, MUFA, PUFA, or CARB on atherosclerotic lesion area and lipoprotein levels. In LDLRKO mice, compared with the SFA diet, the MUFA and CARB diets significantly increased atherosclerosis in both sexes, but the PUFA diet had no effect. The MUFA and CARB diets also increased very low density lipoprotein-cholesterol (VLDL-C) and LDL-cholesterol (LDL-C) in males and VLDL-C levels in females. Analysis of data from LDLRKO mice on all diets showed that atherosclerotic lesion area correlated positively with VLDL-C levels (males: r = 0.47, P < 0.005; females: r = 0.52, P < 0.001). In contrast, in apoEKO mice there were no significant dietary effects on atherosclerosis in either sex. Compared with the SFA diet, the CARB diet significantly decreased VLDL-C in males and the MUFA, PUFA, and CARB diets decreased VLDL-C and the CARB diet decreased LDL-C in females. In summary, in LDLRKO mice the replacement of dietary SFA by either MUFA or CARB causes a proportionate increase in both atherosclerotic lesion area and VLDL-C. There were no significant dietary effects on atherosclerotic lesion area in apoEKO mice. These results are surprising and suggest that, depending on the underlying genotype, dietary MUFA and CARB can actually increase atherosclerosis susceptibility, probably by raising VLDL-C levels through a non-LDL receptor, apoE-dependent pathway.

Adipose Tissue↗
PubMed2003

Dietary trans-18:1 raises plasma triglycerides and VLDL cholesterol when replacing either 16:0 or 18:0 in gerbils.

To compare the relative impact of trans-18:1 with the two main dietary saturated fatty acids it replaces, plasma lipid response was assessed in Mongolian gerbils fed diets rich in 16:0 (24%en),18:0 (10%en), or trans-18:1 (4 or 6%en). The diets were designed such that the 18:0-rich diet substituted 7%en as 18:0 for 16:0, whereas 4%en and 6%en from trans-18:1 was substituted for 16:0 in the two trans diets. The control group was fed a diet formulated according to the fatty acid balance of American Heart Association (AHA), but provided 40%en as fat. Gerbils (n = 10 per dietary group) were fed one of the five diets for 8 weeks. The control diet, with 4 times the polyunsaturated fatty acids (PUFA) content and a P:S ratio about 10 times greater than the test diets, resulted in the lowest plasma TC, LDL cholesterol (LDL-C) and VLDL cholesterol (VLDL-C). Among the test diets, plasma TC and TG were lowest with the 18:0-rich diet. TC in gerbils fed the 16:0-rich diet and 4%en-trans were 20% higher than the 18:0-rich diet, while the 6%en-trans diet was 35% higher. VLDL-C was significantly higher in the 6%en-trans diet compared to all other groups at 8 weeks. Both trans fatty acid diets elevated plasma TG approximately 2- and 3-fold, respectively, compared to the 16:0-rich and 18:0-rich diets at 8 weeks. Further, plasma TG continued to rise over time with trans fatty acids compared to 16:0 or 18:0. Thus, in the fatty acid-sensitive gerbil, impaired TG metabolism represents a major aspect of the hyperlipemia caused by trans fatty acid substitution for major saturated fatty acids.

Animals↗
PubMed1985

Estimation of VLDL cholesterol in hyperlipidemia.

Lipoprotein data from 10947 fasting blood samples drawn between 1968 and 1982 in the Molecular Disease Branch at the National Institutes of Health were used to test the generalizability of estimating very low density lipoprotein cholesterol (VLDL-C) from plasma triglyceride (TG). Patient samples with total cholesterol levels over 500 mg/l and triglyceride values in the 0-100 000 mg/1 range were included in this study. A previously defined linear relationship VLDL-C = 0.20 (TG) was observed in the past by Friedewald and collaborators, allowing estimation of low density lipoprotein cholesterol (LDL-C) without ultracentrifugation for TG values up to 4 000 mg/1. The results from this report extend the use of the Friedewald relationship to higher TG levels, and to various dyslipidemic states. As the VLDL-C estimates become increasingly imprecise for TG values greater than 10 000 mg/l, caution should be exercised using the estimate in the higher TG ranges. Comparisons with an alternative equation VLDL-C = 0.166 (TG) showed equal or improved accuracy with this estimation procedure, particularly at high TG levels.

Adolescent↗
PubMed1985

Familial aortic aneurysms: serum concentrations of triglyceride, cholesterol, HDL-cholesterol and (VLDL + LDL)-cholesterol.

Patients with abdominal aortic aneurysms (AAAs) have been compared with healthy controls with respect to the serum concentrations of triglyceride, cholesterol, HDL-cholesterol and (VLDL + LDL)-cholesterol. The concentrations of triglyceride and (VLDL + LDL)-cholesterol in serum were higher in the patients than in the controls, while the concentration of HDL-cholesterol in serum was lower in the patients than in the controls. There was no statistically significant difference in the serum concentration of total cholesterol between the patients and the controls. Twelve patients had first degree relatives (brothers, sisters and/or parents) with AAAs and six patients had second degree relatives (cousins or brothers and sisters of the parents) with AAAs. There was no statistically significant difference between the patients who had first degree relatives with AAAs and the patients without AAAs in the family in the serum concentrations of triglyceride, cholesterol, HDL-cholesterol and (VLDL + LDL)-cholesterol.

Aged↗
PubMed2001

Dietary plant stanol esters reduce VLDL cholesterol secretion and bile saturation in apolipoprotein E*3-Leiden transgenic mice.

Dietary plant stanols lower serum cholesterol levels in humans and in hyperlipidemic rodents, mainly by inhibition of the intestinal cholesterol absorption. We used female apolipoprotein E*3-Leiden transgenic mice to investigate the consequences of this effect on serum lipid levels and hepatic lipid metabolism. Five groups of 6 or 7 mice received for 9 weeks a diet containing 0.25% cholesterol and 0.0%, 0.25%, 0.5%, 0.75%, or 1.0% (wt/wt) plant stanols (sitostanol 88% [wt/wt], campestanol 10% [wt/wt]) esterified to fatty acids. Compared with the control diet, plant stanol ester treatment dose-dependently reduced serum cholesterol levels by 10% to 33% (P<0.05), mainly in very low density lipoproteins (VLDLs), intermediate density lipoproteins, and low density lipoproteins. Furthermore, 1.0% of the dietary plant stanols significantly decreased the liver contents of cholesteryl esters (-62%), free cholesterol (-31%), and triglycerides (-38%) but did not change the hepatic VLDL-triglyceride and VLDL-apolipoprotein B production rates. However, plant stanol ester feeding significantly decreased the amounts of cholesteryl esters and free cholesterol incorporated in nascent VLDLs by 72% and 30%, respectively, resulting in a net 2-fold decreased VLDL cholesterol output. Liver mRNA levels of low density lipoprotein receptors, 3-hydroxy-3-methylglutaryl coenzyme A synthase, cholesterol 7alpha-hydroxylase, and sterol 27-hydroxylase were not changed by plant stanol ester feeding. Nevertheless, the serum lathosterol-to-cholesterol ratio was significantly increased by 23%, indicating that dietary plant stanol esters increased whole-body cholesterol synthesis. Plant stanol esters also significantly decreased the cholesterol saturation index in bile by 55%. In conclusion, in apolipoprotein E*3-Leiden transgenic mice, plant stanol ester feeding dose-dependently lowered serum cholesterol levels as a result of a reduced secretion of VLDL cholesterol. This was caused by a decreased hepatic cholesterol content that also resulted in a lowered biliary cholesterol output, indicative of a reduced lithogenicity of bile in these mice.

Animals↗
PubMed1994

Impact of monocyte colony-stimulating factor upon beta-very low density lipoprotein (beta-VLDL) cholesterol metabolism in tetradecanoyl phorbol acetate-derived THP-1 cells.

The effect of monocyte colony stimulating factor (M-CSF) on the beta-very low density lipoprotein (beta-VLDL) metabolism in THP-1 cells (human leukemia cell line) was studied. THP-1 cells treated with M-CSF decreased Latex Bead phagocytosis, but the cells incubated with 12-tetradecanoyl-phorbol-13-acetate (TPA) enhanced phagocytosis 2.5-fold. Binding activity of 125I-M-CSF to THP-1 cells was higher than that in THP-1 cells elicited with TPA. THP-1 cells incubated with M-CSF before TPA treatment were designated MT macrophages, and those incubated with M-CSF after TPA treatment were called TM macrophages. When these cells were incubated with beta-VLDL, the cholesterol ester content in MT macrophages was less than in TM macrophages. The uptake of [3H]cholesterol oleate-beta-VLDL in MT macrophages was the same as in TM macrophages. The released radioactivity from [3H]cholesterol oleate-beta-VLDL loaded MT macrophages was higher than that from TM macrophages. Acid cholesterol esterase activity and ACAT activity were the same in both types of macrophages. Neutral cholesterol esterase activity was higher in MT than in TM macrophages. These results suggested that beta-VLDL-induced cholesterol ester deposition in THP-1 cells-derived macrophages was suppressed by M-CSF, when M-CSF acted at the stage of monocytes (THP-1 cells), and that the reduction of cholesterol ester might be due to enhanced release of cholesterol from the cells with high neutral cholesterol esterase activity.

Cell Line↗
PubMed1990

[Analysis of the distribution of HDL-cholesterol and (VLDL + LDL)-cholesterol in hepatic and intestinal disorders].

Total cholesterol (Ch-T), HDL cholesterol (Ch-HDL) and (VLDL + HDL) cholesterol (Ch-(VLDL + LDL) were evaluated in 78 cases of various hepatodigestive diseases (11 icterus, 14 hepatitis, 30 chronic alcoholisms, 8 Crohn's diseases and 15 haemorragic rectocolitis (RCH], and in 76 control subjects. High cholesterol levels were found in icterus, but its distribution between lipoproteic fractions remained unchanged. In the group of hepatitis, a deficit in Ch-(VLDL + LDL) was elicited by a significant decrease of Ch-(VLDL + LDL)/Ch-T ratio. The same was observed in chronic alcoholism. In Crohn's disease the levels of every cholesterol fraction were low, while in RCH they were not significantly different from those of the control group. But, in RCH, the Ch-HDL/Ch-T ratios showed significant low values with concommitant higher values of Ch-(VLDL + LDL)/Ch-HDL ratios, suggesting that, in RCH, the metabolism of cholesterol is unbalanced with a deficit of Ch-HDL. In conclusion, the evaluation of cholesterol in lipoproteic fractions by a simple assay may contribute to specify the diagnostic of these disorders.

Adolescent↗
PubMed2002

A rapid single-step centrifugation method for determination of HDL, LDL, and VLDL cholesterol, and TG, and identification of predominant LDL subclass.

Determination of the circulating levels of plasma lipoproteins HDL, LDL, and VLDL is critical in the assessment of risk of coronary heart disease. More recently it has become apparent that the LDL subclass pattern is a further important diagnostic parameter. The reference method for separation of plasma lipoproteins is ultracentrifugation. However, current methods often involve prolonged centrifugation steps and use high salt concentrations, which can modify the lipoprotein structure and must be removed before further analysis. To overcome these problems we have now investigated the use of rapid self-generating gradients of iodixanol for separation and analysis of plasma lipoproteins. A protocol is presented in which HDL, LDL, and VLDL, characterized by electron microscopy and agarose gel electophoresis, separate in three bands in a 2.5 h centrifugation step. Recoveries of cholesterol and TG from the gradients were close to 100%. The distribution profiles of cholesterol and TG in the gradient were used to calculate the concentrations of individual lipoprotein classes. The values correlated with those obtained using commercial kits for HDL and LDL cholesterol. The position of the LDL peak in the gradient and its shape varied between plasma samples and was indicative of the density of the predominant LDL class. The novel protocol offers a rapid, reproducible and accurate single-step centrifugation method for the determination of HDL, LDL, and VLDL cholesterol, and TG, and identification of LDL subclass pattern.

Centrifugation, Density Gradient↗
PubMed1995

The relation of parental cardiovascular disease to risk factors in children and young adults. The Bogalusa Heart Study.

BACKGROUND: Although cardiovascular risk factors relate to family history of cardiovascular disease, it is not clear how the relation changes from children to young adults. METHODS AND RESULTS: As part of a community study for cardiovascular health, parental history of diseases was obtained from 8276 offspring 5 to 31 years old, 36% black and 64% white. Between 5- to 10-year-old children and 25- to 31-year-old young adults, prevalence of parental heart attack increased from 5% to 25%. More prevalent in blacks than in whites, parental stroke increased from 2% to 9% in whites versus 3% to 19% in blacks; parental diabetes rose from 7% to 19% in whites versus 9% to 33% in blacks; and parental hypertension increased from 26% to 59% in whites versus 40% to 72% in blacks. Offspring with parental heart attack history were significantly overweight after 10 years of age and showed elevated levels of total cholesterol, VLDL cholesterol, LDL cholesterol, insulin, and glucose after 17 years of age, irrespective of weight. Offspring of diabetic parents were significantly overweight, irrespective of age. They showed significant increases in levels of insulin, glucose, triglycerides, total cholesterol, VLDL cholesterol, and LDL cholesterol after age 24 years, independent of weight. Offspring of hypertensive parents displayed overweight regardless of age, higher levels of blood pressure after age 10 years, and elevations of triglycerides and VLDL cholesterol after age 24 years irrespective of weight. Analyzed by race and sex in young adults, parental heart attack related strongly to LDL cholesterol in the white offspring, especially white males, and to insulin in the black offspring. Parental diabetes showed a stronger association with overweight and glucose in black females. Also noted was the relation between parental hypertension and overweight in black females. CONCLUSIONS: Parental history is an important surrogate measure for cardiovascular risk in the offspring. However, parental history information alone is not sufficient to designate younger children for selective screening for high cholesterol, because of the young age of parents.

Adolescent↗