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PubMed1983

Human low density lipoprotein structure: correlations with serum lipoprotein concentrations.

Human low density lipoproteins (LDL) were isolated and purified from individuals having widely differing serum lipid concentrations. Very low density lipoproteins (VLDL) and high density lipoproteins (HDL) were also isolated and quantitated. HDL2 and HDL3 were separated by flotation velocity in the analytical ultracentrifuge and their relative weight percent determined. The mean density of LDL from 41 individuals was determined by flotation velocity at two different solvent densities. The mean density of LDL was directly proportional to the triglyceride (r = 0.65) and VLDL (r = 0.50) concentrations and inversely proportional to the HDL (r = -0.55) and HDL2 (r = -0.74) concentrations (all significant at P less than 0.001). The mean molecular weight of LDL from 42 individuals was determined by flotation equilibrium centrifugation. The mean molecular weight of LDL was directly proportional to the HDL (r = 0.49) and HDL2 (r = 0.48) concentrations and inversely proportional to the serum triglyceride (r = -0.60) and VLDL (r = -0.48) concentrations (all significant at P less than 0.005 except triglyceride--P less than 0.001). The molecular weight of LDL was inversely proportional to its density, and thus inversely proportional to its protein/lipid ratio which was confirmed by composition measurements. The density and molecular weight of LDL had no relationship to the concentration of LDL (r = 0.04 and 0.03).

Adult↗
PubMed1991

An investigation of the role of lecithin:cholesterol acyltransferase and triglyceride-rich lipoproteins in the metabolism of pre-beta high density lipoproteins.

Small high density lipoproteins (HDL) with pre-beta electrophoretic mobility (pre-beta HDL) have recently been shown to be the primary acceptor of cholesterol from cultured cells. We studied the metabolism of these particles by incubating serum at 37 degrees C in the presence and absence of active lecithin: cholesterol acyltransferase (LCAT). We found that the serum pre-beta HDL concentration decreased in the presence of LCAT, but when LCAT was inhibited the concentration remained constant, or increased, depending on the method of inhibition. This suggests that pre-beta HDL are a substrate for LCAT. We also found a significant negative correlation between levels of LCAT activity and pre-beta HDL in 28 fasting healthy subjects, this provides evidence that the activity of LCAT regulates, at least in part the concentration of these particles in vivo. During the early phase of incubation there was a more rapid decrease in pre-beta HDL concentration which was greater in the post-prandial than fasting state. When we infused a triglyceride emulsion into 6 subjects or added this to serum in vitro we observed an immediate fall in pre-beta HDL concentration. These findings suggest that pre-beta HDL interact with triglyceride rich particles. We investigated the origin of pre-beta HDL from blood lipoproteins during their lipolysis, in vivo and in vitro and found that they were produced from both triglyceride-rich and high-density lipoproteins. Formation from triglyceride-rich lipoproteins was evident by the rise in pre-beta HDL concentration during heparin-induced lipolysis when fasting and post-prandially. The rise was greater post-prandially and particularly marked in 4 hypertriglyceridaemic patients following a fat load. Generation from alpha-HDL was evident when we prolonged the action of the heparin-released lipases by incubation of post-heparin sera at 37 degrees C. Continued formation of pre-beta HDL occurred at an equal rate in the fasting and post-prandial samples suggesting release by lipolysis of alpha-HDL. This was supported by the action of lipases on serum and isolated HDL in vitro, where triglyceride lipase rather than phospholipase activity appeared more effective at releasing pre-beta HDL. These findings suggest binding and release of pre-beta HDL by triglyceride-rich lipoproteins depending on the prandial state and production from alpha-HDL through the action of lipases.

Adolescent↗
PubMed2000

High-density lipoprotein cholesterol esterification and transfer rates to lighter density lipoproteins mediated by cholesteryl ester transfer protein in the fasting and postprandial periods are not altered in type 1 diabetes mellitus.

Background: Diabetes mellitus is associated with atherosclerosis that has, in part, been ascribed to abnormalities in the reverse cholesterol transport system. Methods: We determined, in the fasting and post-alimentary periods, rates of HDL cholesterol esterification and transfer to apoB-containing lipoproteins, cholesteryl ester transfer protein (CETP) concentration, and apoB lipoprotein size in 10 type 1 diabetics and 10 well-matched controls. Autologous HDL was labeled with [14C]cholesterol and incubated at 37 degrees C during a period of 30 min for measurement of the cholesterol esterification rate (CER), as well as for 24 h for measurement of the endogenous HDL [14C]cholesteryl ester ([14C]CE) transfer rate to apoB-containing lipoproteins after 2- and 4-h incubations with the subject's own plasma. Exogenous cholesteryl ester transfer activity (CETA) was estimated by incubation of the participant's plasma (CETP source) with [14C]CE-HDL and VLDL from a pool of plasma donors. ApoB lipoprotein size was determined using non-denaturing polyacrylamide gradient gel electrophoresis of whole plasma. Results: Contrary to previous studies, we showed that even not well-controlled type 1 diabetics did not differ from lipid-matched, non-diabetic subjects in HDL-[14C]cholesterol esterification rate, transfer rates, or CETP concentration. CETP concentration correlates with the exogenous method of [14C]CE transfer and with the endogenous method only when the latter is corrected for plasma triacylglycerol (TG) concentration. In addition, during the postprandial phase, diabetic patients' VLDL are smaller and IDL size increases less than in controls. Conclusion: In type 1 diabetes mellitus, CETA is not altered when the plasma levels of donor and/or acceptor lipoproteins are within the normal range.

Journal Article↗
PubMed1997

Theoretical considerations of what regulates low-density-lipoprotein and high-density-lipoprotein cholesterol.

The concentration of cholesterol carried in low-density-lipoprotein cholesterol (LDL-C) is predominantly dictated by metabolic events occurring in liver. LDL-C is derived from the intravascular metabolism of very-low-density lipoproteins, and, in every species, this lipoprotein particle is predominantly cleared by liver through receptor-dependent mechanisms. In addition to cholesterol absorbed from the diet, sterol is also synthesized within the body and this synthesis occurs predominantly in extrahepatic organs. When the amount of cholesterol input into the body is increased, there is expansion of the pools of sterol within liver cells and down-regulation of the receptors responsible for clearing LDL-C from the bloodstream. As a consequence, the concentration of LDL-C in plasma increases. When dietary cholesterol intake is kept constant, some long-chain saturated fatty acids further suppress hepatic LDL receptor activity whereas several unsaturated fatty acids have the opposite effect. These regulatory events are apparently articulated through the ability of these fatty acids to shift intracellular cholesterol between a regulatory and a storage pool. High-density lipoproteins, in contrast, function primarily to move excess cholesterol from the extrahepatic organs to liver for excretion. Although the concentration of high-density-lipoprotein cholesterol in the plasma may be influenced by the rate of apolipoprotein A-I production or the activity of cholesterol ester transfer protein, it is less clear whether dietary long-chain fatty acids have any effect on these processes. The regulatory effects of the saturated and unsaturated long-chain fatty acids on LDL-C concentrations can be shown in a variety of experimental animals and also in humans.

Animals↗
PubMed1998

Association of apolipoprotein E polymorphism with lipoprotein glomerulopathy. Report of 2 cases with a new genotype and comparison of the relative frequencies of apolipoprotein E isoforms in lipoprotein glomerulopathy and in the general population.

Two cases of lipoprotein glomerulopathy with a new apolipoprotein E (Apo E) genotype, epsilon3/epsilon4, were diagnosed recently. These 2 cases, together with other cases documented in English literature made a total of 6 common isoforms of Apo E encountered in lipoprotein glomerulopathy. Although the calculated allele frequency of epsilon2 is relatively high in cases with lipoprotein glomerulopathy as compared with that in the general population (39.3 vs. 6.4-11.4%), the gradual emergence of Apo E isoforms other than E2/E3 in lipoprotein glomerulopathy implicates that the genetic susceptibility of certain Apo E isoforms may not be a crucial factor. An alteration in the local environment of glomerular capillaries may be more important in the pathogenesis of lipoprotein glomerulopathy.

Adult↗
PubMedDate not supplied

Net mass transfer of cholesteryl esters from low density lipoproteins to high density lipoproteins in plasma from normolipidemic subjects.

Net mass transfer of lipids was measured in plasma from fasted, normolipidemic subjects. The plasma was incubated, and lipoproteins were subsequently separated by polyanion precipitation or density gradient ultracentrifugation. Total cholesterol, unesterified cholesterol, and triglycerides were measured in the isolated lipoprotein fractions. The rate of cholesterol esterification was measured simultaneously. All plasma samples showed an increase in high density lipoprotein (HDL) cholesteryl esters during 1-hour incubations. In most cases, this increase was higher than the cholesteryl ester formation in total plasma due to cholesterol esterification. Therefore, we concluded that a net mass transfer of cholesteryl esters occurred from the very low plus low density lipoprotein (VLDL + LDL) fractions to HDL in plasma from most of the subjects studied. Transfer of triglycerides occurred from VLDL + LDL to HDL in plasma from all subjects. The cholesteryl ester transfer (measured after 1 hour) is not related to the activity of cholesteryl ester transfer protein. Inhibition of cholesterol esterification did not change the direction of cholesteryl ester or triglyceride transfer. Ultracentrifugal separation of plasma lipoproteins revealed that both HDL and VLDL are acceptors of cholesteryl esters and that VLDL donates triglycerides to both LDL and HDL. Removal of VLDL from plasma by ultracentrifugation did not affect the cholesteryl ester transfer from LDL to HDL. We conclude that LDL may act as a donor of cholesteryl esters during incubation of normolipidemic plasma.

Adult↗
PubMed1990

Dietary palmitic acid (16:0) enhances high density lipoprotein cholesterol and low density lipoprotein receptor mRNA abundance in hamsters.

In order to examine the qualitative effect of different fats and specific fatty acids on plasma lipids and lipoprotein metabolism, six low fat, cholesterol-free diets were fed to young male hamsters (10/group) for a 4-week period. Fat blends were formulated with coconut oil, palm oil, soybean oil, high oleic acid safflower oil, butter, corn oil, and canola oil. Diets contained 13% energy as fat and dietary polyunsaturate/saturate ratios ranged from 0.12 to 1.04, one of which incorporated the American Heart Association-recommended concentrations of saturates, monoenes, and polyenes and another reflected the current American Fat Blend. In three diets the polyunsaturate/monounsaturate/saturate ratio was held constant while only the 12:0, 14:0, and 16:0 were varied. Plasma lipoproteins and apoproteins were assessed in conjunction with the abundance of specific hepatic and intestinal mRNA for the low density lipoproteins (LDL) receptor and various apolipoproteins associated with cholesterol metabolism. The plasma cholesterol response was lowest with the American Heart Association blend and equally elevated by the more saturated, low polyene diets (polyunsaturate/saturate, 0.12-0.38). Replacing 12:0 plus 14:0 from coconut oil with 16:0 as palm oil induced a significant increase in high density lipoprotein (HDL) cholesterol with a trend toward decreased LDL. These shifts in lipoprotein cholesterol were corroborated by measures of the LDL/HDL ratio, the plasma apolipoprotein B/apolipoprotein A1 ratio, and differences in the synthesis of apolipoproteins and the LDL receptor based on estimates of the mRNA for these proteins in the liver and gut, using specific cDNA probes for apolipoprotein A1, apolipoprotein B, apolipoprotein E, and the LDL receptor. Although it has been suggested that dietary polyenes lower total plasma cholesterol, including HDL, and that saturated fat increases both these pools of cholesterol, the current data represents the first evidence that a specific saturated fatty acid, i.e., palmitic acid, may enhance HDL production.

Animals↗
PubMed1981

Increase in lipolysis and decrease in plasma-heparin lipoprotein lipase activity and alpha 1 lipoprotein level after aminophylline in man.

Intravenous aminophylline 0.48 g produced a sharp increase in plasma free fatty acids. After three days of treatment with aminophylline 0.96 g/day i.v., plasma post-heparin lipoprotein lipase was significantly reduced, and post-heparin hepatic triglyceridase remained unchanged. alpha 1 lipoprotein was reduced by treatment, in parallel with lipoprotein lipase, while other lipoprotein fractions, serum cholesterol and triglycerides were unaffected.

Adult↗
PubMedDate not supplied

Lipid transport in the hypothyroid rat as reflected by the serum concentrations of free fatty acids, lipoproteins, lecithin-cholesterol acyltransferase and lipoprotein lipase activity in adipose tissue.

An experimental model was explored for the study of the effect of thyroid hormone on lipid transport and metabolism in the rat. The development of the hypothyroid state was accompanied by an early decrease in free fatty acids (FFA) followed by an increase in the level of cholesterol and a decrease in triglyceride concentration. Simultaneously, the adipose tissue lipoprotein lipase activity increased while the lecithin-cholesterol acyltransferase was unchanged. The hypothyroid state was also accompanied by a decrease in the concentrations of tryglycerides and cholesterol in very low density lipoproteins (VLDL) while the 2 lipids increased in the low density lipoprotein (LDL) fraction. Administration of triiodothyronine markedly reduced the amount of cholesterol in both the LDL and high density lipoprotein (HDL) fractions. The animal model has been shown to have similarities with findings in human subjects.

Adipose Tissue↗
PubMed2004

Lipoprotein lipase and its role in regulation of plasma lipoproteins and cardiac risk.

For over 50 years, biologists and clinicians have studied lipoprotein lipase (LPL) and learned about its structure, function, cellular production, physiology, and human genetics. LPL is the principal enzyme that removes triglyceride from the bloodstream. It also determines plasma levels of high-density lipoprotein. Surprisingly, within the past several years, a number of new and unexpected proteins have been discovered that regulate the actions of LPL. These include the very low-density lipoprotein receptor, angiopoetin-like protein 3, and apolipoprotein A-V. In addition, mouse genetic studies have confirmed tissue culture findings of nonenzymatic roles of LPL both in lipid metabolism and atherogenesis. These basic observations are now being related to new information on human genetic polymorphism in this gene that is likely to affect clinical evaluation of lipoprotein disorders and cardiac risk.

Angiopoietin-Like Protein 3↗
PubMed1979

Guinea pig very low density lipoproteins are a good substrate for lipoprotein lipase.

In contrast to plasma from most other animals, guinea pig plasma causes little or no stimulation of lipoprotein lipase activity. Very low density lipoproteins (VLDL) isolated by ultracentrifugation of guinea pig serum caused a definite stimulation of lipase activity, whereas the infranatant inhibited the activity. Gel filtration in 5 M guanidinium hydrochloride of delipidated VLDL demonstrated that the activation was caused by a low molecular weight protein. The VLDL themselves were hydrolized at similar rates as human VLDL both by guinea pig and by bovine lipoprotein lipases. Thus, guinea pig VLDL contain an activator for lipoprotein lipase analogous to that in other animals and there is enough of the activator to support rapid hydrolysis of the VLDL lipids by the lipase.

Animals↗
PubMed1991

Interaction of apolipoprotein B-containing lipoprotein secreted by Hep G2 cells with receptors for low-density lipoprotein.

Radioligand and immunoenzymatic techniques were used to characterize the receptor binding properties of apolipoprotein B-containing lipoprotein produced by HepG2 cell line (H-LpB). It was found that compared to plasma low-density lipoprotein (LDL), the interaction of H-LpB nonseparated from conditioned medium with normal fibroblasts was 6-8-times lower and only slightly exceeded the nonspecific binding of LDL modified by malondialdehyde, while the uptake of the indicated lipoproteins by LDL receptor-negative strain of fibroblasts were identical. The uptake of H-LpB by normal fibroblasts increased 1.5-2-times after isolation from the culture medium by immunoaffinity chromatography. The effect of isolation could be explained by the finding that apolipoprotein E-containing lipoprotein secreted by HepG2 cells effectively competed for the binding with LDL-receptors. The obtained results suggest that H-LpB produced by HepG2 cells is poorly recognized by the LDL-receptors.

Apolipoproteins B↗
PubMed1977

Physical, chemical and immunochemical characterization of a lipoprotein lipase activator protein from pig plasma very low density lipoproteins.

Very low density lipoproteins ere isolated from plasma of swine by ultracentrifugal flotation. After delipidation, the lipid-free proteins were separated by chromatography on Sephadex G-150 AND DEAE-cellulose. A major apoprotein was isolated and shown to activate cows' milk lipoprotein lipase. Since human very low density lipoproteins also contain an activator protein, designated, apoC-II, we have called the pig protein, pig apoC-II. Pig apoC-II had a molecular weight of approximately 10 000 as determined by polyacrylamide gel electrophoresis in sodium dodecyl sulfate. The amino acid composistion showed the absence of histidine, cysteine and tryptophan; there was no evidence for carbohydrate. Treatment of pig apoC-II with carboxypeptidase indicated COOH-terminal serine. Rabbit antisera prepared to the pig protein gave single precipitin lines of complete identity to very low density lipoproteins, apoC-11. Using anti-pig apoC-II, a radioimmunoassay was developed which provides a convenient and reproducible method for measuring 5-1000 ng of apoprotein.

Amino Acids↗
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↗
PubMed1994

Lipoprotein (a) displays increased accumulation compared with low-density lipoprotein in the murine arterial wall.

Lipoprotein (a) (Lp(a)) is known to be an independent risk factor for cardiovascular disease, but the mechanisms by which it contributes to this disease remain unclear. Current evidence indicates that the closely related plasma particle, low-density lipoprotein (LDL), may initiate atherosclerosis through deposition in the arterial wall. This study has compared the ability of both lipoproteins to enter and accumulate within the arterial wall. Experiments were conducted in vivo with animals from two strains of mice: C57BL/6 mice, which develop fatty streak lesions upon challenge by a high-fat diet, and C3H/HeJ mice, which are resistant to lesion formation. Animals from both strains were maintained up to 16 weeks either on chow or high-fat diet. The mice were intravenously injected with 125I-labeled human Lp(a) or 125I-labeled human LDL in equimolar amounts and the lipoprotein allowed to circulate in vivo for 2 or 24 h. Transverse sections of the aortic root including sites of predilection for lesion formation at the commissures of the valve were prepared and examined after autoradiography. The autoradiographic grains over lesions and histologically uninvolved areas were enumerated and compared after normalization. Both Lp(a) and LDL demonstrated nearly ten times greater accumulation in lesions compared with histologically uninvolved areas from C57BL/6 mice. Analyses of histologically uninvolved areas from both strains of mice showed a significantly higher accumulation of Lp(a) than LDL. Finally, significantly higher accumulations of both Lp(a) and LDL occurred in the histologically uninvolved intima and subintima of lesion-prone C57BL/6 mice as compared with lesion-resistant C3H/HeJ mice after 5 weeks on the diets. We propose that enhanced accumulation of Lp(a) in the arterial wall accounts, in part, for the increased risk of cardiovascular disease.

Animals↗
PubMed1994

A rapid and simple method for measuring the susceptibility of low-density-lipoprotein and very-low-density-lipoprotein to copper-catalyzed oxidation.

Much evidence has accumulated to suggest a role for the oxidation of low-density-lipoprotein (LDL) and very low-density-lipoprotein (VLDL) in the pathogenesis of atherosclerosis. The susceptibility of lipoprotein to copper-catalyzed oxidation is often used to evaluate its oxidizability. A method was developed which isolates the non-high-density lipoprotein (non-HDL) fraction and removes EDTA by a dextran-magnesium precipitation method. The oxidizability of this fraction is evaluated by monitoring the fluorescence and measuring thiobarbituric acid reactive substances (TBARS) at different intervals of incubation. Those parameters reflect apolipoprotein B (apo B) modification and lipid degradation during LDL and VLDL oxidation. Our assay is sensitive enough to study factors which can influence the oxidizability of LDL and VLDL. The method is simple, rapid and can be easily conducted in a routine laboratory.

Catalysis↗
PubMed1978

Relation of plasma high-density lipoprotein cholesterol to lipoprotein-lipase activity in adipose tissue and skeletal muscle of man.

Lipoprotein-lipase activity (LPL) was measured in biopsies of adipose tissue and skeletal muscle of normal human subjects, and the results were related to concentrations of cholesterol and triglycerides in plasma lipoproteins. Adipose-tissue LPL activity was significantly higher in females than in males, whereas no sex difference was observed in skeletal-muscle LPL activity. A highly significant positive correlation was present between the plasma high density lipoprotein (HDL) cholesterol level and LPL activity in adipose tissue (r = +0.66, P less than 0.001) but not between HDL and skeletal-muscle LPL. The results suggest that the activity of LPL in adipose tissue and the rate of catabolism of triglyceride-rich lipoproteins might be one of the factors that determine the concentration of HDL in plasma and at least partly account for the known sex difference in plasma HDL level.

Adipose Tissue↗
PubMed1984

Accelerated turnover of very low density lipoprotein triglycerides in chronic alcohol users. A possible mechanism for the up-regulation of high density lipoprotein by ethanol.

The concentration of high density lipoproteins (HDL) is related to the catabolism of triglyceride-rich lipoproteins. In order to elucidate the mechanisms by which alcohol increases plasma HDL levels we measured the turnover kinetics of very low density lipoprotein (VLDL) triglycerides in 10 alcoholic men without liver disease and in nonalcoholic control men matched for age, weight and plasma VLDL triglyceride level. The study was repeated in the alcoholics after a 2-week abstinence period. The alcoholic men had elevated HDL cholesterol but reduced low density lipoprotein (LDL) cholesterol as compared to the controls. The fractional catabolic rate and the total turnover (production) rate of VLDL triglycerides were both significantly increased (P less than 0.05) in the alcoholic men before abstinence. After withdrawal of alcohol both the synthetic rate and the catabolic rate of VLDL triglycerides returned to normal and the HDL (HDL2 and HDL3) cholesterol fell. The per cent decrease in HDL2 cholesterol during abstinence was positively correlated to the respective fall of VLDL triglyceride fractional catabolic rate (r = +0.51). The results suggest that the absence of hypertriglyceridemia and the elevated levels of HDL in regular alcohol users may be partly based on increased metabolic clearance of VLDL particles and on subsequent accelerated transfer of the VLDL surface components to HDL.

Adult↗