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PubMed1997

Combined effects of lipoprotein lipase and apolipoprotein E polymorphisms on lipid and lipoprotein levels in the Stanislas cohort.

We have genotyped 1101 supposedly healthy subjects from the Stanislas cohort for the lipoprotein lipase (LPL) gene Ser417(C)-->stop (G) polymorphism and/or for the apolipoprotein (apo)E common polymorphism. Genotypic effects of the two polymorphisms on fasting serum triglycerides (TG), total cholesterol (Tchol), high density lipoprotein-cholesterol (HDLc), low density lipoprotein-cholesterol (LDLc), apoB, apoA-I, and apoE levels were studied separately for each polymorphism and in conjunction. epsilon 4 allele and high apoE levels were associated with high levels of LDLc, Tchol, apoB, and TG. The G allele of LPL was significantly associated with low TG levels. We found a clear interaction between the LPL/apoE polymorphisms and apoE levels on serum TG variation. Total variability of TG levels in women and men of 42.31% and 53.62% respectively, were mainly explained by apoE concentration and these two polymorphisms. ApoE and LPL genes simultaneously modulated TG levels.

Adult↗

PubMed1997

[Effects of oxidatively modified low density lipoprotein and very low density lipoprotein on the expression of MCP-1 in macrophages].

OBJECTIVE: To examine whether oxidatively modified low density lipoprotein (OX-VLDL) and very low density lipoprotein (OX-VLDL) induce the expression of MCP-1 mRNA and protein by rabbit peritoneal exudate macrophages, and to clarify what a role of both lipoproteins play in atherogenesis. METHODS: After exposure of the macrophages to 25 micrograms/ml of LDL, VLDL, OX-LDL and OX-VLDL respectively, and a 24 hour incubation at 37 degrees C, the total RNA was extracted from the cells by guanidinium isothiocyanate method, and the media conditioned by the cultured macrophages were collected. Meanwhile, MCP-1 protein in the conditioned media was determined by using sandwich ELISA. Monocyte migration induced by the media was assayed by micropore filter method using modified Boyden chamber. RESULTS: After a 24 hour exposure to OX-LDL and OX-VLDL, the MCP-1 mRNA expression in macrophages was markedly increased (3.2-fold and 3.4-fold, respectively), and the level of MCP-1 protein was also increased (2.2-fold and 2.5-fold, separately), and furthermore, the monocyte migration distance was significantly increased. However, the expression of MCP-1 mRNA and protein was only slightly increased when exposed to LDL or VLDL. CONCLUSIONS: Rabbit peritoneal exudate macrophages can express MCP-1 mRNA and protein, and OX-LDL and OX-VLDL induce stronger MCP-1 mRNA and protein expression in the cells.

Animals↗

PubMed1999

Analytical capillary isotachophoresis of total plasma lipoproteins: a new tool to identify atherogenic low density lipoproteins.

Plasma low density lipoproteins from 20 patients were separated by capillary isotachophoresis (ITP). In each patient the apparent diameter of the predominant LDL peak on whole plasma was also determined by nondenaturing gradient gel electrophoresis. Furthermore the concentration of the more electronegatively charged in vivo oxidized LDL- was accomplished using anion exchange high pressure liquid chromatography. By analytical capillary ITP of whole plasma lipoproteins, prestained with a lipophilic dye, LDL were separated into four subfractions. Usually, the predominant subfraction was the slow migrating LDL4, followed by LDL3, and then by the faster LDL2 and LDL1. Slow migrating LDL4 correlated negatively with plasma triglycerides and LDL- and positively with plasma high density lipoprotein (HDL) cholesterol and with the LDL diameter, while the faster LDL1 showed an inverse behavior. The LDL1 + LDL2 to LDL3 + LDL4 ratio showed a strong positive correlation with LDL- concentration (r = 0.87; P < 0.001) and a highly significant inverse correlation with the LDL particle diameter (r = -0.74; P < 0.001). At least three highly atherogenic LDL that could be found in human plasma, namely oxidized, glycated and small-dense, are characterized by a greater electric charge. The LDL profile from capillary ITP and the relative prevalence of faster or slower migrating LDL fractions could indicate the presence of more atherogenic LDL.

Adult↗

PubMed1986

Effect of probucol treatment on lipoprotein cholesterol and drug levels in blood and lipoproteins in familial hypercholesterolemia.

Twelve patients with mild and 3 with severe hypercholesterolemia were stabilized with an isocaloric diet containing less than 300 mg cholesterol daily with a P/S ratio of 1.8, and placebo period of 4 weeks. They were administered 1000 mg probucol daily for 12 weeks, followed by placebo for 6 weeks. In patients with mild disease, a significant cholesterol reduction was achieved in serum, LDL, and HDL (maximum decrease, 17%, 13%, and 31%, respectively). While HDL3 cholesterol was reduced significantly throughout the period (P less than 0.001), HDL2 cholesterol showed a significant decrease only at the 4th week of treatment (P less than 0.001), and returned to basal levels at the 8th and 12th treatment weeks. Serum apo B levels decreased only slightly, but the HDL-apo A-I fall was significant with a reduction in the HDL-CH/HDL-apo A-I ratio throughout the treatment period. In 3 patients with severe disease, cholesterol decrease in serum and in VLDL, LDL and HDL fractions varied, but on the whole was lower than in patients with mild disease. A decrease in VLDL-CH and HDL-CH was present in all 3, but LDL-CH levels were only slightly lowered in 2 patients, and unchanged in the third. Serum probucol levels fell 66% from the 4th to the 12th treatment week, and in parallel, the percentage of lipoprotein-bound drug increased about 2-fold. It is suggested that these changes in pharmacokinetics as well as the cholesterol-lowering effect of the drug may be due to a change in lipoprotein composition or structure.

Adult↗

PubMed1995

Effect of intralipid infusion on serum high- and low-density lipoprotein cholesterol, lecithin:cholesterol acyltransferase, and lipoprotein lipase in tumor-bearing rats.

We compared the effects of 0.45% normal saline (NS), 5% Intralipid (IL), and 16.7% glucose (Glu) infusions on total serum triglycerides and cholesterol, serum high-(HDL-c) and low-density lipoprotein cholesterol (LDL-c), and activity of serum lecithin:cholesterol acyltransferase (LCAT), and serum lipoprotein lipase (LPL) in rats implanted with a fibrosarcoma. In tumor-bearing rats given NS, a two-fold increase in total serum cholesterol, a four-fold increase in LDL-c, and a five-fold decrease in the HDL-c/LDL-c ratio were observed compared to tumor-free rats. In tumor-bearing rats administered IL, a two-fold increase in total serum triglyceride and cholesterol, a three-fold increase in HDL-c and HDL-c/LDL-c ratio, and a two-fold increase in LPL activity were observed compared to tumor-bearing rats administered NS. In tumor-bearing rats administered Glu, a two-fold decrease in total serum cholesterol, a two-fold decrease in HDL-c, and a three-fold decrease in LDL-c were observed compared to tumor-bearing rats administered NS. Tumor weights and LCAT activity did not differ significantly between treatment groups. Previous results have demonstrated that lipophilic compounds that interact with plasma lipoproteins have altered pharmacological effects when administered with IL. Therefore, this study suggests that IL infusions alter the HDL-c/LDL-c ratio and could affect the pharmacological behavior of anticancer compounds that predominantly distribute into the LDL fraction upon entrance into the bloodstream.

Animals↗

PubMed1983

Liver lipase and high-density lipoprotein. Lipoprotein changes after incubation of human serum with rat liver lipase.

Human sera were incubated with rat liver lipase after inactivation of lecithin:cholesterol acyltransferase, and the changes in serum lipoprotein composition were measured. In the presence of liver lipase serum triacylglycerol and phosphatidylcholine were hydrolyzed. The main changes in the concentrations of these lipids were found in the high-density lipoprotein fraction. Subfractionation of high-density lipoprotein by rate-zonal ultracentrifugation showed a prominent decrease in all constituents of high-density lipoprotein2, a smaller decrease in the 'light' high-density lipoprotein3 and an increase in the 'heavy' high-density lipoprotein3. These data support a concept in which liver lipase is involved in high-density lipoprotein2 phospholipid and triacylglycerol catabolism and suggest that as a result of this action high-density lipoprotein2 is converted into high-density lipoprotein3.

Animals↗

PubMed1991

Interactions between model triacylglycerol-rich lipoproteins and high-density lipoproteins in rat, rabbit and man.

There are inverse relationships between HDL cholesterol and plasma triacylglycerol concentrations in normal and in hypertriglyceridemic individuals. To investigate the interactions between triacylglycerol-rich lipid particles and HDL, a lipid emulsion model of the triacylglycerol-rich lipoproteins was prepared. When emulsion particles were incubated with rat high-density lipoproteins (HDL) in the presence of lipid transfer activity (d greater than 1.21 g/ml fractions) from rabbit or human plasma there was a rapid bi-directional exchange of cholesteryl oleate (CO) and phospholipid (PL) labels between lighter and heavier fractions of HDL and emulsion particles. The transfers of CO and PL labels between both light and heavy fractions of HDL and the emulsion particles were increased with increasing amounts of emulsion added to the incubations. Incubation with the d greater than 1.21 g/ml fraction from rat plasma resulted in only a small exchange of CO whereas PL exchange was similar to rabbit and human plasma. Retinyl palmitate label was not transferred from emulsion particles to the HDL fractions even in the presence of lipid transfer activity from rabbit or human plasma. The present study shows that the transfer protein-mediated exchanges of surface and core lipids between HDL and the triacylglycerol-rich lipoproteins are affected by the quantity of triacylglycerol-rich particles in the system. This mechanism may contribute to the inverse relationships between plasma triacylglycerol concentrations and HDL concentrations in normal and hypertriglyceridemic individuals.

Animals↗

PubMed1989

Investigation of the role of serum lipoprotein-associated peroxides in Adriamycin cardiotoxicity. Release of reduced glutathione from rat hearts perfused with lipase-hydrolyzed very low density lipoprotein fractions obtained from Adriamycin-treated and control rats.

In a previous study, we demonstrated that the serum of rats treated chronically with the anticancer agent Adriamycin contains lipid peroxides associated with neutral lipids (W. S. Thayer, Biochem Pharmacol 33: 2259-2263, 1984). In the present study, hearts from untreated control rats were perfused with medium containing serum or very low density lipoprotein (VLDL) fractions obtained from either Adriamycin-treated rats or control rats. Release of endogenous glutathione from the perfused heart was tested to evaluate possible metabolism of the serum lipid peroxides through the glutathione peroxidase/glutathione reductase redox cycle. Perfusion with lipoprotein lipase-hydrolyzed serum or VLDL caused glutathione release, the extent of which increased with increasing VLDL concentration in the perfusate. The effect was not unique for VLDL from Adriamycin-treated rats, but instead appeared to be a more general phenomenon since it was also observed with VLDL from control rats. Glutathione was released in the reduced form (GSH), rather than the oxidized form (GSSG) observed during perfusions with model peroxides. Pretreatment of the VLDL with lipoprotein lipase in vitro prior to perfusion was necessary in order to obtain GSH release. Neither lipase alone nor palmitate in the absence of lipase was as effective in promoting GSH release. Simultaneous release of lactate dehydrogenase was quantitatively less than that of GSH. The results suggest an action of components of serum VLDL on cardiac membrane permeability. Peroxide metabolism-linked perturbation of the cardiac glutathione redox cycle does not appear to be the mode of action for the serum lipid peroxides found in Adriamycin-treated rats.

Animals↗

PubMed1978

[Stability of lipid and protein composition of very low-density lipoproteins during the storage after freezing of whole serum and isolated lipoproteins (author's transl)].

The lipid and protein composition of lipoprotein is now regarded with great interest for the identification of hyperlipoproteinemias. Because this relatively time-consuming study cannot be envisaged currently in clinical services, it seems useful to analyse a storage procedure which does not affect the composition of very-low density lipoproteins, whose proportion is very important among subjects with type IV hyperlipoproteinemia. Two studies were considered, one using whole sera stored at -20 degrees C and one using very low-density lipoproteins held in the same conditions. The lipid composition was determined for triglycerides and cholesterol concentrations of total proteins, proteins soluble in tetramethylurea (apoprotein C, "arginine-rich fraction", and apoprotein D), and peptides CII, CIII1 and CIII2 of apoprotein C. For both procedures considered, no significant changes were seen in lipid and protein composition for periods as long as 8 weeks.

Apolipoproteins↗

PubMedDate not supplied

Very low density lipoproteins in normal and cholesterol-fed rabbits: lipid and protein composition and metabolism. Part 2. Metabolism of very low density lipoproteins in rabbits.

The metabolic fate of very low density lipoproteins (VLDL) in normal and hypercholesteremic (h.c.) rabbits has been investigated. VLDL were labelled with 125I in the protein moieties and injected into normal and h.c. animals. The turnover of h.c. VLDL is markedly delayed as compared to that of normal VLDL, and conversion into lipoprotein classes of higher density is considerably decreased. This is observed when h.c. VLDL are injected either into h.c., or into normal rabbits. Arterial uptake of radioactivity is much higher with h.c. VLDL than with the normal lipoproteins, and it is highest when h.c. VLDL are injected into normal recipients. These data, together with those reported in the previous study, support the hypothesis that h.c. VLDL have an inherent atherogenicity. Injection of h.c. VLDL into normal animals also offers an experimental model for testing drugs or diets against atherosclerosis, using untreated animals.

Animals↗

PubMed1991

Desialylated low density lipoprotein--naturally occurring modified lipoprotein with atherogenic potency.

We have recently established that low density lipoprotein (LDL) of most patients with coronary atherosclerosis differs from the LDL of most healthy subjects by its ability to cause primary atherosclerotic changes, i.e. the accumulation of intracellular cholesterol in the cells of smooth muscle origin cultured from unaffected intima of human aorta. Patients' LDL has a 2.5-5-fold lower content of sialic acid as compared with the LDL of healthy subjects. On the other hand, desialylation of native LDL with neuraminidase makes it capable of causing accumulation of intracellular cholesterol similar to patients' LDL. In the present study we showed that LDL of patients and healthy donors did not differ in the content and composition of protein and lipids. Thus, the difference in the content of sialic acid is the only difference observed between atherogenic LDL of patients and nonatherogenic LDL of healthy donors. A low content of sialic acid is characteristic of both protein and lipid moiety of LDL particle. Sialic acid content was determined in individual LDL preparations obtained from patients and healthy donors. The sialic acid of LDL preparations of 25 out of 27 patients was below 18 micrograms/mg protein. LDL from 2 patients with higher sialic acid content proved to be normal. The ability of patients' LDL and LDL desialylated with neuraminidase in vitro to cause the accumulation of intracellular lipids correlated with the degree of lipoprotein desialylation. Apparently, the ability of patients' LDL to stimulate the cellular lipid accumulation may be explained by a deficiency of sialic acid in the lipoprotein particle.

Adult↗

PubMed1994

Effects of alcohol on lipoprotein lipase, hepatic lipase, cholesteryl ester transfer protein, and lecithin:cholesterol acyltransferase in high-density lipoprotein cholesterol elevation.

The mechanism whereby alcohol increases high-density lipoprotein cholesterol (HDL-C) levels is unclear. Lipoprotein lipase (LPL), hepatic lipase (HL), cholesteryl ester transfer protein (CETP) and lecithin:cholesterol acyltransferase (LCAT) act on lipoprotein metabolism. The purpose of the present study is to determine which one or what combination of these factors is responsible for the rise in HDL-C levels following alcohol ingestion. After 3 weeks of abstinence, 12 men consumed 0.5 g/kg bw of alcohol per day for 4 weeks; 13 abstaining men served as controls. Mean plasma total cholesterol (TC) levels were unchanged in either group throughout the study. Among the alcohol consumers, plasma triglycerides (TG), HDL-C, apolipoprotein (apo) A-I and A-II levels increased significantly after 3 weeks of alcohol loading but were unchanged in the control group. High-density lipoprotein3 cholesterol (HDL3-C) levels increased significantly in the alcohol consumers after 4 weeks of alcohol loading whereas high-density lipoprotein2 cholesterol (HDL2-C) levels were unaffected. In the controls, neither HDL2-C nor HDL3-C changed significantly. Post-heparin plasma (PHP) LPL activity and mass increased significantly (P < 0.01) after the alcohol ingestion (controls remained unchanged) without changing LPL specific activity. HL, CETP and LCAT activities were unaffected in both groups. We conclude that of the factors considered, LPL contributed the most to the alcohol-induced rise in HDL-C.

Adult↗

PubMed1987

Lipoprotein receptors in copper-deficient rats: apolipoprotein E-free high density lipoprotein binding to liver membranes.

Twenty-four male weanling Sprague-Dawley rats were randomly and equally divided into two dietary treatments, copper-deficient and adequate (0.7 mg and 8.0 mg Cu/kg diet, respectively). Deionized water and diet were provided ad libitum. After 8 weeks, rats were exsanguinated, membranes prepared from livers, and plasma high density lipoproteins (HDL) isolated by ultracentrifugation and agarose column chromatography. Heparin-sepharose affinity chromatography was used to isolate subfractions of HDL devoid of apolipoprotein E (apo E-free HDL). The apo E-free HDL derived from rats of each dietary treatment were iodinated and bound to liver membranes prepared from rats of both treatment groups. Total binding data, specific binding data, and computer derived estimates of maximum equilibrium binding (Bmax) indicate less binding was observed when lipoproteins and membranes from copper-deficient animals were used in the binding assay compared to controls. In addition, a 2 X 2 factorial analysis of binding parameters derived from all experiments demonstrated a significant lipoprotein effect, indicating the reduction in binding may be associated with apo E-free HDL obtained from copper-deficient rats. The present findings suggest a reduction in binding of apo E-free HDL to their binding sites may contribute to the hypercholesterolemia and hyperlipoproteinemia observed in copper deficiency.

Animals↗

PubMed1993

Increased production of apolipoprotein A-I associated with elevated plasma levels of high-density lipoproteins, apolipoprotein A-I, and lipoprotein A-I in a patient with familial hyperalphalipoproteinemia.

Familial hyperalphalipoproteinemia (FHA) is a heritable trait associated with elevated plasma concentrations of high-density lipoprotein (HDL) cholesterol and possibly with longevity and protection against coronary heart disease (CHD). The metabolic basis and molecular etiology of FHA have not been established in most kindreds. The proband of a kindred with FHA and possible longevity was found to have elevated plasma levels of HDL cholesterol, apolipoprotein (apo) A-I, and lipoproteins containing apo A-I without apo A-II (Lp A-I), but normal levels of apo A-II and lipoproteins containing apo A-I with apo A-II (Lp A-I:A-II). The in vivo kinetics of apo A-I and apo A-II were studied in the FHA proband and in control subjects using both exogenous radiotracer (125I-apo A-I and 131I-apo A-II) and endogenous stable isotope (primed constant infusion of 13C6-phenylalanine) labeling techniques. The production rate (PR) of apo A-I was markedly increased in the FHA subject (28.9 mg/kg.d) compared with the control subjects (12.0 +/- 2.1 mg/kg.d), whereas the apo A-II PR was not substantially increased. The primary sequence of the proband's apo A-I gene, including 1.2 kb of the 5'-flanking sequence, was normal. We conclude that a selective upregulation of apo A-I production is one metabolic cause of FHA, and results in high plasma concentrations of HDL cholesterol, apo A-I, and Lp A-I and possibly in protection from atherosclerotic CHD.

Apolipoprotein A-I↗

PubMed1994

The amount of cholesterol relative to apolipoprotein B in low-density lipoproteins relates primarily to high-density lipoprotein cholesterol in children: the Bogalusa Heart Study.

Serum low-density lipoprotein (LDL) particles vary in size, composition, and atherogenic potential. Relationships between the ratio of cholesterol to apolipoprotein B (apo B) within LDL, and levels of other lipoprotein variables in serum were examined in a biracial (black-white) sample (N = 2,053) of 8- to 17-year-olds whose median triglyceride level remained relatively low (56 mg/dL). The LDL cholesterol to apo B ratio showed a significant positive association with high-density lipoprotein (HDL) cholesterol (r = .36 to .44), HDL2 cholesterol (r = .34 to .50), HDL3 cholesterol (in whites only, r = .24 to .28), and apo A-I (r = .17 to .27), and a significant inverse association with triglycerides (except in black girls, r = -.15 to -.19). The best predictor of the LDL cholesterol to apo B ratio was HDL cholesterol or HDL2 cholesterol in all four race-gender groups; triglycerides entered as a predictor variable only in black boys. Since relationships of LDL and HDL to coronary heart disease (CHD) risk are considered interdependent, a subgroup of children with apo B-enriched LDL and low HDL cholesterol may be potentially at increased risk.

Adolescent↗

PubMed1983

Plasminogen-binding lipoprotein: isolation and characterization of a plasma very low density lipoprotein which co-chromatographs with plasminogen on lysine-sepharose.

By lysine-Sepharose chromatography, approximately 20% of normal plasma samples yield epsilon-aminocaproic acid (EACA) eluates which are opalescent, rather than clear, suggesting the presence of an additional, non-plasminogen component. This material has been isolated and characterized as a plasma lipoprotein of the very low density (VLDL) class on the basis of density ( less than 1.006 g/ml), size (greater than or equal to 5 X 10(7) daltons by gel filtration), electrophoretic mobility (pre-beta), chemical composition (mean cholesterol:triglyceride protein ratio, 1:3.4:1) and immunochemical evidence for apoproteins B, C, and E. Uniform particles, 100-200 Angstroms in diameter, were seen by electron microscopy. In contrast with VLDL in general, this lipoprotein co-chromatographed with plasminogen on lysine-Sepharose, where its binding was plasminogen-dependent, and from which it was eluted by EACA, but at lower concentrations than was plasminogen, suggesting a lysine-binding process. This plasminogen-binding lipoprotein (PBLP) was found in both male and female plasma samples, and increased post-prandially. Its properties suggest that it is a unique subclass of plasma VLDL. Although its isolation explains a laboratory phenomenon, and it exhibits interesting interactions with an important plasma zymogen, its function remains to be determined.

Carrier Proteins↗

PubMed1992

Effect of lithocholic acid feeding on plasma lipoproteins and binding of radioiodinated human lipoproteins to hepatic membranes in rats.

1. Male Sprague-Dawley rats fed diets containing 0.25% lithocholic acid for 6 weeks exhibited elevated serum cholesterol. 2. The rats were fed diets containing 5 or 20% fat with and without the lithocholate and/or oxytetracycline-HCl. 3. The cholesterol elevation was associated with high density lipoprotein (HDL) and not very low density lipoprotein (VLDL) or low density lipoprotein (LDL). 4. Specific binding of human [125I]HDL to hepatic membranes was lowered in lithocholate-fed rats, but binding of human [125I]LDL to these membranes was not affected.

Animals↗

PubMed1992

Liver metabolism of cholesterol taken up from lipoproteins in Wistar rats. An in vivo comparison between rat and human lipoproteins.

1. This study compares liver uptake, biliary secretion and blood decay of VLDL, LDL, HDL2 and HDL3 lipoprotein fractions isolated from both rat and human plasma and labelled with [14C]-cholesterol following the i.v. administration to the bile-fistulated rat model. 2. The present results demonstrate that the use of heterologous lipoproteins in bile-fistulated rat can be helpful in administering in a small volume large amounts of free and esterified cholesterol and in evaluating specific aspects of lipoprotein cholesterol metabolism by liver.

Animals↗