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PubMed2000

The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: a current review.

Three major interconnected pathways are involved in lipoprotein metabolism: (1) the transport of dietary or exogenous fat; (2) the transport of hepatic or endogenous fat; and (3) reverse cholesterol transport. These pathways are interdependent and disruptions in one will affect the function and products of the others. For example, a mutation such as one in the ABC1 protein can disrupt normal transport and processing of cholesterol. High-density lipoprotein cholesterol (HDL-C) appears to have cardioprotective properties because of its involvement in certain processes such as reverse cholesterol transport and inhibition of low-density lipoprotein cholesterol (LDL-C) oxidation. Certain agents, such as niacin, which increases HDL-C, lowers lipoprotein (a), and targets specific enzymes or receptors, may be highly beneficial for patients at risk of cardiovascular disease.

Cholesterol↗

PubMed2002

Rates of cholesterol esterification and esterified cholesterol net mass transfer between high-density lipoproteins and apolipoprotein B-containing lipoproteins in Type 1 diabetes.

AIMS: Type 1 diabetes is associated with a high incidence of coronary heart disease (CHD) despite paradoxically normal or high high-density lipoprotein (HDL) cholesterol concentrations. Triglyceride (TG) concentrations have been shown to be important determinants of two aspects of HDL metabolism: cholesterol esterification rate and esterified cholesterol (EC) net mass transfer rate between HDL and the apolipoprotein B-containing lipoproteins. In order to try to explain the paradox, we aimed to assess the relationships between plasma TG and these two processes in Type 1 diabetic compared with non-diabetic subjects. METHODS: Rates of cholesterol esterification and EC net mass transfer between HDL and the apolipoprotein B-containing lipoproteins were assessed by incubating whole plasma at 37 degrees C; intra-assay coefficients of variation were 6% and 30%, respectively. RESULTS: Ten Type 1 diabetic and 10 non-diabetic subjects, with similar ages, sex distributions, body mass indices and total cholesterol and TG concentrations, were assessed. Apolipoprotein A1, HDL unesterified cholesterol, and HDL phospholipid concentrations were greater in the Type 1 diabetic subjects. There were no significant differences in the rates of cholesterol esterification or EC net mass transfer between the groups. There were strong associations between plasma TG and the rate of cholesterol esterification and between plasma TG and the rate of EC net mass transfer in Type 1 diabetic subjects (r = 0.83, P = 0.0027 and r = 0.88, P = 0.0009, respectively) and in non-diabetic subjects (r = 0.91, P = 0.0002 and r = 0.79, P = 0.0070, respectively). However, the slopes of the associations with plasma TG were significantly steeper in the Type 1 diabetic subjects (analyses of covariance P = 0.0053 and P = 0.0146, respectively). CONCLUSIONS: Increases in TG may therefore promote more EC enrichment of atherogenic apolipoprotein B-containing lipoproteins in Type 1 diabetes while also promoting more cholesterol esterification, thereby maintaining HDL cholesterol concentrations. This could contribute to the paradox of high CHD incidence despite normal or high HDL cholesterol concentrations in Type 1 diabetes.

Adult↗

PubMed1998

Effect of hypochlorite (HOCl)-modified low density lipoproteins and high density lipoproteins on platelet function.

As hypochlorous acid (HOCl) might be a potential candidate for generation of modified (lipo)proteins in vivo , the present study was aimed at investigating the effects of HOCl-modified lipoproteins on platelet function in vitro. Lipoproteins modified with HOCl at concentrations that occur physiologically did not induce spontaneous platelet aggregation. However, low density lipoproteins (LDL; 100 to 500 microg protein/ml) increased platelet aggregation and fluorescence anisotropy in response to ADP (1 and 10 microM) and thrombin (0.1 and 0.5 U/ml) as well as malondialdehyde (MDA) formation as a function of increasing HOCl-concentrations (0.2 to 1.6 mM). HOCl-modified high density lipoprotein subfraction 3 (HDL3) had no effect on platelet function.

Journal Article↗

PubMed2006

Platelet activation by low density lipoprotein and high density lipoprotein.

Cardiovascular disease is the main cause of death and disability in the Western society. Lipoproteins are important in the development of cardiovascular disease since they change the properties of different cells involved in atherosclerosis and thrombosis. The interaction of platelets with lipoproteins has been under intense investigation. Particularly the initiation of platelet signaling pathways by low density lipoprotein (LDL) has been studied thoroughly, since platelets of hypercholesterolemic patients, whose plasma contains elevated LDL levels due to absent or defective LDL receptors, show hyperaggregability in vitro and enhanced activity in vivo. These observations suggest that LDL enhances platelet responsiveness. Several signaling pathways induced by LDL have been revealed in vitro, such as signaling via p38 mitogen-activated protein kinase and p125 focal adhesion kinase. High density lipoprotein (HDL) consists of two subtypes, HDL(2) and HDL(3), which have opposing effects on platelet activation. This review provides a summary of the activation of signaling pathways after platelet-LDL and platelet-HDL interaction, with special emphasis on their role in the development of thrombosis and atherosclerosis.

Atherosclerosis↗

PubMed1997

Fasting during Ramadan induces a marked increase in high-density lipoprotein cholesterol and decrease in low-density lipoprotein cholesterol.

We demonstrated for the first time in a Moroccan population that fasting during Ramadan, the ninth lunar month of the Muslims' year, affected lipid and lipoprotein metabolism in a group of 32 healthy adult male volunteers. This investigation was conducted to study the changes in serum total cholesterol, triglycerides, cholesterol in high-density lipoprotein (HDL) and low-density lipoprotein (LDL), glucose, and body weight during Ramadan. The results showed a significant decrease (7.9%, p < 0.001) in serum total cholesterol concentration during Ramadan as compared with the prefasting period. Also, we obtained a significant decrease of serum triglyceride concentration (30%, p < 0.001) during Ramadan fasting as compared to the period before Ramadan. The reduction of both serum triglycerides and total cholesterol was maintained 1 month after Ramadan. By the end of Ramadan, serum HDL cholesterol had markedly increased (14.3%, p < 0.001) and remained elevated 1 month after Ramadan in contrast to LDL cholesterol which showed a significant decrease (11.7%, p < 0.0001) also maintained 1 month after Ramadan. Mean body weight declined by 2.6% (p < 0.01) on day 29 of Ramadan, whereas during Ramadan, the diet pattern used by our subjects showed an increase of total energy intake due to carbohydrates (+ 1.4% of total energy), proteins (+ 0.4% of total energy) but not fat (-0.7% of total energy) compared to a usual diet used throughout the rest of the year. Moreover, the fat diet is high in monounsaturated (p < 0.05) and polyunsaturated fatty acid in contrast to saturated fatty acid which significantly (p < 0.05) decreased during Ramadan. These findings suggest that feeding behavior that occurs during Ramadan beneficially affects plasma lipids and lipoproteins.

Adult↗

PubMed1984

Mechanism of localization of major outer membrane lipoprotein in Escherichia coli. Studies with the OmpF-lipoprotein hybrid protein.

A chimera gene consisting of the ompF promoter, the coding regions for the signal peptide and the NH2-terminal 11 amino acid residues of outer membrane OmpF protein, and the coding region for the major outer membrane lipoprotein devoid of the NH2-terminal 7 amino acid residues was constructed. Escherichia coli carrying the cloned chimera gene produced a hybrid protein with the predicted chemical structure. The protein was localized in the periplasmic space with an interaction with the peptidoglycan layer. These results indicate that the hybrid protein was expressed, secreted across the cytoplasmic membrane, and processed for the signal peptide normally. The hybrid protein, however, was not incorporated into the outer membrane, suggesting the importance of the lipid domain in the assembly of the lipoprotein into the outer membrane. Although a larger part of the protein was extractable with sodium dodecyl sulfate, a part of the hybrid protein was covalently bound to the peptidoglycan layer as the lipoprotein is. Upon treatment with lysozyme of the envelope the hybrid protein became water soluble. The solubilized protein most probably existed as a trimer. These results most likely suggest that the major lipoprotein exists as a trimer in the periplasmic space with interactions with the peptidoglycan layer through the protein domain on one side and with the outer membrane through the lipid domain on the other side.

Amino Acid Sequence↗

PubMed1995

Purification of the apolipoprotein B-67-containing low density lipoprotein particle and its affinity for the low density lipoprotein receptor.

Naturally occurring mutant forms of apolipoprotein B (apoB)-100 may be able to provide valuable information on the structure-function relationships of apoB with the low density lipoprotein (LDL) receptor. ApoB-67, recently identified in a kindred displaying apoB levels 25% of normal (Welty et al. J. Clin. Invest. 1991. 87: 1748-1754), is predicted to contain 3040 amino acids and therefore, contains part of the epitope for antibody 4G3, which blocks binding of LDL to the LDL-receptor. To determine whether the amino terminal 67% of apoB-100 is important for binding to the LDL receptor, the apoB-67-containing lipoprotein particle was purified from plasma by gradient ultracentrifugation. The fractions containing apoB-67 were in the density range 1.049-1.070 g/ml. These fractions were pooled and adsorbed onto an affinity chromatography column containing the monoclonal antibody, MB-47. The epitope for MB-47 is two nonlinear domains between amino acids 3429 to 3453 and 3507 to 3523; therefore, apoB-100 will bind to the MB-47 column but apoB-67 will not. The resulting apoB-67-containing particles were completely devoid of apoB-100. In competitive binding studies, the apoB-67 lipoprotein particle did not compete with 125I-labeled apoB-100-containing LDL particles for binding, uptake, or degradation by normal human fibroblast monolayers. We conclude that the amino terminal 67% of apoB-100 in the naturally occurring lipoprotein particle does not appear to contain a functionally relevant epitope of the LDL-receptor binding domain.

Apolipoproteins↗

PubMed1997

Variation at the lipoprotein lipase and apolipoprotein AI-CIII gene loci are associated with fasting lipid and lipoprotein traits in a population sample from Iceland: interaction between genotype, gender, and smoking status.

The effects of polymorphisms in the lipoprotein lipase (LPL) gene (HindIII and S447X) and in the apolipoprotein (apo) AI-CIII gene cluster (G75A and C1100T) on levels of fasting plasma triglycerides, apoCIII, high density lipoprotein cholesterol (HDL-C), and apoAI were examined in 315 healthy men and women from Iceland. Non-smoking and smoking men and women were examined separately because of the strong effects of smoking status and gender on lipoproteins. For the LPL gene, there were no significant associations between plasma traits and genotypes of the S447X polymorphism, but the LPL-HindIII polymorphism was associated with significant effects on levels of all traits, with the effect of genotype on triglycerides and apoAI being modulated by smoking status, (genotype x smoking interaction, P < .02). The H- allele was generally associated with slightly lower levels of apoCIII, with a lowering effect on triglycerides only in smokers and with a raising effect on ApoAI in non-smoking and smoking men and in non-smoking women. For the apoCIII C1100T polymorphism, smoking and non-smoking men with one or more T alleles had levels of triglycerides roughly 10% higher than those with only the C allele; in contrast, the women with the T allele had lower levels of triglycerides (15.7% lower in non-smokers, P = .04; gender x genotype interaction, P = .02). In males and females and in smokers and non-smokers, the T allele was associated with levels of apoCIII that were 9-20% higher than those with only the C allele (P = .004 overall). In the non-smoking men, nonlinear additive effects were observed with combinations of genotypes at the LPL and apoAI-CIII loci, with the HDL-C and apoAI raising effect associated with the A75 allele and H- allele seen only in those men with both alleles, and the apoCIII raising effect associated with the H+ and T alleles seen only in those with both alleles. Thus, variations at both of the LPL and apoAI-apoCIII loci influence levels of triglycerides, apoCIII, HDL-C, and apoAI, but these effects are strongly modulated by smoking and are different between men and women. The mechanisms for these interactions between smoking or gender and genes are unknown, but future studies should take such interactions into account.

Adolescent↗

PubMed1996

Higher level of plasma cholesteryl ester transfer activity from high-density lipoprotein to apo B-containing lipoproteins in subjects with angiographically detectable coronary artery disease.

BACKGROUND AND HYPOTHESIS: Plasma high-density lipoprotein cholesterol (HDL-C) levels correlate inversely with the incidence of coronary artery disease. In order to ascertain whether the transfer activity is related to coronary atherosclerosis, we studied plasma cholesteryl ester transfer activity (CETA) from HDL to apo B-containing lipoproteins in a consecutive series of 64 Japanese men aged < 60 years who had undergone diagnostic coronary angiography. METHODS: The subjects were divided into two groups: those who had > or = 50% luminal stenosis in one or more coronary arteries (Group 1) and those who had < 50% stenosis (Group 2). RESULTS: CETA was 20.8 +/- 6.0%/2 h in 38 subjects in Group 1, significantly higher than 17.4 +/- 6.9%/2 h in 26 subjects in Group 2 (p < 0.05). Plasma HDL-C levels in Group 1 were significantly lower than those in Group 2 (p < 0.05). CETA correlated inversely with HDL-C levels (r = -0.46, p < 0.001). Plasma total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and Lp(a) levels did not differ significantly between the two groups. There was no significant correlation between CETA and either LDL-C or TG levels. CONCLUSION: Results suggest that high CETA is related to low plasma HDL-C levels and may lead to the development of coronary atherosclerosis. Also, CETA was independent of plasma LDL-C or TG levels.

Apolipoproteins B↗

PubMed1994

The soluble form of Alzheimer's amyloid beta protein is complexed to high density lipoprotein 3 and very high density lipoprotein in normal human plasma.

The amyloid fibrils of Alzheimer's neuritic plaques and cerebral blood vessels are mainly composed of aggregated forms of a 39 to 44 amino acids peptide, named amyloid beta (A beta). A similar although soluble form of A beta (sA beta) has been identified in plasma, cerebrospinal fluid and cell culture supernatants, indicating that it is produced under physiologic conditions. We report here that sA beta in normal human plasma is associated with lipoprotein particles, in particular to the HDL3 and VHDL fractions where it is complexed to ApoJ and, to a lesser extent, to ApoAI. This was assessed by immunoprecipitation experiments of purified plasma lipoproteins and lipoprotein-depleted plasma and confirmed by means of amino acid sequence analysis. Moreover, biotinylated synthetic peptide A beta 1-40 was traced in normal human plasma in in vitro experiments. As in the case of sA beta, biotinylated A beta 1-40 was specifically recovered in the HDL3 and VHDL fractions. This data together with the previous demonstration that A beta 1-40 is taken up into the brain via a specific mechanism and possibly as an A beta 1-40-ApoJ complex indicate a role for HDL3- and VHDL-containing ApoJ in the transport of the peptide in circulation and suggest their involvement in the delivery of sA beta across the blood-brain barrier.

Amino Acid Sequence↗

PubMed2000

Contribution of the carboxy-terminal domain of lipoprotein lipase to interaction with heparin and lipoproteins.

The C-terminal domain of lipoprotein lipase (LPL) is involved in several important interactions. To assess its contribution to the binding ability of full-length LPL we have determined kinetic constants using biosensor technique. The affinity of the C-terminal domain for heparin was about 500-fold lower than that of full-length LPL (K(d) = 1.3 microM compared to 3.1 nM). Replacement of Lys403, Arg405 and Lys407 by Ala abolished the heparin affinity, whereas replacement of Arg420 and Lys422 had little effect. The C-terminal domain increased binding of chylomicrons and VLDL to immobilized heparin relatively well, but was less than 10% efficient in binding of LDL compared to full-length LPL. Deletion of residues 390-393 (WSDW) did not change the affinity to heparin and only slightly decreased the affinity to lipoproteins. We conclude that the C-terminal folding domain contributes only moderately to the heparin affinity of full-length LPL, whereas the domain appears important for tethering triglyceride-rich lipoproteins to heparin-bound LPL.

Animals↗

PubMed1982

Lipoprotein lipase activity and serum lipoproteins in untreated type 2 (insulin-independent) diabetes associated with obesity.

Serum lipoproteins and the heparin-releasable lipoprotein lipase (LPL) activity of adipose tissue and skeletal muscle were measured in 36 untreated obese patients with Type 2 (insulin-independent) diabetes and the values were compared with those of non-diabetic subjects of similar age, sex and relative body weight. In diabetic men, the LPL activity of adipose tissue was significantly reduced when expressed per tissue weight or per fat cell (p less than 0.01). Diabetic females had slightly but not significantly lower LPL activity in adipose tissue than the non-diabetic females. The muscle LPL activity was similar in diabetic and non-diabetic subjects of both sexes. When the diabetic men were classified according to fasting blood glucose, the patients with high glucose levels had lower adipose tissue LPL activity than those with moderate hyperglycemia. In both diabetic and non-diabetic subjects, there was a significant positive correlation between HDL cholesterol concentrations and adipose tissue LPL activity. It is concluded that Type 2 diabetes influences adipose tissue LPL activity and plasma lipoprotein concentrations and that this effect is superimposed on the similar changes produced by obesity alone.

Adult↗

PubMed2001

Effect of low-density lipoprotein buoyant density and cholesterol content on the formation of lipoprotein(a) particles.

Lipoprotein(a) [Lp(a)] is a unique lipoprotein which resembles low-density lipoprotein (LDL) both in lipid composition and the presence of apolipoprotein B-100 (apo B-100). Lp(a) is, however, distinguishable from LDL by the presence of an additional glycoprotein apolipoprotein(a) [apo(a)], which is covalently attached to apo B-100 by a single disulfide bond. It is now generally accepted that Lp(a) assembly is a two-step process in which the initial non-covalent interaction between apo(a) and apo B-100 is mediated by the weak lysine binding sites present in kringle IV types 6, 7 and 8 of apo(a). In the present study, we have investigated the effect of LDL heterogeneity on Lp(a) assembly in a group of 111 individuals. The three parameters of LDL composition assessed in this study were the cholesterol content, the apo B content, and the relative flotation rate (a measure of LDL buoyancy and thus size). We found no correlation between the size of LDL particles and the extent of Lp(a) formation; a weak negative correlation was observed between cholesterol content of LDL and Lp(a) formation (P=0.042). This may suggest a role for free (i.e., surface-associated) cholesterol in the ability of LDL to form Lp(a) particles.

Cholesterol↗

PubMed1989

Efficient electroblotting of human very-low-density lipoproteins and low-density lipoproteins from composite gradient gels to nylon membranes.

Rinsing of gradient composite acrylamide/agarose gels with 1% Triton X-100 permits the efficient electrotransfer of very-low-density and low-density lipoproteins from the gels and does not appear to interfere with subsequent capture of the lipoproteins by charged nylon membranes. Overall efficiency of the transfer/capture process can approach 95% and does not appear to be significantly affected by total lipoprotein concentrations up to 5000 mg/dl. Direct immunoquantification of transferred apolipoproteins on the membrane is feasible as well. The nylon membranes used, however, must be pretested to ensure capture efficiency.

Detergents↗

PubMed1979

Association of lysolecithin acyltransferase with the high density lipoproteins and its activation by the low density lipoproteins in normal human plasma.

The lysolecithin acyltransferase of human plasma is shown to be associated with the high-density lipoprotein fraction. Although the low density lipoproteins do not have intrinsic enzyme activity, their presence activated the enzyme 3--7-fold. This activation is not affected by heat-treatment of the low density lipoproteins, but is abolished by the addition of heparin.

1-Acylglycerophosphocholine O-Acyltransferase↗

PubMed1980

Net mass transfer of esterified cholesterol from human low density lipoproteins to very low density lipoproteins incubated in vitro.

In 37 degrees C incubations of either human or rabbit very low density lipoproteins (VLDL), low density lipoproteins (LDL) and lipoprotein-free plasma thee was a net mass transfer of esterified cholesterol from LDL to VLDL which in the human studies resulted in an approximate doubling of the VLDL esterified cholesterol concentration after 24 h. There was also a net mass transfer of triacylglycerol in the reverse direction, from VLDL to LDL.

Animals↗

PubMed1981

Origin and pattern of glucocorticoid-induced hyperlipidemia in rats. Dose-dependent bimodal changes in serum lipids and lipoproteins in relation to hepatic lipogenesis and tissue lipoprotein lipase activity.

Rats maintained for five days on a low dose of triamcinolone (0.5 mg/kg) showed a 2-fold increase in serum triacylglycerol concentration, paralleled by a rise in all very low density lipoprotein (VLDL) components but no significant change in serum cholesterol or high density lipoproteins (HDL). In contrast, a high dose of triamcinolone (12.5 mg/kg) produced a fall in triacylglycerol and VLDL to the range of control levels coincident with doubling in serum cholesterol and HDL. The rise in VLDL was attributed in a large part to enhanced hepatic fatty acid synthesis as evident from the marked rises in activity of rate-limiting enzymes of lipogenesis and in 3H incorporation into liver and serum fatty acids from in vivo administered 3H2O. The induction of fatty acid synthesis was linked to pronounced hyperinsulinemia, elicited by the triamcinolone treatment, to which the liver remained selectively responsive, contrary to the general insulin antagonism in peripheral tissues. Triamcinolone treatment also resulted in small rises in serum glucagon but these changes did not appear to be of importance for the observed bimodal serum lipoprotein perturbations. Dexamethasone, prednisolone and cortisol, administered in doses equipotent to 0.5 mg/kg triamcinolone, produced similar changes in the levels of serum triacylglycerol and insulin and activities of hepatic enzymes of lipogenesis.

Acetyl-CoA Carboxylase↗

PubMed1983

Relative rates of incorporation of esterified cholesterol into human very low density lipoproteins and low density lipoproteins. In vitro studies of two separate pathways.

It has been shown previously that there are two pathways by which the esterified cholesterol formed in human plasma in the reaction catalysed by lecithin: cholesterol acyltransferase may be delivered to very low density lipoproteins (VLDL) and low density lipoproteins (LDL): (a) an indirect pathway in which esterified cholesterol which was incorporated initially into high density lipoproteins (HDL) is transferred subsequently to VLDL and LDL in a process mediated by an esterified cholesterol transfer/exchange protein and (b) a direct pathway in which a small proportion of the esterified cholesterol formed in the lecithin:cholesterol acyltransferase reaction is delivered to VLDL and LDL directly from its site of synthesis via a pathway which bypasses the bulk HDL fraction. These present studies have been designed to examine the incorporation of esterified cholesterol into VLDL relative to that into LDL via each of these two pathways. It has been found that a delivery of esterified cholesterol from HDL to VLDL and LDL via the indirect pathway has a marked preference for VLDL over LDL; equating the concentrations of esterified cholesterol in the two fractions revealed an incorporation into VLDL which was 7-11 times greater than that into LDL. By contrast, delivery via the direct pathway showed a marginal preference for LDL over VLDL.

Adult↗