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PubMed1975

Metabolism of lipoproteins in nonhuman primates. Studies on the origin of low density lipoprotein apoprotein in the plasma of the squirrel monkey.

The plasma of squirrel monkeys contains extremely low levels of very low density lipoproteins. The delipidated apoproteins from the different lipoprotein density classes of this species show a heterogeneity similar to that of man and the rat. The biosynthesis of the apoproteins of squirrel monkey lipoproteins was studied in fasted normal and Triton WR1339-treated animals. After intravenous injection of [3-H] leucine, maximal labeling of very low density lipoproteins occurred after 1 h, intermediate density lipoproteins (d 1.006--1.019) in 2 h, and low density lipoproteins after 3 h. At all times, however, low density lipoproteins had the greatest percentage of radioactivity. Polyacrylamide gel electrophoresis revealed that the apoprotein B moiety of very low density and intermediate density lipoproteins contained 62% and 81% of the total radioactivity in these lipoproteins whereas the fast-migrating peptides were minimally labeled. In monkeys injected with Triton WR1339, 70--80% of the radioactivity incorporated into d smaller than 1.063 lipoproteins was in very low density lipoproteins with only 10--15% in intermediate and low density lipoproteins. After injection of 3-H-labeled very low density lipoproteins and [14-C] leucine into Triton-treated monkeys, catabolism of 3-H-labeled very low density lipoprotein to intermediate and low density lipoproteins was small and was significantly less than corresponding values for the incorporation of [14-C] leucine. Thus, breakdown of very low density lipoproteins could not account for all the labeled apoprotein B present in the intermediate and low density lipoprotein fractions. The results indicate that most, but not all, of the newly synthesized apoprotein B enters plasma in very low density lipoproteins and that the low concentrations of this lipoprotein in squirrel monkey plasma are a consequence of its rapid turnover.

Animals↗
PubMed1987

High-cholesterol diet-induced lipoproteins stimulate lipoprotein lipase secretion in cultured rat alveolar macrophages.

We have previously shown that cultured rat alveolar macrophages synthesize and secrete lipoprotein lipase into the medium. The purpose of the present experiments is to examine whether cholesterol-enriched lipoproteins from cholesterol-fed animals have any effects on the lipoprotein lipase secretion and the lipid accumulation in macrophages. Macrophages incubated with the VLDL obtained from rats fed a normal diet secreted 2-fold higher amounts of lipoprotein lipase than those without lipoproteins. Intermediate-, low- and very-low-density lipoproteins from rats fed a high-cholesterol diet also enhanced the lipoprotein lipase secretion. Normal high- and low-density lipoproteins, and high-density lipoproteins from hypercholesterolemic animals did not cause any increase in the lipoprotein lipase secretion. The lipoproteins which stimulated the lipoprotein lipase secretion caused intracellular accumulation of both triacylglycerol and cholesterol. It is speculated that macrophages residing in the environment rich in lipoproteins, especially hypercholesterolemic lipoproteins, take them up and accumulate lipids intracellularly, and that this process links with the lipoprotein lipase secretion. The secreted lipoprotein lipase could facilitate, by degrading lipoproteins, the uptake of lipoprotein lipase-modified lipoproteins. Probably such a series of events is of importance in the foam cell formation of macrophages.

Animals↗
PubMed1999

Sialic acid-containing components of lipoproteins influence lipoprotein-proteoglycan interactions.

Sialic acid is a negatively charged sugar associated with the protein and lipid portions of lipoproteins. Sialic acid has been hypothesised to play an anti-atherogenic role in lipoprotein metabolism through the electrostatic inhibition of lipoprotein interactions with chondroitin-6-sulphate-rich arterial proteoglycans (APG). We conducted a series of studies using native and modified lipoproteins (VLDL1 Sf 60-400, VLDL2 Sf 20-60, IDL1 Sf 16-20, IDL2 Sf 12-16, LDL(A) Sf 8-12, and LDL(B) Sf0-8) that vary in their sialic acid content to examine the relationship between lipoprotein sialic acid content and its interaction with APG. Lipoprotein sialic acid was greatest in VLDL1 and decreased progressively with particle density until the IDL2 fraction (VLDL1 > VLDL2 > IDL1 > IDL2 = LDL(A) = LDL(B)). The pattern of reactivity of each fraction with APG was different from the pattern observed for lipoprotein sialic acid content (IDL2 > LDL(A) > LDL(B) > IDL1 > VLDL2 > VLDL1). Levels of sialic acid were lower in subjects with CHD as compared to control subjects but the presence of CHD had no effect on lipoprotein-APG complex formation when sex and plasma triglyceride levels were taken into account. There was also no significant relationship between the lipoprotein sialic acid content and the reactivity with APG within each lipoprotein fraction. Treatment of hypertriglyceridaemic subjects with ciprofibrate decreased lipoprotein-APG complex formation in all lipoprotein fractions. This was associated with a decrease in the total sialic acid content of apo B100-containing lipoproteins suggesting that the total sialic acid content of apo B100-containing lipoproteins has no influence on lipoprotein-APG complex formation. We next conducted in vitro experiments to manipulate LDL sialic acid content. Enzymatic removal of sialic acid from LDL with neuraminidase resulted in an increase in LDL-APG complex formation. This was accompanied by an increase in the exposure of free amino groups on LDL possibly due to disruption of interactions between free amino groups and sialic acid-containing components on LDL. Increasing LDL sialic acid content through incubation with ganglioside resulted in a decrease in lipoprotein-APG complex formation without any changes in the exposure of free amino groups on LDL. We conclude that total sialic acid content of lipoproteins is not a major determinant of their binding to APG. However, specific sialic acid-containing components on lipoproteins can affect their interaction with APG.

Apolipoprotein B-100↗
PubMed1985

Endogenous plasma lipoprotein lipase activity in fed and fasting rats may reflect the functional pool of endothelial lipoprotein lipase.

In this study, a correlation was sought between the circulating lipoprotein lipase activity and nutritional state in the rat. In fed rats, the plasma lipoprotein lipase activity was between 30 and 120 munits/ml, whereas after an overnight fast in restraining cages, the lipoprotein lipase plasma levels were between 280 and 500 munits/ml. The plasma lipoprotein lipase activity was inhibited by a specific high titre goat antiserum to rat lipoprotein lipase. No effect of fasting was seen on the plasma hepatic triacylglycerol lipase. 6 h after fasting, adipose tissue lipoprotein lipase decreased maximally, but plasma lipoprotein lipase was not changed and rose only after 16 h. Thus, it seems that most of the lipoprotein lipase activity in the fasting plasma was related to the 3-fold rise in lipoprotein lipase activity in the heart, which may represent total muscle lipoprotein lipase. The increase in heart lipoprotein lipase was due in part to an increase in the t1/2 of the enzyme from 1.2 to 2.9 h. To determine whether the high plasma levels in the fasting rats might result from impaired clearance of the enzyme by the liver, functional hepatectomy was carried out. 15 min after hepatectomy, plasma lipoprotein lipase rose up to 20-fold in fed and about 6-fold in fasting rats. Lipoprotein lipase activity extracted by the liver was calculated to be 30-60 munits/ml in the fed and 171-247 munits/ml plasma per min in fasting rats. An increase in lipoprotein lipase activity in extrahepatic tissues (heart, lung, kidney, diaphragm and adrenal) occurred 30 min after hepatectomy in fed rats. The increase in heart lipoprotein lipase was due to an increase in heparin-releasable fraction. Since no impairment of hepatic clearance of circulating plasma lipoprotein lipase was found, the high fasting plasma lipoprotein lipase activity may be related to an increase in enzyme synthesis, decreased enzyme turnover and an expansion of the functional pool in tissues such as the heart and probably muscle. The present findings indicate that measurement of endogenous plasma lipoprotein lipase can provide information with respect to the size of the functional pool under normal and pathological conditions.

Animals↗
PubMed1991

Race and gender differences in serum lipoproteins of children, adolescents, and young adults--emergence of an adverse lipoprotein pattern in white males: the Bogalusa Heart Study.

METHODS: Serum lipoprotein profiles in 4,231 individuals, ages 5-26 years, were studied cross-sectionally in a biracial community to describe the race- and gender-specific changes from adolescence into young adulthood. RESULTS: White children and adolescents of both genders showed significantly higher covariates--adjusted triglycerides (9-11 mg/dl) and very-low-density lipoprotein cholesterol (1-2 mg/dl)--and lower total cholesterol (3-14 mg/dl) and high-density lipoprotein cholesterol (6-10 mg/dl) levels than their black counterparts. These black-white differences persisted among young adults of both genders with the exception of total cholesterol levels (higher triglycerides: 23-32 mg/dl; higher very-low-density lipoprotein cholesterol: 5-7 mg/dl; lower high-density lipoprotein cholesterol: 9-11 mg/dl); in addition, white young adult males began to show higher levels of low-density lipoprotein cholesterol (14 mg/dl) than black young adult males. A consistent gender-related pattern emerged only among white young adults with males showing higher triglyceride levels (22 mg/dl), very-low-density lipoprotein cholesterol (5 mg/dl), and low-density lipoprotein cholesterol (10 mg/dl) and lower high-density lipoprotein cholesterol (10 mg/dl) than females. Lipoprotein changes from adolescence into young adulthood were more pronounced among white males than other race-gender groups, resulting in higher triglyceride, very-low-density lipoprotein cholesterol, and low-density lipoprotein cholesterol, a higher total cholesterol/high-density lipoprotein cholesterol ratio, and a lower high-density lipoprotein cholesterol in their young adulthood. According to the National Cholesterol Education Program criteria, a relatively higher proportion of young adult white males was classified as borderline-high (22.6%) or high (9.1%) for low-density lipoprotein cholesterol. Adiposity was the major contributor to the adverse lipoprotein pattern, especially among white males. Sexual maturation and age influenced the lipoprotein levels to a greater extent among white males. Cigarette smoking, alcohol intake, and oral contraceptive use began to emerge as minor but significant factors contributing to the lipoprotein levels in adolescents and young adults. CONCLUSION: These results underscore the desirability of early targeting for primary prevention.

Adolescent↗
PubMed1996

Dimeric lipoprotein lipase is bound to triglyceride-rich plasma lipoproteins.

Lipoprotein lipase hydrolyzes the triglyceride-rich core of chylomicrons and very low density lipoproteins. It is also a ligand, in vitro, for binding of lipoproteins to the low density lipoprotein receptor-related protein and may play a central role in the receptor-mediated removal of triglyceride-rich lipoproteins. The aim of the present study was to determine to which lipoprotein subclass the enzyme is bound in preheparin plasma and when released into plasma by heparin injection. Tetrahydrolipstatin, a potent inhibitor of serine lipases, was used to block lipolytic activity, thereby preventing changes in plasma lipoproteins due to ex vivo lipolysis. To analyze the distribution pattern of lipoprotein lipase dimers among lipoprotein classes, a specific ELISA was used and gel filtration was performed in pre- and postheparin plasma from five subjects with triglyceride ranging from 69 to 522 mg/dl. When lipolytic activity was not inhibited, lipoprotein lipase dimers eluted in association with low and high density lipoproteins, reproducing results previously obtained by several groups of investigators. However, in pre- and postheparin samples treated with tetrahydrolipstatin, most of the dimeric enzyme was found associated with very low density lipoprotein particles. In conclusion in pre- and postheparin samples most of the lipoprotein lipase dimers are associated with very low density lipoproteins when ex vivo lipolytic activity is inhibited, which supports the hypothesis that, in vivo, lipoprotein lipase may affect the receptor-mediated removal of these particles. Moreover, it suggests that the association between lipoprotein lipase and cholesterol-rich lipoproteins might be an ex vivo phenomenon due to lack of inhibition of lipolytic activity.

Adult↗
PubMed2000

Preventing, stopping, or reversing coronary artery disease--triglyceride-rich lipoproteins and associated lipoprotein and metabolic abnormalities: the need for recognition and treatment.

A substantial number of treated patients with or at high risk for coronary artery disease continue to have fatal and nonfatal coronary artery events in spite of significant reduction of elevated levels of low-density lipoprotein cholesterol. Other lipoprotein abnormalities besides an elevated level of low-density lipoprotein cholesterol contribute to risk of coronary artery disease and coronary artery events, and the predominant abnormalities that appear to explain much of this continued risk are an elevated serum triglyceride level and a low level of high-density lipoprotein cholesterol. Most patients with coronary artery disease have a mixed dyslipidemia with hypertriglyceridemia, which is associated and metabolically intertwined with other atherogenic risk factors, including the presence of triglyceride-rich lipoprotein remnants, low levels of high-density lipoprotein cholesterol, small, dense, low-density lipoprotein particles, postprandial hyperlipidemia, and a prothrombotic state. Aggressive treatment of these patients needs to focus on these other lipoprotein abnormalities as much as on low-density lipoprotein cholesterol. Combination drug therapy will usually be required. Reliable assessment of risk of coronary artery disease from lipoprotein measurements and response to therapy requires inclusion of all atherogenic lipoproteins in laboratory measurements and treatment protocols. At present this may be best accomplished by use of non-high-density lipoprotein cholesterol (total cholesterol minus high-density lipoprotein cholesterol) calculated from standard laboratory lipoprotein values. Ultimately, a more comprehensive assessment of coronary artery disease risk and appropriate therapy may include measurement of lipoprotein subclass distribution including determination of low-density lipoprotein particle concentration and sizes of the various lipoprotein particles.

Arteriosclerosis↗
PubMedDate not supplied

Transfer of plasma lipoprotein components and of plasma proteins into aortas of cholesterol-fed rabbits. Molecular size as a determinant of plasma lipoprotein influx.

The arterial influx of esterified and free cholesterol from low density lipoproteins and very low density lipoproteins in 20 hypercholesterolemic rabbits was measured simultaneously by the use of lipoproteins labeled in vivo with [3H]- and [14C]-cholesterol. The simultaneous arterial influx of either [3H]-leucine-labeled very low density lipoproteins, low density lipoproteins, high density lipoproteins, or plasma proteins was also measured in each rabbit. The arterial influx was calculated as intimal clearance, i.e., the influx of a given fraction divided by its plasma concentration. The intimal clearance of low density lipoprotein esterified cholesterol was equal to that for the apolipoproteins of that fraction, which is compatible with an arterial influx of intact low density lipoprotein molecules. The intimal clearance of very low density apolipoprotein or cholesteryl ester was less than that for low density lipoprotein, whereas high density lipoprotein and albumin clearances exceeded low density lipoprotein clearance by 1.5- to 3-fold. The intimal clearances of plasma proteins, high density, low density, and very low density lipoproteins decreased linearly with the logarithm of the macromolecular diameter. This indicates that the arterial influx of three plasma lipoprotein fractions and of plasma proteins proceeds by similar mechanisms. Apparently the relative intimal clearances of lipoproteins are more dependent on their size relative to pores or vesicular diameters at the plasma-artery interface than on specific interactions between lipoproteins and the arterial intimal surface.

Animals↗
PubMed1992

Distribution of apolipoprotein(a) in the plasma from patients with lipoprotein lipase deficiency and with type III hyperlipoproteinemia. No evidence for a triglyceride-rich precursor of lipoprotein(a).

Lipoprotein(a) consists of a low-density lipoprotein containing apolipoprotein (apo) B-100 and of the genetically polymorphic apo(a). It is not known where and how lipoprotein(a) is assembled and whether there exists a precursor for lipoprotein(a). We have determined the phenotype, concentration, and distribution of apo(a) in plasma from patients with lipoprotein lipase (LPL) deficiency (type I hyperlipoproteinemia, n = 14), in apo E 2/2 homozygotes with type III hyperlipoproteinemia (n = 12) and in controls (n = 16). In the two genetic conditions, there is grossly impaired catabolic conversion of apo B-100-containing precursor lipoproteins to low-density lipoproteins. Considering apo(a) type, the plasma concentration of apo(a) was normal in type III patients but significantly reduced in LPL deficiency. Despite the defects in the catabolism of other apo B-containing lipoproteins, the distribution of apo(a) was only moderately affected in both metabolic disorders, with 66.7% (type I) and 74.7% (type III) being present as the characteristic lipoprotein(a) in the density range of 1.05-1.125 g/ml (controls 81.6%). The remainder was distributed between the triglyceride-rich lipoproteins (type I 12.4%, type III 8.5%, controls 4.7%) and the lipid-poor bottom fraction (type I 19.3%, type III 15.3%, controls 12.6%). In all conditions most apo(a) (57-88%) dissociated from the triglyceride-rich lipoproteins upon recentrifugation and was recovered as lipoprotein(a). These data suggest that lipoprotein(a) is not generated from a triglyceride-rich precursor. Lipoprotein(a) may be secreted directly into plasma or may be formed by preferential binding of secreted apo(a) to existing low-density lipoprotein.

Apolipoproteins↗