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PubMed1985

High density lipoprotein and coronary artery disease risk factors in children with different lipoprotein profiles: Bogalusa Heart Study.

Serum high density lipoprotein-cholesterol (HDL-C) and apoprotein A-1 (apo A-1) profiles were examined in subgroups of children (n = 338), initially aged 2-14 years, whose earlier beta-lipoprotein cholesterol (beta-LPC) and pre-beta-lipoprotein cholesterol (pre-beta-LPC) measurements were in extreme percentiles of values from a biracial community. Relationships of HDL-C and apo A-1 to serum lipoprotein lipids, apoprotein B (apo B), subscapular skinfold thickness, fasting and 1/2 hr postglucose plasma insulin, and fasting and 1 hr postglucose plasma glucose and free fatty acids were examined. Clustering of several coronary artery disease risk factors in these children was observed. HDL-C levels tended to be low in children having high pre-beta-LPC levels and apo A-1 levels were low in boys having high pre-beta-LPC levels. Within beta- and pre-beta-LPC strata, differences were also observed with respect to race, but not sex, in the mean levels of both HDL-C and apo A-1. HDL-C and apo A.1 were related inversely to subscapular skinfold thickness and plasma insulin levels in all children except those with low levels of both beta-LPC and pre-beta-LPC. Ratios of low density lipoprotein-cholesterol/HDL-C and of apo B/apo A-1 were related positively with other coronary artery disease risk factors except in children having low levels of both beta-LPC and pre-beta-LPC. The magnitude of these associations was greater in whites than in blacks. These observations may help to identify, at an early age, children at high risk of developing coronary artery disease in adulthood.

Adolescent↗
PubMed1989

Plasma lipoproteins in healthy octogenarians: lack of reduced high density lipoprotein cholesterol levels: results from the Framingham Heart Study.

Genetic low density lipoprotein (LDL) deficiency and high density lipoprotein (HDL) excess have been associated with enhanced longevity. This investigation assessed the prevalence of lipoprotein abnormalities in octogenarians free of clinical evidence of cardiovascular disease (CVD) in the Framingham Heart Study. Plasma lipid and lipoprotein cholesterol determinations were carried out by standard techniques between 1971 and 1974. Participants who were free of clinical evidence of CVD in an examination approximately 10 years later (1981 to 1982) had their lipoprotein values tabulated based on the earlier examination. There were 106 women and 57 men who met these criteria, with mean ages of 83.3 and 82.9 years, respectively, at examination 16 (called cases). Mean levels (+/- SEM) of LDL cholesterol in cases were 152 +/- 3 mg/dL for women, and 147 +/- 5 mg/dL for men. For HDL cholesterol, these values were 57 +/- mg/dL for women and 46 +/- 2 mg/dL for men. These values were not statistically different from those of other study subjects (who did not meet the CVD criteria or were decreased) or middle-aged controls. In contrast, HDL cholesterol levels below the tenth percentile of normal were not observed in any male cases and in only 1.0% of female cases (P less than .05) as compared with observations in control subjects. The data are consistent with the concept that there is not an overrepresentation of either decreased LDL cholesterol or elevated HDL cholesterol values in subjects who subsequently become healthy octogenarians, but that these subjects are exceedingly unlikely to have reduced HDL cholesterol levels.

Aged↗
PubMed2004

Differential effect of two nicotinic acid preparations on low-density lipoprotein subclass distribution in patients classified as low-density lipoprotein pattern A, B, or I.

We tested the hypothesis that treatment with nicotinic acid results in a differential blood lipid response in subjects classified as having a low-density lipoprotein (LDL) pattern A or B. One hundred eighty hypercholesterolemic subjects were randomized to placebo (n = 61), immediate-release niacin (3,000 mg/day, n = 59), or extended-release niacin (1,500 mg/day, n = 60) for 14 weeks. Lipids and lipoprotein cholesterol were determined with enzymatic methods. LDL subclass distribution was determined with 2% to 16% polyacrylamide gradient gel electrophoresis. Extended- and immediate-release niacin had significant effects on the decrease of triglycerides, total cholesterol, LDL cholesterol, apoprotein B, lipoprotein(a), and apoprotein A-I and significantly increased high-density lipoprotein cholesterol. The 2 nicotinic acid compounds and doses significantly increased mean LDL peak particle diameter and percent distribution in large LDL I and IIa, with a significant decrease in small LDL IIIa, IIIb, and IVb. In patients with LDL pattern B compared with those with pattern A, extended-release niacin (1,500 mg/day) increased LDL peak particle diameter significantly more and decreased the percent distributions of small LDL IIIa, LDL IIIb, and LDL IVa significantly more. With 3,000 mg/day, immediate-release nicotinic acid in patients with LDL pattern B exhibited a significantly greater increase in LDL peak particle diameter and large LDL IIa and IIb and significantly greater decreases in small LDL IIIa, IIIb, and IVa compared with patients with pattern A. These differences in response between patients with LDL pattern A and those with pattern B were not reflected by changes in the standard lipid profile, including apoproteins A-I and B. Nicotinic acid has a significantly different effect on lipids and lipoprotein subclass distribution in subjects classified as having LDL subclass pattern A or B. Nicotinic acid has a significantly greater effect on the decrease of small LDL subclass distribution and increase in LDL peak particle diameter in pattern B versus pattern A.

Adult↗
PubMed2004

Smooth muscle cell biglycan overexpression results in increased lipoprotein retention on extracellular matrix: implications for the retention of lipoproteins in atherosclerosis.

Lipoprotein retention on extracellular matrix (ECM) may play a central role in atherogenesis, and a specific extracellular matrix proteoglycan, biglycan, has been implicated in lipoprotein retention in human atherosclerosis. To test whether increased cellular biglycan expression results in increased retention of lipoproteins on ECM, rat aortic smooth muscle cells (SMCs) were transduced with a human biglycan cDNA-containing retroviral vector (LBSN) or with an empty retroviral vector (LXSN). To assess the importance of biglycan's glycosaminoglycan side chains in lipoprotein retention, ECM binding studies were also performed using RASMCs transduced with a retroviral vector encoding for a mutant, glycosaminoglycan-deficient biglycan (LBmutSN). Human biglycan mRNA and protein were confirmed in LBSN and LBmutSN RASMCs by Northern and Western blot analyses. HDL3+E binding to SMC ECM was increased significantly (as determined by 95% confidence intervals for binding curves) for LBSN as compared to either LXSN or LBmutSN cells; the increases for LBSN cell ECM were due primarily to an approximately 50% increase in binding sites (increased Bmax) versus LXSN cell ECM and of approximately 25% versus LBmutSN cell ECM. These results are consistent with the hypothesis that biglycan, through its glycosaminoglycan side chains, may mediate lipoprotein retention on atherosclerotic plaque ECM.

Animals↗
PubMed2002

Usefulness of lipoprotein changes during acute coronary syndromes for predicting postdischarge lipoprotein levels.

The aim of our study was to evaluate the lipoprotein changes that occur during acute coronary events, and to determine the lipoprotein threshold levels that identify patients who require future statin therapy. Lipoprotein levels were measured at admission, at 6 hours, the morning after admission, before discharge, and 3 months after discharge in patients with myocardial infarction and unstable angina. Patients with myocardial infarction on thrombolytic therapy (n = 63) and patients with unstable angina (n = 33) had a decrease in low-density lipoprotein (LDL) cholesterol levels < or = 24 hours after admission (-12 +/- 20% and -6 +/- 23%, respectively), but these levels returned to baseline before discharge. In patients with myocardial infarction who did not receive thrombolytic therapy (n = 37), the decrease was more gradual and peaked before hospital discharge (-7 +/- 19%). There was good correlation between LDL cholesterol levels at admission and after discharge, especially in normotriglyceridemic patients. Over 90% of patients with LDL cholesterol > or = 125 mg/dl on the morning after admission were candidates for statin therapy after discharge. Thus, the need for future statin therapy can be predicted with fair reliability during the initial 24 hours after admission. However, elevated baseline triglyceride levels significantly affect these LDL cholesterol changes and complicate prediction of long-term lipoprotein levels.

Anticholesteremic Agents↗
PubMed1998

Relative contribution of low-density lipoprotein receptor and lipoprotein lipase gene mutations to angiographically assessed coronary artery disease among French Canadians.

Men with low-density lipoprotein receptor gene mutations causing familial hypercholesterolemia (FH) are at high risk of premature coronary artery disease (CAD). The dyslipidemic state found among patients who are heterozygous for mutations in the lipoprotein lipase (LPL) gene may also increase the risk of CAD. In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain. The frequency of FH as well as of LPL gene mutations tended to increase with the number of narrowed coronary arteries. However, CAD occurred earlier in FH patients than in partly LPL-deficient patients. Indeed, the proportion of men affected by FH was of 16.4% in those <45 years of age, and solely 4.3% among those between 56 and 60 years of age (p <0.0001). In contrast, the LPL gene defect was found in only 4.0% of men aged <45 years, whereas this prevalence reached 8.3% among those aged 56 to 60 years. In multivariate analyses, the association of LPL with CAD was not independent of age, high-density lipoprotein cholesterol concentrations, and other covariates included at baseline, and was not affected by the type of mutation in the LPL gene. In contrast, FH was associated with CAD with minimal contribution of other cardiovascular risk factors. However, the relation between FH and CAD was at least partly dependent on plasma apolipoprotein B concentrations. In the different regression models, fasting insulin and plasma high-density lipoprotein cholesterol concentrations were important covariates of CAD, whether or not patients were affected by FH or LPL deficiency. In conclusion, the association of LPL gene mutations with CAD was delayed compared with FH, appeared to be markedly exacerbated by the presence of additional risk factors, and was not affected by the type of mutation in the LPL gene.

Alleles↗
PubMed2001

Apolipoprotein-E phenotype and basal activity of low-density lipoprotein receptor are independent of changes in plasma lipoprotein subfractions after cholesterol ingestion in Japanese subjects.

We investigated whether the apolipoprotein-E (apoE) phenotype and the basal activity of low-density lipoprotein (LDL) receptor, which were reported to be the major determinants for increase in plasma LDL levels by cholesterol ingestion, have the same role in Japanese subjects whose diet is low in fat and cholesterol. Cholesterol (750 mg/d) was added to the ordinary diet as a dried egg-yolk supplement for 4 wk to 110 subjects. Plasma levels of lipids, apolipoproteins, and cholesterol in lipoprotein subfractions were measured at the beginning and end of the test period. Phenotyping of apoE was determined by an isoelectric focusing-immunoblotting method, and LDL receptor activity in lymphocytes was determined by flow cytometry. Plasma levels of cholesterol in less-dense LDL (LDL(1)) and less-dense high-density lipoprotein (HDL(2)) were slightly but significantly increased, 3.4% and 4.1%, respectively, by cholesterol ingestion, but the increases were not statistically significant in any of E2, E3, and E4 groups. The distribution of the apoE phenotype was equivalent in all three LDL-cholesterol groups (no change, increase, and decrease by cholesterol ingestion). Plasma levels of LDL, LDL(1), and LDL(2) cholesterol were not significantly increased in the three groups of subjects with lymphocyte LDL-receptor activities (low, medium, and high). As with apoE phenotype, LDL-receptor activities were the same in all three LDL-cholesterol groups. In addition, there were no significant correlations between LDL-receptor activity and changes in plasma levels of lipids, apolipoproteins, and cholesterol in lipoprotein subfractions. Therefore, we concluded that cholesterol ingestion significantly increases plasma levels of less-dense LDL and HDL, but neither apoE phenotype nor basal LDL-receptor activity explain the variability in changes in plasma lipoprotein subfractions by cholesterol ingestion in Japanese subjects.

Apolipoproteins E↗
PubMed2003

Role of helices and loops in the ability of apolipophorin-III to interact with native lipoproteins and form discoidal lipoprotein complexes.

The structure of Locusta migratoria apolipophorin-III consists of a five-helix bundle connected by four short loops. The role of the conformational flexibility of helices and loops on the lipid-binding activity of this apolipoprotein was investigated by disulfide mediated tethering experiments. One disulfide mutant tethering the second and fourth loops (L2-L4), and two disulfide mutants restricting the flexibility of the neighboring alpha-helices 3 and 4 (H3-H4) and 1 and 5 (H1-H5), were studied. The ability of the disulfide mutants to interact with phospholipid vesicles, mixed micelles of phosphatidylcholine and cholate, and in vivo with native spherical lipoprotein particles was studied. The L2-L4 mutant was active with native lipoproteins as well as being able to form discoidal lipoproteins upon incubation with either liposomes or discoidal micelles. The H3-H4 mutant was not able to interact with liposomes or native lipoproteins but interacted with discoidal micelles. The H1-H5 mutant was unable to interact with lipid in any of the three systems. Three conclusions were reached: (1) opening of the helix bundle does not require the separation of loops 2 and 4 as recently proposed by others and (2) alpha-helices 3 and/or 4 are involved in the insertion of apoLp-III in both phospholipid bilayers and monolayers. The conformational flexibility of helices 3 and 4 is required for the lipid-binding activity of apoLp-III. (3) Interaction of helices 1 and/or 5 with the lipid surface is required to the formation of stable lipoprotein complexes of any kind.

Animals↗
PubMed2001

Phospholipid composition of high-density lipoproteins reflects lipolysis of triglyceride-rich lipoproteins during hyperlipidemia.

We studied phospholipid composition of high-density lipoproteins in patients with normo- and hypertriglyceridemia treated with various hypolipidemic preparations (simvastatin and fenofibrate). Both preparations changed phospholipid composition of high-density lipoproteins and improved their functional activity. The differences in the phospholipid composition of high-density lipoproteins were probably related to lipolysis of triglyceride-rich lipoproteins catalyzed by lipoprotein lipase and, in particular, hepatic lipase.

Adult↗
PubMed2001

Triacylglycerol-rich lipoproteins alter the secretion, and the cholesterol-effluxing function, of apolipoprotein E-containing lipoprotein particles from human (THP-1) macrophages.

Elevated plasma levels of triacylglycerol-rich lipoproteins (TGRLP) are associated with increased risk of atherogenesis and abnormal reverse cholesterol transport, as illustrated in Type II diabetes. Here we examine the effect of plasma triacylglycerol-rich or cholesteryl ester-rich lipoproteins on the secretion of nascent apolipoprotein E (apoE)-containing lipoprotein E (LpE) particles by human (THP-1) macrophages. As expected, preincubation with low-density lipoprotein (LDL) yielded small but significant increases in total cellular cholesterol content and also the secretion of apoE by macrophages. By contrast, preincubation with TGRLP resulted in higher, dose-dependent, increases in apoE secretion that reflected, but were not dependent on, cellular triacylglycerol accumulation. Secreted apoE was incorporated into a pre-beta migrating LpE fraction that differed in lipid composition and flotation density depending on preincubation conditions. Specifically, the LpE-containing lipoprotein fraction produced by macrophages preincubated with TGRLP was cholesterol-poor, markedly heterogeneous and of higher peak flotation density (d 1.14-1.18) when compared with particles produced after preincubation with LDL. Both the conditioned medium and the isolated (d<1.21) LpE-containing fraction, yielded by macrophages preincubated with TGRLP, seemed poorer at inducing cholesterol efflux than the equivalent fractions from cells preincubated with LDL, as judged by [(3)H]cholesterol efflux from untreated 'naïve' macrophages. Thus, although the interaction of TGRLP with macrophages can enhance apoE output from these cells, the LpE particles produced seem to be relatively inefficient mediators of cholesterol efflux. These factors might contribute to the increased risk of atherosclerosis in individuals with Type II diabetes.

Apolipoproteins E↗
PubMed1980

Effect of tunicamycin on the metabolism of low-density lipoproteins by control and low-density-lipoprotein-receptor-deficient human skin fibroblasts.

Preincubation of normal human skin fibroblasts with tunicamycin, which inhibits N-glycosylation of glycoproteins, resulted in a dose-dependent and reversible inhibition of binding and internalization of homologous low-density lipoproteins by the cells. The degradation of the internalized lipoproteins was not affected by the drug. Comparative studies with fibroblasts deficient in low-density-lipoprotein receptors indicated that tunicamycin exerts its inhibitory effect only via the receptor-mediated high-affinity binding and uptake of lipoproteins. These results suggest that expression of low-density-lipoprotein receptors on the cell surface of human skin fibroblasts depends on intact N-glycosylation.

Cell Line↗
PubMed2002

Measurement of apolipoprotein B-48 in the Svedberg flotation rate (S(f))>400, S(f) 60-400 and S(f) 20-60 lipoprotein fractions reveals novel findings with respect to the effects of dietary fatty acids on triacylglycerol-rich lipoproteins in postmenopausal women.

The present study was designed to examine whether the type of fat ingested in an initial test meal influences the response and density distribution of dietary-derived lipoproteins in the Svedberg flotation rate (S(f))>400, S(f) 60-400 and S(f) 20-60 lipoprotein fractions. A single-blind randomized within-subject crossover design was used to study the effects of palm oil, safflower oil, a mixture of fish and safflower oil, and olive oil on postprandial apolipoprotein (apo) B-48, retinyl ester and triacylglycerol responses in each lipoprotein fraction following an initial test meal containing one of the oils and a second standardized test meal. For all dietary oils, late postprandial (300 min) concentrations of triacylglycerol and apo B-48 were significantly higher in the S(f) 60-400 fraction than in the S(f)>400 fraction (P<0.02). Significantly greater apo B-48 incremental areas under the curve (IAUCs) were also observed in the S(f) 60-400 fraction than in the S(f)>400 fraction following palm oil, safflower oil and olive oil (P<0.04), with a similar non-significant trend for fish/safflower oil. Olive oil resulted in a significantly greater apo B-48 IAUC in the S(f)>400 fraction (P<0.02) than did any of the other dietary oils, as well as a tendency for a higher IAUC in the S(f) 60-400 fraction compared with the palm, safflower and fish/safflower oils. In conclusion, we have found that the majority of intestinally derived lipoproteins present in the circulation following meals enriched with saturated, polyunsaturated or monounsaturated fatty acids are of the density and size of small chylomicrons and chylomicron remnants. Olive oil resulted in a greater apo B-48 response compared with the other dietary oils following sequential test meals, suggesting the formation of a greater number of small (S(f) 60-400) and large (S(f)>400) apo B-48-containing lipoproteins in response to this dietary oil.

Aged↗
PubMed1995

The very low density lipoprotein receptor mediates the cellular catabolism of lipoprotein lipase and urokinase-plasminogen activator inhibitor type I complexes.

The very low density lipoprotein (VLDL) receptor binds apolipoprotein E-rich lipoproteins as well as the 39-kDa receptor-associated protein (RAP). Ligand blotting experiments using RAP and immunoblotting experiments using an anti-VLDL receptor IgG detected the VLDL receptor in detergent extracts of human aortic endothelial cells, human umbilical vein endothelial cells, and human aortic smooth muscle cells. To gain insight into the role of the VLDL receptor in the vascular endothelium, its ligand binding properties were further characterized. In vitro binding experiments documented that lipoprotein lipase (LpL), a key enzyme in lipoprotein catabolism, binds with high affinity to purified VLDL receptor. In addition, urokinase complexed with plasminogen activator-inhibitor type I (uPA.PAI-1) also bound to the purified VLDL receptor with high affinity. To assess the capacity of the VLDL receptor to mediate the cellular internalization of ligands, an adenoviral vector was used to introduce the VLDL receptor gene into a murine embryonic fibroblast cell line deficient in the VLDL receptor and the LDL receptor-related protein, another endocytic receptor known to bind LpL and uPA.PAI-1 complexes. Infected fibroblasts that express the VLDL receptor mediate the cellular internalization of 125I-labeled LpL and uPA.PAI-1 complexes, leading to their degradation. Non-infected fibroblasts or fibroblasts infected with the lacZ gene did not internalize these ligands. These studies confirm that the VLDL receptor binds to and mediates the catabolism of LpL and uPA.PAI-1 complexes. Thus, the VLDL receptor may play a unique role on the vascular endothelium in lipoprotein catabolism by regulating levels of LpL and in the regulation of fibrinolysis by facilitating the removal of urokinase complexed with its inhibitor.

Adenoviruses, Human↗
PubMed2000

Mechanisms of hepatic very low density lipoprotein overproduction in insulin resistance. Evidence for enhanced lipoprotein assembly, reduced intracellular ApoB degradation, and increased microsomal triglyceride transfer protein in a fructose-fed hamster model.

A novel animal model of insulin resistance, the fructose-fed Syrian golden hamster, was employed to investigate the mechanisms mediating the overproduction of very low density lipoprotein (VLDL) in the insulin resistant state. Fructose feeding for a 2-week period induced significant hypertriglyceridemia and hyperinsulinemia, and the development of whole body insulin resistance was documented using the euglycemic-hyperinsulinemic clamp technique. In vivo Triton WR-1339 studies showed evidence of VLDL-apoB overproduction in the fructose-fed hamster. Fructose feeding induced a significant increase in cellular synthesis and secretion of total triglyceride (TG) as well as VLDL-TG by primary hamster hepatocytes. Increased TG secretion was accompanied by a 4.6-fold increase in VLDL-apoB secretion. Enhanced stability of nascent apoB in fructose-fed hepatocytes was evident in intact cells as well as in a permeabilized cell system. Analysis of newly formed lipoprotein particles in hepatic microsomes revealed significant differences in the pattern and density of lipoproteins, with hepatocytes derived from fructose-fed hamsters having higher levels of luminal lipoproteins at a density of VLDL versus controls. Immunoblot analysis of the intracellular mass of microsomal triglyceride transfer protein, a key enzyme involved in VLDL assembly, showed a striking 2.1-fold elevation in hepatocytes derived from fructose-fed versus control hamsters. Direct incubation of hamster hepatocytes with various concentrations of fructose failed to show any direct stimulation of its intracellular stability or extracellular secretion, further supporting the notion that the apoB overproduction in the fructose-fed hamster may be related to the fructose-induced insulin resistance in this animal model. In summary, hepatic VLDL-apoB overproduction in fructose-fed hamsters appears to result from increased intracellular stability of nascent apoB and an enhanced expression of MTP, which act to facilitate the assembly and secretion of apoB-containing lipoprotein particles.

Animals↗
PubMed2000

Oxidized low density lipoproteins regulate synthesis of monkey aortic smooth muscle cell proteoglycans that have enhanced native low density lipoprotein binding properties.

Oxidized low density lipoproteins (Ox-LDL) affect several biological processes involved in atherogenesis. However, it is not known whether Ox-LDL can regulate proteoglycan expression and thus affect arterial wall lipoprotein retention. This study evaluated whether Ox-LDL, as compared with native LDL, regulates proteoglycan expression by monkey arterial smooth muscle cells in vitro and whether proteoglycans synthesized in the presence of Ox-LDL exhibit altered lipoprotein binding properties. Ox-LDL stimulated glycosaminoglycan synthesis, as measured by (35)SO(4) incorporation, by 30-50% over that of native LDL. The effect was maximal after 72 h of exposure to 5 microg/ml of Ox-LDL. The molecular sizes of versican, biglycan, and decorin increased in response to Ox-LDL, as indicated by size exclusion chromatography and SDS-polyacrylamide gel electrophoresis. These effects could be mimicked by the lipid extract of Ox-LDL. These size increases were largely due to chain elongation and not to alterations in the ratio of (35)SO(4) to [(3)H]glucosamine incorporation. Affinity chromatography indicated that Ox-LDL stimulated the synthesis of proteoglycans with high affinity for native LDL. Ox-LDL also specifically stimulated mRNA expression for biglycan (but not versican or decorin), which was correlated with increased expression of secreted biglycan. Thus, Ox-LDL may influence lipoprotein retention by regulating synthesis of biglycan and also by altering glycosaminoglycan synthesis of vascular proteoglycans so as to enhance lipoprotein binding properties.

Animals↗
PubMed1999

Lipoprotein hydrolysis and fat accumulation in chicken adipose tissues are reduced by chronic administration of lipoprotein lipase monoclonal antibodies.

The lipoprotein lipase (LPL) catalyzed hydrolysis of plasma lipoproteins is a rate-limiting step in the lipid transport into peripheral tissues. The aim of the present study was to isolate monoclonal antibodies against chicken adipose LPL and to investigate whether chronic infusion of the LPL monoclonal antibodies inhibits adipose LPL activity and consequently reduces fat accumulation in broiler chickens. The LPL catalyzed very low density lipoprotein (VLDL) hydrolysis was completely inhibited by the addition of 100 microg/mL of monoclonal antibodies (CLP10, CLP14, CLP16) in the in vitro incubation with plasma VLDL and LPL. A single injection of CLP10 and CLP16 into chickens fed or starved for 24 h elevated plasma triacylglycerol concentrations for 24 h, whereas that of CLP14 was ineffective. Intravenous injection every other day and continuous infusion by osmotic minipump with CLP16 maintained higher plasma triacylglycerol concentration for 5 d than that of the control group and extensively reduced LPL activity in adipose tissues and abdominal fat pad weight. Lipoprotein lipase mRNA and protein levels in adipose tissue were not modified by chronic administration of anti-LPL antibody. The results indicate that chronic administration of anti-LPL antibodies is effective in retarding fatness in broiler chickens, and the antibodies are a proper subject for studies of lipoprotein metabolism.

Adipose Tissue↗
PubMed1976

Immunogenetic polymorphism of lipoproteins in swine. 1. Four additional serum beta-lipoprotein allotypes (Lpp2, Lpp4, Lpp5 and Lpp15) in the Lpp system.

Four additional swine serum lipoprotein allotypes are described. Specific anti-allotype reagents were obtained from alloimmune precipitating sera produced in lipoprotein-defined-type recipients immunized with normal sera and subsequently with lipoprotein fractions. Identification studies indicate that the four serologically defined low-density lipoprotein (LDL) variants, designated Lpp2, Lpp4, Lpp5 and Lpp15, are members of a previously described Lpp system. The individual specificities, Lpp2, Lpp4 and Lpp5, are determined by three co-dominant autosomal genes, Lpp2, Lpp4 and Lpp5, respectively, whereas the common specificity, Lpp15, is controlled by a complex of genetic information of the Lpp2 and Lpp4 genes, and by the two previously described alleles, Lpp1 and Lpp3; Lpp15 occurs on the same molecule with respective individual specificity. The Lpp5 and Lpp15 antigens behave as a pair of alternative allotypic specificities. The double immunodiffusion test in agar was employed to demonstrate independent phenotypic expression of each allelic gene in the Lpp heterozygous animals, for the analysis of the immune sera, and for lipoprotein testing of 3305 sera. Marked differences in gene frequencies were found between the swine breeds tested. As a result of characteristic frequencies, only nine of 15 possible Lpp genotypes were found in the breeding herds tested; the remaining six genotypes were obtained from testcross matings.

Alleles↗
PubMed2004

Atorvastatin reduces remnant lipoproteins and small, dense low-density lipoproteins regardless of the baseline lipid pattern.

Elevated plasma levels of remnant lipoproteins and small, dense low-density lipoprotein (LDL) particles increase the risk of atherosclerosis. This prospective, placebo-controlled, crossover trial evaluated the effect of atorvastatin on various lipid parameters including remnant lipoproteins and small, dense-LDL cholesterol levels. Forty-five subjects were enrolled in the study. These subjects fell into three distinct lipid patterns: atherogenic dyslipidemia, isolated hypercholesterolemia, and mixed dyslipidemia. Regardless of the baseline lipid profile, atorvastatin (10 mg q x d) reduced levels of remnant lipoproteins by 25%, LDL-cholesterol by 27%, and the three LDL subfractions by 23%-28% (p<0.0001 for all). Combining all patients, atorvastatin did not significantly alter the overall LDL subfraction pattern; however, in the isolated hypercholesterolemia group, the proportion of LDL present as the small, dense fraction increased by 23% (p=0.01) with treatment, whereas it did not change significantly in the other two groups. Overall, atorvastatin reduced triglycerides by 18% and apolipoprotein-B100 by 23% and increased high-density lipoproteins by 6.2% (p<0.001 all). Since atorvastatin is known to reduce the risk for coronary heart disease events and these data suggest that it does not appear to alter the LDL subfraction pattern, it is unclear whether or not the latter is an important risk predictor independent of LDL-cholesterol concentrations. Increased attention should be paid to absolute concentrations of LDL subfraction cholesterol, which may be a more sensitive indicator of coronary heart disease risk than total LDL or an LDL pattern.

Adult↗