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PubMedDate not supplied

Low density lipoprotein metabolism in familial combined hyperlipidemia. Mechanism of the multiple lipoprotein phenotypic expression.

Plasma low density lipoprotein (LDL) kinetics and their relation to plasma very low density lipoprotein (VLDL) and LDL composition were determined in patients with familial combined hyperlipidemia (FCHL) of varying lipoprotein phenotypes. In both Type II and IV subjects, LDL apolipoprotein B (apo B) synthesis was greater than normal. In Type IV, the VLDL triglyceride/apo B ratio was normal and almost all of the LDL apo B was derived from VLDL. LDL cholesterol/apo B ratio was diminished and LDL apo B fractional catabolic rate (FCR) was sufficiently increased to prevent a rise in plasma LDL concentration. In Type II, VLDL triglyceride/apo B was reduced and 14% to 50% of the LDL was formed by direct synthesis. LDL cholesterol/apo B was normal and LDL apo B FCR was lower than in Type IV subjects. In four patients whose plasma lipid levels became normal with carbohydrate restriction and intake of a fibric acid derivative, plasma VLDL and LDL composition and LDL kinetic measurements remained unchanged. By contrast, VLDL triglyceride-apo B decreased and direct LDL synthesis increased in four patients whose phenotype changed to Type IIa. LDL cholesterol/apo B also increased and LDL FCR declined. Among patients with FCHL, significant correlations between VLDL triglyceride/apo B, LDL apo B derived by direct synthesis, LDL cholesterol/apo B, and LDL apo B FCR were found. Thus, increased apo B synthesis is a characteristic feature of FCHL. The phenotypic expression is determined by the availability of triglyceride for hepatic coupling to apo B which could influence the source, composition, and removal rate of circulating LDL. Despite normalization of their plasma lipid levels, some patients continued to show the compositional and kinetic features of FCHL.

Adult↗

PubMed2004

Remnant lipoprotein particles induce apoptosis in endothelial cells by NAD(P)H oxidase-mediated production of superoxide and cytokines via lectin-like oxidized low-density lipoprotein receptor-1 activation: prevention by cilostazol.

BACKGROUND: Remnant lipoprotein particles (RLPs), products of lipolytic degradation of triglyceride-rich lipoprotein derived from VLDL, exert atherogenesis. In this study, we observed how RLPs induced cytotoxicity in human umbilical vein endothelial cells (HUVECs) and cilostazol prevented cell death. METHODS AND RESULTS: RLPs were isolated from the plasma of hyperlipidemic patients by use of an immunoaffinity gel mixture of anti-apolipoprotein A-1 and anti-apolipoprotein B-100 monoclonal antibodies. RLPs (50 microg/mL) significantly increased superoxide formation in HUVECs associated with elevated gp91phox mRNA and protein expression and Rac1 translocation, accompanied by increased production of tumor necrosis factor (TNF)-alpha and interleukin-1beta, DNA fragmentation, and cell death. Cilostazol (1 to 100 micromol/L) significantly suppressed not only NAD(P)H oxidase-dependent superoxide production but also TNF-alpha and interleukin-1beta release and restored viability. RLPs activated a lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), which was not inhibited by cilostazol. Treatment of HUVECs with monoclonal antibody for LOX-1 attenuated RLP-mediated production of superoxide, TNF-alpha, and interleukin-1beta and DNA fragmentation. CONCLUSIONS: RLPs stimulated NAD(P)H oxidase-dependent superoxide formation and induction of cytokines in HUVECs via activation of LOX-1, consequently leading to reduction in cell viability with DNA fragmentation, and cilostazol exerts a cell-protective effect by suppressing these variables.

Adult↗

PubMed1993

High density lipoprotein reverses inhibitory effect of oxidized low density lipoprotein on endothelium-dependent arterial relaxation.

We have recently reported that oxidized low density lipoprotein (ox-LDL) inhibits endothelium-dependent arterial relaxation through its increased lysophosphatidylcholine (LPC). In this study we examined whether high density lipoprotein (HDL) has any effect on the inhibition of endothelium-dependent relaxation by ox-LDL in isolated strips of rabbit thoracic aorta. Both low density lipoprotein (LDL) and HDL were isolated from normal human plasma, and LDL was oxidized by exposure to copper. Preincubation of arterial strips with ox-LDL (0.1-0.5 mg protein/ml) inhibited endothelium-dependent relaxation to acetylcholine (ACh) in a concentration-dependent manner. HDL (1 mg protein/ml) by itself had no effect on the relaxation to ACh. In the presence of HDL, the inhibition by ox-LDL was markedly reduced. Although synthetic L-alpha-palmitoyl LPC (5 micrograms/ml) completely abolished a relaxation to ACh, the preincubation of arterial strips with HDL completely prevented the LPC-induced inhibition. Moreover, a relaxation to ACh was almost completely recovered when the strips were washed with buffer containing HDL even after LPC-induced inhibition had occurred. HDL markedly reduced the incorporation of [1-14C]palmitate-labeled LPC ([14C]LPC) into cultured bovine aortic endothelial cells and promoted the release of cell-incorporated [14C]LPC into the medium, resulting in a reduction of the remaining [14C]LPC in the cells. Agarose electrophoresis after incubation of a mixture of ox-LDL labeled with [14C]LPC and unlabeled HDL demonstrated a transfer of [14C]LPC from ox-LDL to HDL. These results indicate that HDL reverses the ox-LDL-induced impairment of endothelium-dependent relaxation by removing LPC from ox-LDL and preventing LPC from acting on the endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1988

Uptake of cholesterol-rich remnant lipoproteins by human monocyte-derived macrophages is mediated by low density lipoprotein receptors.

The uptake and degradation of cholesterol-rich remnant lipoproteins, referred to as beta-VLDL, are shown in the present study to be mediated by LDL receptors (apoB,E(LDL) receptors), not by unique beta-VLDL receptors. Human blood monocytes cultured for 5-7 d bound apoB- and/or apoE-containing lipoproteins from different species with affinities equivalent to those demonstrated for the receptors on cultured human fibroblasts. Low density lipoproteins competed effectively and completely with 125I-beta-VLDL for binding to and degradation by monocyte-derived macrophages. Specific polyclonal antibodies to bovine apoB,E(LDL) receptors abolished both LDL and beta-VLDL uptake by normal human monocyte-macrophages. Immunoblots of monocyte-macrophage extracts with these antibodies revealed a single protein in human macrophages with an apparent molecular weight identical to that of the apoB,E(LDL) receptor found on human fibroblasts. Like receptors on cultured human fibroblasts, the apoB,E(LDL) receptors on monocyte-macrophages responsible for 125I-beta-VLDL and 125I-LDL uptake were efficiently down regulated by preincubation of the cells with beta-VLDL or LDL. Finally, monocyte-macrophages from seven homozygous familial hypercholesterolemia subjects were unable to metabolize beta-VLDL or LDL, but demonstrated normal uptake of acetoacetylated LDL. The classic apoB,E(LDL) receptors on human monocyte-macrophages thus mediate the uptake of beta-VLDL by these cells.

Adult↗

PubMed1993

Native and modified (acetylated) low density lipoprotein-supported steroidogenesis by macaque granulosa cells collected before and after the ovulatory stimulus: correlation with fluorescent lipoprotein uptake.

We recently reported that uptake of fluorescent-tagged low density lipoprotein (DiI-LDL) by macaque granulosa cells (GC) was greatly enhanced within 27 h of an ovulatory stimulus (hCG injection). The present study was designed to determine whether increased DiI-LDL uptake correlated with an increased capacity for LDL-supported steroidogenesis. We also tested whether modified [acetylated (ac)] LDL or high density lipoprotein (HDL), which are not ligands for the LDL receptor, supported progesterone (P) production. Beginning at menses, adult female rhesus macaques were treated with human (h) FSH and hLH for 9 days to promote development of multiple follicles. On day 10, monkeys were injected with hCG (1000 IU) or received no ovulatory stimulus. Large follicles were aspirated on day 10 (nonluteinized GC) or 27-34 h after hCG administration (luteinizing GC). GC (2 x 10(4)/0.2 ml) were cultured in Dulbecco's Modified Eagle's Medium-Ham's F-12 plus insulin, transferrin, H2SeO3, and aprotinin, with 0-100 micrograms hLDL, ac-hLDL, or hHDL. P concentrations in medium were determined by RIA. LDL (1-25 micrograms/ml) dose-dependently increased (up to 15-fold; P < 0.05) basal and hCG-stimulated P production by luteinized GC on days 1-8 of culture. However, LDL (25 micrograms/ml) did not alter basal P production by nonluteinized GC and increased (2-fold; P < 0.05) hCG-stimulated P secretion only on days 4-8. Basal and hCG-stimulated P production by luteinized GC were initially (days 1-2) increased (up to 2-fold; P < 0.05), but later (days 6-8) suppressed (P < 0.05) in a dose-dependent manner by 1-100 micrograms ac-LDL/ml. Ac-LDL did not alter basal or hCG-stimulated P production by nonluteinized GC. HDL (1-100 micrograms/ml) did not alter P production by either luteinized or nonluteinized GC. The number of viable luteinized GC on day 8 was reduced (30-50%; P < 0.05) after exposure to 10 micrograms ac-LDL/ml or more, whereas only the highest dose (100 micrograms/ml) of LDL or HDL reduced cell survival. Ac-LDL did not alter the survival of nonluteinized GC in culture. Flow cytometric analyses using fluorescent-tagged lipoproteins (DiI-LDL/DiI-ac-LDL) demonstrated the uptake of both native and ac-LDL by luteinized GC. Uptake of DiI-LDL was competitively suppressed in a dose-dependent manner by unlabeled LDL, but not by ac-LDL. In contrast, DiI-ac-LDL uptake was competitively inhibited by both ac-LDL and LDL.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2002

Prolonged stimulation of the adrenals by corticotropin suppresses hepatic low-density lipoprotein and high-density lipoprotein receptors and increases plasma cholesterol.

Pituitary ACTH has been shown to strongly stimulate adrenal receptors for low-density lipoprotein (LDL) and high-density lipoprotein (HDL) scavenger receptor class B type 1(SR-BI) to provide precursor cholesterol for glucocorticoid synthesis. The present study aimed to determine the effects of ACTH on hepatic cholesterol metabolism and plasma lipoproteins. Treatment of Sprague Dawley rats or normal C57BL/6J mice with ACTH for 3.5 d reduced hepatic SR-BI and LDL receptors. Simultaneously, cholesterol in plasma LDL and HDL was increased. None of these effects could be reproduced using glucocorticoids instead of ACTH, and they were abolished in adrenalectomized rats, indicating an obligate role of the adrenals for the effects of ACTH observed in the liver. When ACTH was given to LDL receptor-deficient mice, plasma LDL did not increase and the increase in HDL cholesterol remained, as did the suppression of hepatic SR-BI. Our data show that prolonged ACTH treatment suppresses hepatic SR-BI and LDL receptors in vivo in rodents, resulting in elevated plasma HDL and LDL. The adrenals are obligate for these effects, suggesting that ACTH releases some factor(s) that suppresses hepatic LDL and SR-BI receptors. Hypothetically, this novel mechanism would further promote channeling of cholesterol to the adrenals in situations of prolonged stress.

Adrenal Glands↗

PubMed2004

The influence of lipoprotein lipase gene variation on postprandial lipoprotein metabolism.

Lipoprotein lipase (LPL) is one of the key enzymes in the metabolism of triacylglycerol-rich lipoproteins (TRL). We evaluated whether the association of LPL HindIII (H1/H2) and Serine447-Stop (S447X) polymorphisms may explain the interindividual variability observed during postprandial lipemia. Fifty-one healthy male volunteers (26 with the H2S447 genotype, 15 with the H1X447 genotype, and 10 with the H1S447 genotype) were subjected to a vitamin A-fat load test consisting of 1 g fat/kg body weight and 60,000 IU vitamin A. Blood was drawn every hour until the 6th hour and every 2 h and 30 min until the 11th hour. Data revealed that subjects that are homozygous for the H2 allele (H2H2) showed a higher postprandial response for small TRL, retinyl palmitate (RP), large TRL-RP, large TRL-B48, and small TRL-B48 levels. Furthermore, in the case of the S447X polymorphism, 447Ter carriers had a lower postprandial response for small TRL-RP, large TRL-B48, and small TRL-RP. Subjects with the LPL H2S447 genotype had higher plasma triacylglycerol, large TRL-triacylglycerol, large TRL-RP, small TRL-RP, and large TRL-B48 (P < 0.037) than H1X447 subjects. The modifications observed in postprandial lipoprotein metabolism in young normolipemic males with LPL polymorphism could be involved in the lower risk of coronary artery disease associated with the H1X447 genotype.

Adolescent↗

PubMed2004

Antiretroviral treatment reduces very-low-density lipoprotein and intermediate-density lipoprotein apolipoprotein B fractional catabolic rate in human immunodeficiency virus-infected patients with mild dyslipidemia.

The relationship between antiretroviral treatment of HIV infection, body fat distribution, insulin resistance, and very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) apolipoprotein-B (apoB) kinetics was investigated in 55 HIV-infected patients taking two nucleoside analogs plus either a protease inhibitor (n = 15) or a nonnucleoside reverse transcriptase inhibitor (n = 25), 15 antiretroviral therapy-naive patients, and 12 HIV-negative controls. Compared with the controls, high-density lipoprotein cholesterol was reduced in all groups (P < 0.01). Plasma triglyceride was increased in patients taking protease inhibitors (P < 0.05). VLDL and IDL apoB fractional catabolic rate (FCR) was lower in all treatment groups (P < 0.05) compared with controls. Trunk fat, VLDL apoB absolute secretion rate, and insulin resistance were not different between groups. Peripheral fat was lower in the treated patients (P < 0.05) and correlated with duration of therapy (r = -0.55; P < 0.001). There was a positive correlation between peripheral fat and VLDL apoB FCR (P = 0.002) and IDL apoB FCR (P = 0.002) and a negative correlation with VLDL apoB pool size, VLDL cholesterol, and triglyceride (P < 0.03; P < 0.01; P < 0.002). These results suggest that mild dyslipidemia resulting from antiretroviral therapy is caused by a decrease in VLDL and IDL apoB FCR, which is associated with a loss of peripheral fat.

Adult↗

PubMed2000

Hypertriglyceridemia characterized by low-density lipoprotein phenotype and lipoprotein lipase gene mutation.

A high serum triglyceride (TG) concentration is associated with an increased serum concentration of small, dense low-density lipoprotein (LDL). To further characterize the hypertriglyceridemic condition, we examined sera from 240 subjects for small, dense LDL using non-denaturing polyacrylamide gradient gel electrophoresis. We focused on determining the frequency of the pattern B, which is characterized by a higher proportion of small, dense LDL, among hypertriglyceridemic individuals. The subjects were divided into four groups: a control group (TG < or = 1.65 mmol/l, high-density lipoprotein cholesterol (HDL-C) > or =1.17 mmol/l; n = 71), a high TG group (TG > 1.65 mmol/l, HDL-C > or = 1.17 mmol/l; n = 36), a group with high TG and low HDL-C (TG > 1.65 mmol/l, HDL-C < or = 0.91 mmol/l; n = 106), and a low HDL-C group (TG < or = 1.65 mmol/l, HDL-C < or = 0.91 mmol/l; n = 27). We found that pattern B occurs at a high frequency mainly in individuals with high TG and low HDL-C levels. We also observed an increased percentage of LDL within the 20.0 nm to 25.5 nm particle diameter range in this group. Analysis of the lipoprotein lipase gene in this group showed that some mutations seem to be associated with small, dense LDL, resulting in LDL pattern B.

Densitometry↗

PubMed1989

Evidence for differences in low density lipoprotein processing by porcine granulosa and luteal cells in vitro: effect of addition of serum for plating of granulosa cells on lipoprotein metabolism.

The present studies were carried out to compare the low density lipoprotein (LDL) metabolism by freshly isolated immature porcine granulosa cells with that by luteal cells. Furthermore, we have examined the effect of serum used for plating of granulosa cells on lipoprotein degradation and utilization. In incubation studies, addition of LDL as an exogenous substrate had a mild stimulatory effect on progesterone accumulation by granulosa cells, while it exhibited a dose-dependent stimulatory effect on luteal cells. When granulosa and luteal cells were incubated with 125I-labelled LDL, membrane binding of LDL occurred in both cell types, but only luteal cells were capable of internalizing the bound LDL. Granulosa cells in incubation degraded LDL much less in comparison with luteal cells, and the amount varied with the maturity of the cells. When granulosa cells were plated with graded amounts of serum which was withdrawn for 48 h following plating, they exhibited enhanced LDL degradation in a serum concentration-dependent fashion. Addition of serum for plating selectively enhanced utilization of LDL, but not high density lipoprotein (HDL) for progesterone accumulation by the cells in culture. Time-course studies on LDL degradation by granulosa cells following serum withdrawal indicate that the ability of cells to degrade LDL decreased in a time-dependent fashion. Serum withdrawal selectively decreased utilization of LDL but not HDL for progesterone secretion. It is concluded that immature granulosa cells have a limited capability to utilize cholesterol carried by LDL.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Role of lipoprotein lipase and apolipoprotein E secretion by macrophages in modulating lipoprotein uptake. Possible role in acceleration of atherosclerosis in diabetes.

Because the accumulation of lipid in macrophages is a characteristic feature of atherosclerosis, the mechanisms by which this lipid accumulation occurs have been intensively studied. This paper reviews the receptor- and non-receptor-mediated pathways that promote lipid accumulation in macrophages. Particular emphasis is placed on the contributions of two secretory products of macrophages, lipoprotein lipase and apolipoprotein E, to both receptor- and non-receptor-mediated uptake of triglyceride-rich lipoproteins by macrophages. The hormonal, lipid, and immunological factors that regulate the secretion of LpL and apoE by macrophages are discussed, as are how changes in the secretion of apoE and LpL that can modulate the uptake of triglyceride-rich lipoproteins by macrophages might influence the atherosclerotic process in people with diabetes.

Apolipoproteins E↗

PubMed1999

Human apolipoprotein A-I kinetics within triglyceride-rich lipoproteins and high density lipoproteins.

Stable isotope methodology was used to determine the kinetic behavior of apolipoprotein (apo) A-I within the triglyceride-rich lipoprotein (TRL) fraction and to compare TRL apoA-I kinetics with that of apoA-I in high density lipoprotein (HDL) and TRL apoB-48. Eight subjects (5 males and 3 females) over the age of 40 were placed on a baseline average American diet and after 6 weeks received a primed-constant infusion of [5,5,5-(2)H(3)]-l-leucine for 15 h while consuming small hourly meals of identical composition. HDL and TRL apoA-I and TRL apoB-48 tracer/tracee enrichment curves were obtained by gas chromatography;-mass spectrometry. Data were fitted to a compartmental model to determine the fractional secretion rates of apoA-I and apoB-48 within each lipoprotein fraction. Mean plasma apoA-I levels in TRL and HDL fractions were 0. 204 +/- 0.057 and 134 +/- 15 mg/dl, respectively. The mean fractional catabolic rate (FCR) of TRL apoA-I was 0.250 +/- 0.069 and HDL apoA-I was 0.239 +/- 0.054 pools/day, with mean estimated residence times (RT) of 4.27 and 4.37 days, respectively. The mean TRL apoB-48 FCR was 5.2 +/- 2.0 pools/day and the estimated mean RT was 5.1 +/- 1.8 h. Our results indicate that apoA-I is catabolized at a slower rate than apoB-48 within TRL, and that apoA-I within TRL and HDL fractions are catabolized at similar rates.

Adult↗

PubMed1992

Distinct properties of the recognition sites for beta-very low density lipoprotein (remnant receptor) and alpha 2-macroglobulin (low density lipoprotein receptor-related protein) on rat parenchymal cells.

The properties of the recognition sites for alpha 2-macroglobulin (alpha 2-macroglobulin receptor; low density lipoprotein receptor-related protein) and beta-migrating very low density lipoprotein (beta-VLDL) (remnant receptor) on rat parenchymal cells were directly compared to analyze whether both substrates are recognized and internalized by the same receptor system. In cholesterol-fed rats, the large circulating pool of beta-VLDL is unable to diminish the liver uptake of 125I-labeled alpha 2-macroglobulin, while liver uptake of 125I-labeled beta-VLDL in these rats is reduced by 87.3% at 10 min after injection. In vitro competition studies with isolated parenchymal liver cells demonstrate that the binding of 125I-labeled alpha 2-macroglobulin to rat parenchymal cells is not effectively competed for by beta-VLDL, whether this lipoprotein is additionally enriched in apolipoprotein E or not. Binding of alpha 2-macroglobulin to parenchymal cells requires the presence of calcium, while binding of beta-VLDL does not. Incubation of parenchymal cells for 1 h with proteinase K reduced the subsequent binding of alpha 2-macroglobulin by 90.1%, while the binding of beta-VLDL was reduced by only 20.2%. In the presence of monensin, the association of alpha 2-macroglobulin to parenchymal cells at 2 h of incubation was reduced by 64.7%, while the association of beta-VLDL was not affected. Preincubation of parenchymal cells with monensin for 60 min at 37 degrees C reduced the subsequent binding of alpha 2-macroglobulin by 54.5%, while binding of beta-VLDL was only reduced by 14.6%. The results indicate that the recognition sites for alpha 2-macroglobulin and beta-VLDL on rat parenchymal cells do exert different properties and are therefore likely to reside on different molecules.

Animals↗

PubMedDate not supplied

Normal levels of lipoproteins including lipoprotein(a) after liver-heart transplantation in a patient with homozygous familial hypercholesterolaemia.

A 33-year-old female with severe diffuse coronary artery disease and left ventricular outflow tract obstruction secondary to homozygous familial hypercholesterolaemia underwent liver and heart transplantation. During a post-operative follow-up period of 13 months, apart from one episode of cardiac rejection at 3 weeks, she has remained well and without evidence of accelerated coronary disease on angiography. By 3 months after transplantation serum total cholesterol, low density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) levels had decreased and apolipoprotein A-I and high density lipoprotein cholesterol levels had increased, all to within the normal range. These changes were accompanied by marked regression of xanthomata and were maintained at 13 months. Liver transplantation provides an effective means of correcting serum lipids in patients with homozygous familial hypercholesterolaemia and is an important adjunct to cardiac transplantation.

Adult↗

PubMed1992

Normal variation of plasma lipoproteins: postural effects on plasma concentrations of lipids, lipoproteins, and apolipoproteins.

We examined the effects of postural change on the concentrations of plasma cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, apolipoproteins (apo) A-I and B, and lipoprotein(a) [Lp(a)] in six volunteers who fasted 12 h before blood sampling. Baseline samples were drawn in the standing position; the subjects then assumed the supine or sitting position, and additional blood samples were drawn at intervals up to 40 min. They then returned to the standing position and were again sampled at intervals up to 40 min. In the supine position, lipid, lipoprotein, and apolipoprotein concentrations decreased rapidly within the first 5 min and stabilized after 20 min. Total and HDL cholesterol, apoA-I, apoB, and Lp(a) decreased by as much as 7-12% in the supine position and returned to baseline values 20-40 min after the standing position was resumed. Smaller changes (5-9%) were observed when the subjects were sitting, and returned to baseline within 20 min after the subjects resumed the standing position. The decrease in triglycerides was 17% in the supine position and 10-11% in the sitting position. Lp(a) concentrations decreased 7-8% in either the supine or sitting position and returned to baseline more slowly than did the other components. For all components the changes were most rapid within the first 10 min after changing posture.

Adult↗

PubMed1976

The action of arterial hypertension on lipid and lipoprotein metabolism. II. Qualitative and quantitative alterations of blood serum, liver and aortic lipids and lipoproteins in Okamoto-Aoki rats with spontaneous hypertension.

The purpose of the study was to investigate alterations in the content of the basic lipid fractions, and of the low density lipoproteins (LDL) in the liver, the blood serum and aorta, as well as to determine by acrylamide disc electrophoresis the hyperlipoproteinaemic type of spontaneously hypertensive rats (SHR) which are considered as the most suitable model of essential hypertension. The experiments were carried out on 25 normotensive control Wistar rats and 30 SHR (Okamoto-Aoki strain). An augmentation of lipid metabolism in the liver and a moderate hyperlipidaemia mainly due to an increase in triglycerides was found. The quantitative alterations of the lipid fractions corresponded with the qualitative alterations of the lipoproteins, an intensive and permanent pre-beta-LP fraction being established. In all the SHR a peculiar pattern of hyperlipoproteinaemia differing from the basic Fredickson-Lees patterns by a LP-fraction located between tha alpha- and beta-LP fractions was also established. The alterations in the lipid and lipoprotein metabolism in SHR are considered as connected with the hypertensive state itself since no accompanying atherosclerosis was observed.

Animals↗

PubMedDate not supplied

[Lipoprotein lipase fractionation of very low density serum lipoproteins from healthy subjects and persons afflicted with atherosclerosis].

In vitro experiments showed that blood sera of the patients with atherosclerosis contained rather often the fraction of very low density lipoproteins (VLDL) with sf 100-400 S, which were cleaved by the lipoprotein lipase at the decreased rate as compared with that of normal people. The decrease in cleavage of the VLDL fraction was usually observed in patients with the increased concentration of the lipoprotein fraction in blood sera. These data suggest that separate constituents occurring in the VLDL fraction (sf 100-400 S) may be nonuniformly increased in hyperlipoproteinemia.

Adult↗

PubMed1979

Low density lipoprotein metabolism and lipoprotein cholesterol content in southwestern American Indians.

The prevalence of ischemic heart disease is significantly lower in southwestern American Indians than in Caucasians. To investigate this difference, the metabolism of low density lipoprotein apoprotein (apo-LDL) and plasma lipoprotein cholesterol composition were studied in 10 southwestern American Indians and 5 Caucasian controls. The plasma concentration of LDL cholesterol in American Indians was 88 +/- 5 mg/dl (mean +/- SEM) and 111 +/- 7 mg/dl in Caucasians. The corresponding values of apo-LDL concentrations were 53 +/- 3 mg/dl and 77 +/- 4 mg/dl, respectively. Conversely, high density lipoprotein cholesterol (HDL) concentrations were significantly higher in American Indians (56 +/- 4 mg/dl) than in Caucasians (37 +/- 3 mg/dl). There were no statistically significant differences in the biological half-life of apo-LDL, calculated from the second exponential of the plasma die-away curve (3.06 +/- 0.15 days vs. 3.45 +/- 0.11 days), the fractional catabolic rate of apo-LDL (0.432 +/- 0.01 vs. 0.411 +/- 0.01), or the fraction of total exchangeable apo-LDL in the intravascular space (70 +/- 1 vs. 67 +/- 3%). As derived from the absolute catabolic rate under steady-state conditions, the synthetic rate of apo-LDL in American Indians was, however, significantly lower than in Caucasians (334.6 +/- 7.8 mg/m(2) per day vs. 507.2 +/- 6.7 mg/m(2) per day; P < 0.001). These data indicate that the lower levels of plasma LDL cholesterol and apo-LDL in American Indians are due to a reduced rate of apo-LDL synthesis rather than to differences in fractional catabolic rates. These differences, in combination with higher HDL cholesterol levels, may contribute to the lower prevalence of ischemic heart disease in American Indians.

Adult↗