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At least 19 recordsLinked to original sources
PubMed1979

Uptake and degradation of low density lipoproteins (LDL) by confluent, contact-inhibited bovine and human endothelial cells exposed to physiological concentrations of LDL.

Metabolism of low density lipoproteins (LDL) was studied in cultures of endothelial cells derived from bovine aorta or heart and from human umbilical veins. At low LDL concentrations nonconfluent cultures of bovine endothelial cells catabolized more LDL protein than contact-inhibited confluent cultures but this difference was reduced at high LDL concentrations. Nonconfluent human endothelial cells displayed also a higher rate of LDL degradation than their contact-inhibited counterparts, but this difference was less pronounced than in the bovine cells. Bovine endothelial cells grown in the presence of fibroblast growth factor metabolized less LDL than those cultured without fibroblast growth factor (FGF), but this difference was not consistent in the human endothelial cells. The data presented provide evidence that contact-inhibited confluent human endothelial cells are capable of catabolizing LDL when exposed to physiological concentrations of this lipoprotein.

Animals↗
PubMed1978

Degradation of low-density lipoproteins (LDL) and LDL - protamine complexes by lysosomal protease.

Native LDL are degraded by the protease of the lysosomal extract but they are not sensitive to isolated cathepsin D. Protamine increases the sensitivity of LDL to the effect of lysosomal protease and makes them sensitive to the effect of cathepsin D. Degradation of LDL by lysosomal protease is most intensive between pH 4.0 and 4.5 but in case of LDL bound with protamine it is most intensive at pH 4.5--5.0.

Cathepsins↗
PubMedDate not supplied

[Inhibiting effect of low density lipoproteins (LDL) on neutrophil function (author's transl)].

LDL preparations obtained from normal individuals of known genetic type have been added to neutrophils from healthy donors. After incubation at 37 degrees C for 30 min, and washing in Hank's solution, in order to evaluate metabolic and bactericidal activities neutrophils were assayed by the nitroblue tetrazolium (NBT) quantitative test, using latex particles, and by E. coli killing test. LDL in aliquots of 100-500 microgram/2 x 10(6) neutrophils, inhibited NBT reduction and reduced neutrophil killing of E. coli by more than 50%. No difference was observed in the degree of inhibition using LDL and neutrophils obtained from donors of either the same or of different Ag phenotype. These data suggest that the immunoregulatory activity of LDL affects lymphocyte as well as neutrophil function.

Blood Bactericidal Activity↗
PubMed1979

Lipoprotein (a) is not a metabolic product of other lipoproteins containing apolipoprotein B.

125I-Labeled autologous very low density lipoprotein (VLDL) was injected intravenously into three lipoprotein (a) positive individuals. One other lipoprotein (a) positive subject received 125I-labeled VLDL from a a lipoprotein (a) negative donor. Specific activity of apolipoprotein B in VLDL, low density lipoprotein (LDL) and lipoprotein (a) was measured for 5 days. In the lipoprotein (a) fraction only traces of radioactivity could be detected, which were caused by contamination with labeled LDL. No precursor-product relationship existed between apolipoprotein B in VLDL or LDL and apolipoprotein B in lipoprotein (a). One lipoprotein (a)-positive individual was kept on a fat-free diet for 4 days to prevent chylomicron formation; no change in the serum level of lipoprotein (a) could be detected under these conditions. The data of this study indicate that lipoprotein (a) is not a metabolic product of VLDL or LDL. Also chylomicrons are not likely to play role as a precursor for lipoprotein (a). It is concluded that lipoprotein (a) is synthesized as a separate lipoprotein.

Adult↗
PubMed1979

Low density lipoprotein binding, internalization, and degradation in human adipose cells.

Human adipose tissue derives its cholesterol primarily from circulating lipoproteins. To study fat cell-lipoprotein interactions, low density lipoprotein (LDL) uptake and metabolism were examined using isolated human adipocytes. The 125I-labelled LDL (d = 1.025-1.045) was bound and incorporated by human fat cells in a dose-dependent manner with an apparent Km of 6.9 + 0.9 microgram LDL protein/mL and a Vmax of 15-80 microgram LDL protein/mg lipid per 2 h. In time-course studies, LDL uptake was characterized by rapid initial binding followed by a linear accumulation for at least 4 h. The 125I-labelled LDL degradation products (trichloroacetic acid soluble iodopeptides) accumulated in the incubation medium in a progressive manner with time. Azide and F- inhibited LDL internalization and degradation, suggesting that these processes are energy dependent. Binding and cellular internalization of 125I-labelled LDL lacked lipoprotein class specificity in that excess (25-fold) unlabelled very low density lipoprotein (VLDL) (d less than 1.006) and high density lipoprotein (HDL) (d = 1.075-1.21) inhibited binding and internalization of 125I-labelled LDL. On an equivalent protein basis HDL was the most potent. The 125I-labelled LDL binding to an adipocyte plasma membrane preparation was a saturable process and almost completely abolished by a three- to four-fold greater concentration of HDL. The binding, internalization, and degradation of LDL by human adipocytes resembled that reported by other mesenchymal cells and could account for a significant proportion of in vivo LDL catabolism. It is further suggested that adipose tissue is an important site of LDL and HDL interactions.

Adipose Tissue↗
PubMed1977

The composition of low (LDL) and very low (VLDL) density lipoprotein subfractions in type III hyperlipoproteinaemia: comparison with normal subjects.

The lipid and protein composition of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) subfractions (Sf greater than 100, 60--100 and 20--60 VLDL and Sf 10.4--20, 5.7--12 and 3.5--6.5 LDL) in six subjects with type III hyperlipoproteinaemia (HLP) was compared to that of 12 normal subjects. In type III HLP all VLDL subfractions contained increased concentrations of cholesterol and triglycerides and were relatively enriched in cholesterol. VLDL of Sf 20--60 also contained and increased concentration of B-protein. The tetramethylurea (TMU) soluble apolipoproteins of the VLDL subfractions were separated by polyacrylamide disc gel electrophoresis. In the subjects with type III HLP the proportion of arginine rich protein (ARP) was increased in all subfractions. The concentrations of cholesterol and triglycerides were increased in the LDL subfraction of Sf 10.4--20 and cholesterol was decreased in LDL of Sf 5.7--12, but the ratios of cholesterol to triglycerides were not significantly different from those in the LDL subfractions of the normal subjects and the protein composition was also similar. These results provide further evidence that in type III HLP abnormalities are not confined to the stage of conversion of VLDL to LDL, but occur throughout the VLDL spectrum.

Adult↗
PubMed1977

Familial hypo-beta-lipoproteinemia: a family detected by cord blood tests.

A family with low-density lipoprotein (LDL) deficiency was detected during the course of screening cord blood samples. The initial diagnosis in the proband was based on the cord blood LDL cholesterol and lipoprotein electrophoretic pattern, and was confirmed by repeated studies at the age of 8 months. The infant had none of the clinical abnormalities previously ascribed to the condition. Further investigation did not disclose any other significant biochemical or histological abnormalities. Hypo-beta-lipoproteinemia was found to exist in the proband's mother and only sibling. Hence the diagnosis of familial hypo-beta-lipoproteinemia is possible by unselected cord blood LDL cholesterol measurement and lipoprotein electrophoresis in conjunction with kindred studies.

Adult↗
PubMed1979

Lipid metabolic studies in oophorectomized women. Effects of three different progestogens.

Ten oophorectomized women (ranging in age from 27 to 45 years, having a mean age of 34.5 years with a standard deviation of 5.3) were given three different progestogens (norgestrel, norethisterone and medroxyprogesterone) in treatment periods of 3 weeks' duration immediately preceded by 3 weeks "wash out" periods. Venous blood samples were drawn before and after each treatment period. Free and total cholesterol, triglycerides and phospholipids were determined in the three lipoprotein fractions: Very low density lipoproteins (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL). Individual phosphatides were determined after thin layer chromatography. In addition, the relative fatty acid composition of serum lecithin and cholesterol esters were assessed by gas-liquid-chromatography. Both norethisterone and norgestrel caused a decrease in alpha-lipoprotein cholesterol. The relative fatty acid composition of serum lecithin revealed an increase of biochemical pathway 1 for liver lecithin synthesis on norgestrel and norethisterone but no major changes on medroxyprogesterone. With norgestrel an increase in serum-lysolecithin concomitant with a decrease in lecithin was observed, while the two other progestogens did not induce any significant changes. From the present data it is suggested that the 19-norethisterone derivatives, norethisterone and especially norgestrel, have androgen-like influences on lipid metabolism. Medroxyprogesterone, being a 17-alpha-hydroxyprogesterone, caused less changes and consequently less disturbance of lipid metabolism.

Adult↗
PubMed1977

The influence of crude cottonseed oil in the feed on the blood and egg yolk lipoproteins of laying hens.

Lipovitellin, very low density lipoproteins (VLDL), low density lipoproteins (LDL), high density lipoproteins (HDL), and proteins of d greater than 1.20 were isolated from blood plasma and egg yolks obtained from hens fed a normal diet or one containing 2.5% of crude cottonseed oil. The amounts and compositions of each fraction were determined. Hen blood plasma and egg yolk VLDL and LDL obtained from hens fed a normal diet contained similar levels of lipid, and the fatty acid compositions of those lipids were, for the most part, similar. The percentages of VLDL and LDL in total lipoproteins were similar for plasma and egg yolk obtained from hens fed the normal diet. Separation of VLDL from LDL was not clear-cut in eggs from hens fed the diet which contained crude cottonseed oil. Lipovitellin, as it is isolated from egg yolk, did not appear to be present in any appreciable amount in hen blood plasma. Hen plasma appeared to contain about 10% of a liproprotein d greater than 1.20, the lipid of which was similar in fatty acid composition to that of lipovitellin except for palmitic and oleic acids. Lipids of all the different lipoproteins isolated from plasma and egg yolks of hens fed diets which contained 2.5% of crude cottonseed oil contained more stearic acid and less palmitoleic and oleic acids than did those from normal hens. The increased content of stearic acid increased the density of the lipoproteins so that a larger proportion of the lipoproteins were in the LDL and a smaller proportion were in the VLDL than in lipoproteins from normal plasma and eggs.

Animals↗
PubMed1979

Study of the atherogenic dyslipoproteinemia induced by dietary cholesterol in rhesus monekys (Macaca mulatta).

Hypercholesterolemia was induced in adult male rhesus monkeys with a high-fat diet containing an elevated cholesterol level (0.5%). Plasma lipoproteins were chromatographically separated into four size populations (regions) that were subdivided by density until fractions with single electrophoretic mobilities were obtained. The region III lipoproteins (LDL) contained 80% of plasma cholesterol and were present in the highest concentration of all fractions. Their molecular weight was increased over that of controls so that each particle averaged 1.8 times the number of cholesteryl ester molecules as did control LDL. Region II lipoproteins, a heterogeneous group, were present in next highest concentration. Most were cholesteryl ester-rich, beta-migrating lipoproteins that overlapped the VLDL and LDL density ranges; apoB was the predominant apoprotein. One region II subfraction had pre beta 2 migration and the density range. 1.050 less than d less than 1.10. Another subfraction, cholesteryl ester-rich VLDL including only about 1% of plasma cholesterol, had pre beta 1 migration and apoB and apoC as the predominant apoproteins with no apoprotein E. Region I lipoproteins were larger sized, slow beta-migrating cholesteryl ester-rich VLDL that included 5% of plasma cholesterol. ApoB and apoE were the predominant apoproteins. Region IV lipoproteins (HDL) contained 4% of the plasma cholesterol; their concentration was decreased to about 1/3 of the control level. Atherogenic features of the diet-induced dyslipoproteinemia included the increased plasma concentrations and cholesteryl ester contents of the region I, II, and III lipoproteins in addition to the decreased HDL concentration.

Animals↗