Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

(1) Lipoproteins from the serum of male turkeys maintained on a normal diet were separated by sequential preparative ultracentrifugation into VLDL (d less than 1.006 g/ml), LDL (d = 1.006-1.063 g/ml), HDL (d = 1.063-1.21 g/ml) and VHDL (d greater than 1.21 g/ml). Lipoprotein density classes were characterized by analytical ultracentrifugation, agarose electrophoresis, immunodiffusion and immunoelectrophoresis, and by quantitative determination of protein, lipids and individual phosphatides. (2) HDL were the major density class representing 75% of the total lipoprotein content, LDL accounted for approximately 20% and VLDL for only 3-5% of the total lipoproteins. (3) VLDL were characterized by a relatively low content of glyceride (34%). Cholesterol esters were the major lipid (38%) of LDL, and the phospholipids (26%) of HDL. Glycerides of all major density classes consisted of equal amounts of triglycerides and diglycerides. (4) Phosphatidylcholine was the major phosphatide in all density classes. The composition of phosphatides was very similar in the VLDL and LDL, but it was different in the HDL. The ratio of phosphatidylcholine/sphingomyelin was higher in HDL than in VLDL and LD. (5) Immunological and electrophoretic studies showed that all three major density classes consisted of two lipoprotein families designated, in analogy to the human serum lipoprotein system [1], as LP-A and LP-B. The exception was HDL3 (d = 1.125-1.21 g/ml) which contained only LP-A. (6) ApoB was insoluble in aqueous buffers but could be solubilized after reduction and carboxymethylation. No C- or N-terminal amino acids were released by the usual chemical methods. The carbohydrate moiety of ApoB contained mannose, galactose and galactosamine. (7) ApoA consisted of a non-identical polypeptides designated in analogy to the human polypeptides as A-I and A-II. A-I was the major ApoA polypeptide and had a molecular weight of about 27,000. This polypeptide contained no half cystine, and the aspartic acid as the N-terminal and alanine as the C-terminal amino acids. A-II had a molecular weight of about 10,000, contained no half cystine and had alanine as the C-terminal amino acid. A-II showed no N-terminal amino acid by either dansylation, dinitrophenylation or Edman's procedure. Neither A-I nor A-II contained neutral sugars or hexosamines. (8) Concentrations of polypetides analogous to human ApoC, ApoD and "arginine-rich" polypeptide, if present, were too low for their unequivocal chemical characterization.
Atherosclerosis
PMID:Lipid transport in the avian species. Part I. Isolation and characterization of apolipoproteins and major lipoprotein density classes of male turkey serum. 18 83

Serum lipids, lipoproteins, and lipoprotein subfractions were measured in a group of 18 women aged 20 through 39 who were users of oral contraceptive drugs, and in 19 age-matched controls. Concentrations of the major lipid and lipoprotein classes were higher in the users, but the elevation was statistically significant only in the case of the high density lipoproteins. This increase was shown to be due to a highly significant increase (275 +/- 9 vs. 223 +/- 9 mg/100 ml, (p less than 0.005) in the denser high density lipoprotein subfraction (HDL3). Levels of the other subfraction (HDL2) were similar in users and controls. Thus, anovulatory steroids have selective effects on individual types of high density lipoproteins. Studies of such specific effects may help to further define the functional properties of the high density lipoproteins such as their apparent protective role in atherosclerosis.
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PMID:Changes in serum high density lipoproteins in women on oral contraceptive drugs. 19 81

A relatively short, simple procedure is presented to separate serum high-density lipoproteins discretely into the two main classes, those with densities between 1.063 and 1.125 g/ml (HDL2) and those with densities between 1.125 and 1.210 g/ml (HDL3). A 3.5% polyacrylamide gel in 10 cm glass tubes and the use of Tris/glycine buffer, pH 8.4, will accomplish this separation. The components can be identified in several different ways, examples of which are given. This procedure will give rapid and reliable estimations of both HDL2 and HDL3, and can be used to relate their levels and proportional amounts to incidence or risk of atherosclerosis, coronary-artery disease and possibly cancer.
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PMID:Discrete separation of HDL2 from HDL3 of human serum by means of polyacrylamide gel. 20 17

The influence of treatment with polyunsaturated lecithin (EPL) and with saturated lecithin on the lipoprotein composition and fatty acid profile was investigated in 4 male chimpanzees. The animals were successively given 3 isocaloric diets containing the same amount of fat with a degree of saturation varying from 1 in the control diet to 0.2 in the diet enriched with polyunsaturated lecithin, to 4 in the diet enrich with saturated lecithin. The VLDL, LDL and HDL3 fractions were isolated by ultracentrifugal flotation; changes in their lipid and fatty acid composition were followed and their microviscosity was measured. The treatment with polyunsaturated lecithin increases the cholesterol esters and lysolecithin content in HDL3, presumably via activation of the enzyme LCAT. These modified HDL particles have a more fluid surface and a denser core and are susceptible to act as better cholesterol carriers. A complementary effect of this treatment is a decrease of the plasma triglycerides and VLDL concentration, an increase in the unsaturation ratio of the triglycerides which might take place via activation of triglyceride lipase. The saturated lecithin treatment increases the plasma VLDL and LDL concentrations and the triglyceride levels and increases mostly the saturation ratio of the cholesterol esters. These effects are likely to enhance the progression of atherosclerosis.
Atherosclerosis 1979 Feb
PMID:Influence of oral polyunsaturated and saturated phospholipid treatment on the lipid composition and fatty acid profile of chimpanzee lipoproteins. 22 3

High density lipoprotein (HDL) was fractionated by ion exchange column chromatography using a continuous NaCl gradient of 0.06--0.13 M. It was found that, on the basic C apoprotein content, HDL is comprised of 3 subfractions. All 3 subfractions contain apo A-I and apo A-II but the apo A-I/apo A-II ratio is different in each subfraction and in the case of subfraction c, that fraction which eluted at highest NaCl concentrations, the A-I/A-II ratio varied even within this subfraction. Subfraction a contained no C apoprotein, subfraction b contained apo C-II and apo C-III-1 but no apo C-III-2 while subfraction c contained apo C-III-2 and trace amounts of apo C-II and C-III-1. Analysis of HDL2 and HDL3 shows that both contain all 3 lipoprotein subfractions, but in differing quantities.
Atherosclerosis 1979 Aug
PMID:Protein content and composition of human high density lipoprotein subfractions. 22 80

This study on 4 type II hyperlipoproteinaemic subjects examines the effects of pharmacologic doses (8 g twice daily) of the bile acid sequestrant cholestyramine on the plasma distribution and chemical composition of the high density lipoprotein subfractions, HDL2 and HDL3, and describes the influence of the drug on the metabolism of the major HDL aporoteins, apolipoprotein A-I and A-II. Cholestyramine lowered plasma low density lipoprotein cholesterol (32%; P less than 0.05) without affecting the level of that lipid in very low density or high density lipoproteins. However, the plasma HDL2/HDL3 ratio and apolipoprotein A-I concentration rose significantly on treatment, while apolipoprotein A-II remained unchanged. The rise in apolipoprotein A-I derived from an increase in its synthetic rate and produced a relative enrichment of the protein with respect to apolipoprotein A-II in both HDL subfractions. These results demonstrate the cholestyramine treatment affects HDL metabolism in a way which, according to current concepts, may prove beneficial to the recipient.
Atherosclerosis 1979 Aug
PMID:The effects of cholestyramine on high density lipoprotein metabolism. 22 82

Low density lipoprotein (LDL) and high density lipoprotein (HDL3) were tested for their ability to induce inositol phospholipid turnover and inositol phosphate production in bovine aortic endothelial cells (BAEC). The production of inositol phosphates following hydrolysis of the phosphoinositides was demonstrated by two methods; release of [3H]inositol phosphates after labelling with [3H]myo-inositol and by a direct binding assay for inositol 1,4,5-trisphosphate (InsP3). Acute exposure to LDL induced InsP3 release at low concentrations of the lipoprotein within the physiological range of LDL in tissues. HDL3 did not cause any release of the inositol phosphates. Pre-incubation of BAEC with HDL3 suppressed bradykinin- and LDL-induced inositol phosphate production in BAEC in a concentration-dependent manner. It is concluded that LDL acutely stimulates phosphoinositide breakdown and that pre-incubation of cells with HDL3 inhibits this effect. The mechanism responsible for these effects remains to be elucidated.
Atherosclerosis 1992 Jan
PMID:The effects of low density lipoprotein and high density lipoprotein on phosphoinositide hydrolysis in bovine aortic endothelial cells. 131 50

Many preclinical and clinical studies reveal that changes in lipoprotein metabolism are a major contributing factor to atherosclerosis. Hormones in oral contraceptive (OC) formulations strongly influence lipoprotein metabolism. Specifically, estrogens bring about increases in plasma triglycerides which then cause a rise in the very low density lipoprotein. They also decrease levels of the intermediate and low density lipoprotein which cause build up of plaque on arterial walls. Estrogens also lead to rising high density lipoprotein (HDL) levels, especially the HDL2 subspecies. Increased HDL levels are associated with lower mortality rates from cardiovascular conditions in women who have already experienced menopause and are on hormone replacement therapy. Combination OCs used in the US increase plasma triglycerides, low density lipoprotein, and HDL3. The estrogen dose and the relative androgenicity of the progestin together influence the changes in HDL and HDL2. Even though low dose combined OCs bring about lipoprotein changes which are lower than those of higher dose OCs, the changes often remain significant. The progestin component of OCs is responsible for most changes in carbohydrate metabolism. Specifically OC use can lead to increased levels of plasma insulin, insulin resistance, and relative glucose intolerance. A curve analysis of glucose tolerance tests reveals this intolerance effect of OCs. The changes in carbohydrate metabolism are not as great in women using the lower dose OCs or formulations using the new progestins, however.
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PMID:The metabolic impact of oral contraceptives. 141 43

High density lipoprotein subfraction 2 (HDL1)-cholesterol level is usually decreased in Type 2 (non-insulin-dependent) diabetes. A study was carried out in 251 Type 2 diabetic patients (106 males [M], 145 females [F]) and in 120 non diabetic controls in order to determine the influence of hypertriglyceridaemia and obesity on the HDL2-cholesterol level and to analyse the relationship between HDL2-cholesterol level and atherosclerosis (coronary heart disease, peripheral atherosclerosis or cerebral vascular disease), in Type 2 diabetes. Influence of hypertriglyceridaemia and obesity on HDL2-cholesterol level was studied by comparing the mean values of HDL2-cholesterol between diabetics and controls, after controlling for hypertriglyceridaemia and obesity, and by a multiple linear regression test. A stepwise logistic regression was performed to analyse the association between the prevalence of atherosclerosis and several variables: age, duration of diabetes, hypertension, cigarette smoking, body mass index, mean glycaemia, total cholesterol, triglyceride, HDL-cholesterol, HDL2-cholesterol and HDL3-cholesterol levels. In both men and women, when both of the factors (hypertriglyceridaemia and obesity) were present of when only one was, HDL2-cholesterol level was significantly lower in the diabetic population, compared with controls. But when obesity and hypertriglyceridaemia were absent, HDL2-cholesterol level, in the diabetic population, was not significantly different from controls (M: 17.9 +/- 13.3 vs 20.5 +/- 13.8 mg/dl: NS; F: 30.1 +/- 21.5 vs 27.6 +/- 14.2 mg/dl: NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of obesity and hypertriglyceridaemia on the low HDL2-cholesterol level and on its relationship with prevalence of atherosclerosis in type 2 diabetes. 145 17

Human endothelial cells (EA.hy 926 line) were enriched with cholesterol using cationized low density lipoprotein (LDL). Cholesterol-loaded cells interacted with native apolipoprotein (apo) E-free high density lipoprotein3 (HDL)3 as well as with dimethyl suberimidate-modified HDL3 (DMS-HDL3). At 4 degrees C both HDL preparations showed a saturable high affinity binding with a KD of 31 and 50 micrograms of protein/ml and a Bmax of 226 and 436 ng/mg cell protein for native HDL3 and DMS-HDL3 particles, respectively. Competition of binding of 5 micrograms apo E-free 125I-labelled HDL3/ml by unlabelled DMS-HDL3 and tetranitromethane-treated HDL3 (TNM-HDL3) was very poor, whereas unlabelled native HDL3 competed very effectively with 125I-labelled HDL3 binding. Thus, both types of modified HDL did not compete for the high affinity binding sites for native HDL. Unlabelled native HDL3 and unlabelled DMS-HDL3 both competed for the binding of 125I-labelled DMS-HDL3 very effectively. These experiments indicate that there are two distinct high affinity binding sites for HDL on cationized LDL-loaded EA.hy 926 cells: one specific HDL binding site, which only binds native HDL, and a second binding site for both native HDL and DMS-HDL. The modified HDL fractions were used to study the relation between HDL binding and HDL-mediated efflux. Efflux of cell cholesterol was measured as the increase of cholesterol mass in the medium after 24 h of incubation with 0.2 mg native HDL3/ml, or the same amount of modified HDL3. DMS-HDL3-mediated efflux was identical to efflux mediated by native HDL3. TNM-HDL3 also induced efflux of cell cholesterol; however, efflux induced by TNM-HDL3 was only 45-50% of the amount obtained with native HDL3. So both DMS- and TNM-modified HDL3 induced efflux of cholesterol, although these particles do not bind to the specific high affinity sites for native HDL. These results do not indicate a link between binding of HDL to specific receptors for native HDL and HDL-mediated efflux of cholesterol from loaded endothelial cells.
Atherosclerosis 1992 Dec
PMID:Binding of modified high density lipoproteins to endothelial cells: relation with cellular cholesterol efflux? 146 59


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