Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Plasma levels of dehydroepiandrosterone sulfate (DHEA-S), testosterone, dihydrotestosterone (DHT) androstenedione, sex hormone-binding globulin (SHBG), lipoproteins, apolipoproteins and high density lipoprotein (HDL) subfraction were measured in 32 men aged 26-40 years after myocardial infarction (MI) suffered at least 3-4 months prior to the study, who were normocholesterolemic and had angiographically demonstrated coronary occlusion. The control group consisted of 76 healthy men aged 25-40 years. Blood samples were obtained in the morning from fasting subjects. A significant decrease in plasma DHEA-S and DHT levels were found in MI patients. Also, a significant decrease in HDL-cholesterol, HDL2-cholesterol (HDL2-C) and apolipoprotein A-I, an increase in apolipoprotein B and LDL-cholesterol (LDL-C) levels were observed in those patients as compared with healthy men. However, there were no differences in testosterone, androstenedione and SHBG concentrations between the groups. Significant correlations between testosterone and HDL2-C (r = 0.46, P less than 0.01), as well as between DHEA-S and HDL3-C (r = 0.39, P less than 0.05) levels in MI patients were observed. These results suggest that decreased levels of plasma DHEA-S and DHT may promote the development of coronary atherosclerosis in men.
Atherosclerosis 1989 Oct
PMID:Decreased plasma dehydroepiandrosterone sulfate and dihydrotestosterone concentrations in young men after myocardial infarction. 253 16

Human erythrocytes were incubated for 5 h at 37 degrees C with lipoproteins (LP), preliminary oxidized to different extent, as assessed by thiobarbituric acid (TBA) test. Cholesterol content in the cells was increased by 12-14% after incubation with low-density lipoproteins (LDL) along with augmentation of order parameter and rotational correlation time of spin-labeled stearic acids incorporated into membranes. If erythrocytes were incubated with oxidized LDL, containing 2.5-4 times more TBA-reactive material than native ones, cellular content of cholesterol was increased by 24-28%. In contrast, high-density lipoproteins (HDL2 and HDL3) removed cholesterol from cell membranes, when incubated with erythrocytes. This was followed by increased fluidity of membrane lipid phase as detected by the spin probe method. Oxidation of HDL2 and HDL3 decreased their ability to accept cholesterol from cell membranes. No detectable accumulation of TBA-reactive material was observed in the samples during the incubation. The antioxidant, butylated hydroxytoluene (BHT), in the concentration of 10(-5) M did not influence the cholesterol transfer between LP and erythrocytes. Hence, the effects of lipid peroxidation (LPO) on the cholesterol transfer seem to result from LP alterations by oxidation rather than from free radical reactions occurring during the incubation. By increasing cholesterol-donating ability of LDL and inhibition of cholesterol-accepting capacity of HDL lipid peroxidation in LP may activate cholesterol accumulation in blood vessel cells and thus contribute to atherosclerosis.
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PMID:Free radical lipid oxidation affects cholesterol transfer between lipoproteins and erythrocytes. 255 Mar 31

Digestion of the human apolipoprotein (apo) A-II gene with the endonuclease MspI produces fragments of 3.0 or 3.7 kb, reflecting the presence or absence of a polymorphic site within an Alu sequence 3' to the gene. Patients with hypertriglyceridemia have been shown to have an increased prevalence of the 3.0 kb allele. To explore this observation further, plasma lipoprotein lipids were studied in a random sample of fasted middle-aged Caucasian men, of which 59 were 3.0 kb homozygotes, 24 were heterozygotes, and 2 were 3.7 kb homozygotes. After adjusting for the effects of age, height, weight, alcohol intake and cigarette consumption by covariance analysis, no statistically significant associations were present between genotype and the concentrations of triglyceride in whole plasma or the d less than 1.019 g/ml fraction of plasma (i.e., VLDL + IDL). Nor were the cholesterol concentrations in VLDL + IDL, low density lipoprotein (LDL, d = 1.019-1.063 g/ml), high density lipoprotein (HDL), HDL2 or HDL3 related to genotype. In an independent comparison of eight 3.0 kb homozygotes and eight 3.7 kb homozygotes (all Caucasians) drawn from a different community, genotype was unrelated to the triglyceride or cholesterol concentrations in VLDL (d less than 1.006 g/ml), IDL + LDL (d = 1.006-1.063 g/ml) or HDL, after adjustment for the effects of covariates. These results suggest that the MspI polymorphism of the apo A-II gene is not associated with genetic variation that significantly affects triglyceride transport in the majority of men.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1989 May
PMID:Plasma lipoprotein lipids in relation to the MspI polymorphism of the apolipoprotein AII gene in Caucasian men. Lack of association with plasma triglyceride concentration. 256 9

The structure of lipoproteins is described, followed by a description of the structure and function of low density lipoproteins (LDL) which carry cholesterol to cells, and high density lipoproteins (HDL) which remove cholesterol. The process of atherosclerosis is then indicated. When LDL accumulates in plasma, it is deposited in macrophages which metabolize all the components of LDL except the cholesterol ester which becomes a foam cell. HDL converts foam cells back to macrophages. The presence of HDL and HDL2 allows foam cells to secrete cytoplasmic cholesterol and an apoprotein E which coats HDL2 and allows the recognition and removal of cholesterol in blood and by receptors in he liver. Atherosclerosis can be predicted from the effect of the HDL and LDL on foam cell formation, i.e., more foam cells means more HDL, particularly HDL2, and the less likely atherosclerosis will develop. The link between oral contraceptives (OCs) and atherosclerosis is that with estrogen LDL cholesterol levels decrease, while there are increases with progestins; HDL and HDL2 increase with estrogen and decrease with progestins. HDL3 is unaffected by estrogen. The effects of progestins are dependent on a number of other factors. Longterm clinical trials of OCs and their effects on lipoproteins are identified from Johns Hopkins and George Washington University studies. The longterm trail results are given. Total cholesterol rose regardless of the 3 different progestins. Compounds containing dl-norgestrel in higher doses raised LDL levels more than ethynodiol diacetate or norethindrone. In low doses, levels of LDL also rose but ethynodiol diacetate rose least in 6 months. Apoprotein B also rose in a similar fashion. Norgestrel lowers HDL considerably and HDL2 in higher or lower doses; there were more differences in ethynodiol diacetate or norethindrone. All 3 preparations raised HDL3 similarly. Norgestrel decreases apoprotein levels in high doses and apoprotein is unaffected at low doses; low apoprotein is linked to coronary artery disease. Increases occurred with ethynodiol diacetate and norethindrone. New triphasic compounds are under investigation, and show low HDL at 6 but not 12 months, but consistently raise LDL. Lipoprotein phospholipids research findings are also revealed as well as other related research. Adverse effects may be seen for many years after OC use, so low doses are recommended.
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PMID:Effects of oral contraceptives on circulating lipids and lipoproteins: maximizing benefit, minimizing risk. 257 64

Although the triglyceride-lowering actions of n-3 fatty acids of marine lipids are now well-recognized, their effects on plasma lipoproteins have not been studied systematically in patients with hypercholesterolemia. To address this question, we supplemented the Phase 1 American Heart Association diets of 14 hypercholesterolemic ambulatory outpatients with a commercially available preparation of marine lipid concentrate (SuperEPA) containing 7.5 g n-3 fatty acids per day and studied their plasma lipids and lipoproteins before and after 30 days of treatment. Both plasma triglyceride and cholesterol levels fell uniformly in all patients while the mean VLDL- and LDL-cholesterol decreased by 58% (P less than 0.005) and 13% (P less than 0.025) respectively. The decrease in whole plasma cholesterol was significantly correlated with the fall in LDL-cholesterol (r = 0.85, P less than 0.01), and not VLDL-cholesterol (r = 0.39, NS). Among the other potentially beneficial actions observed was an increase in HDL2 in all patients (mean increment 41%, P less than 0.005), and an increase in the HDL2/HDL3 ratio (+46%, P less than 0.001) and decreases in the LDL/HDL ratio (-14%, P less than 0.005) and in the unesterified cholesterol/lecithin ratio (-17%; P less than 0.001) in plasma. The increase in the unesterified cholesterol/esterified cholesterol ratio in VLDL and HDL3 suggested that marine lipid therapy resulted in a reduction in the size of lipoprotein particles in these fractions. Since these changes may reduce cardiovascular risk, these findings suggest that marine lipids may prove useful in the treatment of certain patients with hypercholesterolemia.
Atherosclerosis 1989 Oct
PMID:Effects of dietary supplementation with marine lipid concentrate on the plasma lipoprotein composition of hypercholesterolemic patients. 259 25

The effects of insulin on the lipid values of nonobese non-insulin-dependent diabetic (NIDDM) Arab women requiring insulin was investigated to find whether these patients have the same coronary artery risk factor related to lipid levels. In this study, 55 NIDDM women on insulin therapy (mean age 28 +/- 8.1 yr and duration of disease 5 +/- 1.2 yr) and 70 control subjects (matched for sex, age, and body mass index) were studied for their plasma levels of lipids, lipoproteins, and apolipoproteins. Concentrations of total cholesterol, very-low-density lipoprotein cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride (TG), LDL TG, high-density lipoprotein triglyceride (HDL TG), phospholipid, glucose, glycosylated hemoglobin (HbAtc), apolipoprotein B (apoB), LDL-apoB, and apoB/apoAl were significantly elevated in diabetic women compared with control subjects. There was no significant change in the levels of apoAll in plasma and lipoprotein fractions. Concentrations of HDL cholesterol (chol), HDL2-chol, HDL3-chol, plasma apoAl, HDL2-apoAl, HDL3-apoAl, and HDL-apoAl were significantly lower in diabetic women than in control subjects. There was no significant correlation between glucose or HbAtc and most of the lipids, lipoprotein lipids, and apolipoproteins measured. Despite normal body weight and insulin therapy, abnormalities in lipids, lipoprotein lipids, and apoB persisted in NIDDM patients compared with control subjects. Our data may favor an enhanced affinity toward atherosclerosis in these patients.
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PMID:Lipoproteins and apolipoproteins in young nonobese Arab women with NIDDM treated with insulin. 265 41

We followed 19 men and 19 women with asymptomatic carotid stenosis up to 30 months to determine whether hematologic or lipid abnormalities could identify those individuals developing progressing carotid atherosclerosis (defined as an increase in mean percent stenosis greater than or equal to 19% or an increase in a single region of greater than or equal to 23%) on B-mode carotid ultrasonography performed at 2- to 6-month intervals. Our patients demonstrated increased beta-thromboglobulin, platelet factor 4, and fibrinogen compared with age-matched controls. Eight patients developed progression of carotid stenosis, and this group had higher baseline low-density lipoprotein (LDL) and fibrinogen than the 30 nonprogressing patients. Multiple regression analyses of age, sex, smoking, coronary artery disease, peripheral vascular disease, diabetes, hypertension, and baseline high-density lipoprotein (HDL), HDL2, HDL3, LDL, beta-thromboglobulin, platelet factor 4, and fibrinogen identified coronary artery disease and elevated LDL and fibrinogen as the only independent variables significantly associated with the progressing group. We conclude that, in patients with carotid atherosclerosis, a combination of coronary artery disease and elevated LDL and fibrinogen will predict with 88% accuracy whether the patient will have progressing carotid stenosis.
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PMID:Prediction of carotid stenosis progression by lipid and hematologic measurements. 218 78

In a group of 40 newly detected middle-aged diabetics the authors recorded reduced HDL cholesterol levels and elevated triglyceride and total cholesterol levels. After compensation of diabetes the cholesterol and triglyceride levels became normal, the HDL cholesterol levels remained, however, low. By comparison of the sub-fractions of HDL cholesterol in diabetics with the control group it was revealed that in the diabetic group the HDL2 cholesterol levels were significantly reduced. The HDL3 cholesterol was not significantly altered. The reduction of the total HDL cholesterol was due mainly to low HDL2 cholesterol, while the HDL3 cholesterol level was normal. Low HDL cholesterol levels and those of the HDL2 sub-fraction in newly detected diabetics indicate the increased risk of development of atherosclerosis.
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PMID:[Levels of HDL cholesterol and the HDL2 and HDL3 subfractions in newly detected type 2 diabetes]. 273 99

It is established in the in vitro experiments that subfraction of HDL3 is able of accepting cholesterol from the atherosclerosis-afflicted aorta intima. Apoprotein E has no effect on the acceptance of cholesterol from the intima by HDL3 particles. The role of the protein under its joint incubation with the aorta intima and HDL3 is reduced to the uptake of cholesterol esters from HDL3-particles enriched by cholesterol. It is assumed that apoprotein E under certain metabolic conditions can transfer esterified cholesterol from HDL-particles on other lipoproteins as well as into tissues impoverished in the cholesterol content.
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PMID:[Participation of apolipoprotein E in the transport of cholesterol esters]. 274 12

Plasma and lipoprotein cholesterol, triglycerides, apolipoproteins (apo) A-I, A-II, B and phospholipid concentrations were measured at 10 days and 4 months after myocardial infarction (MI) in 60 young Kuwaiti male MI survivors below the age of 40 years. Controls were matched for age, relative weights, smoking, dietary habits and physical activities. The young MI survivors had significantly higher levels of total and LDL-cholesterol, and ratios of LDL/HDL- and LDL/HDL2-cholesterol. Total VLDL and LDL triglycerides, and phospholipids were also elevated in MI survivors compared to controls. Similarly, plasma and LDL-apo B as well as the ratios of apo B/apo A-I were higher in the MI group. There was no significant change in the levels of VLDL and HDL3-cholesterol and of apo A-II in these patients compared to their controls. Concentrations of HDL- and HDL2-cholesterol and of plasma and HDL apo A-I were significantly lower in the young MI survivors compared to the control subjects. The better discriminating lipoproteins and apolipoproteins in MI patients in descending order were HDL2-cholesterol greater than apo B greater than apo A-I greater than VLDL-triglyceride greater than HDL-cholesterol greater than LDL/HDL2-cholesterol greater than triglycerides. The data indicate that measurement of HDL2-cholesterol, apo B and apo A-I may be useful indicators in assessing coronary artery disease risk than triglycerides (TG), total cholesterol (TC), LDL-cholesterol and HDL-cholesterol.
Atherosclerosis 1989 Jun
PMID:Lipoproteins and apolipoproteins in young male survivors of myocardial infarction. 275 45


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