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)

Untreated hypertension in age groups below 60 years has been shown to be associated with significant elevations in serum cholesterol and triglyceride levels. Drug therapy of hypertension has also been shown to have adverse effects on lipoproteins. We have investigated lipid and lipoprotein levels in a community-based sample of men and women 60 years and older belonging to one of the following groupings: (a) normal blood pressure (n = 1075); (b) untreated hypertension (n = 329); (c) drug-treated hypertension (n = 880). Serum lipid, lipoprotein, apolipoprotein or plasma glucose levels did not vary significantly between untreated hypertensives and normotensives of either sex. In a multiple regression model controlling for possible influences of age, overweight, alcohol and tobacco usage, and presence of coronary heart disease, anti-hypertensive drug therapy significantly predicted increased serum triglycerides (P less than 0.001) and reduced high density lipoprotein (HDL) cholesterol levels (P less than 0.01) in both sexes, reduced apolipoprotein A-I levels in males (P less than 0.001), and increased apolipoprotein B (P less than 0.01) and plasma glucose levels (P less than 0.001) in females. Adjusted triglycerides were 20% higher and HDL cholesterol was 7% lower in the presence of anti-hypertensive drug therapy. These effects were partially consistent with the known actions of thiazide diuretics and beta-blockers which were used by more than 50% and 40% of subjects, respectively.
Atherosclerosis 1992 Jan
PMID:Dubbo Study of the elderly: hypertension and lipid levels. 134 82

A DNA restriction fragment length polymorphism (RFLP), observed with the XbaI restriction enzyme digestion of peripheral lymphocyte genomic DNA and a 3.5 kb probe 3' end of the apolipoprotein B gene, was investigated in 228 normal healthy males. Lipoprotein measurements were conducted on fasting plasma and related to the genotype; the X2X2 homozygotes (the X2 allele contains the enzyme cutting site) had significantly higher plasma cholesterol, low density (LDL) cholesterol and LDL apolipoprotein B. Thirty subjects (10 from each of the X1X1, X1X2 and X2X2 groups) were recalled and the LDL receptor activity measurements, conducted on peripheral venous blood lymphocytes, indicated no significant differences between the genotypes. However, when LDLs isolated from these individuals were assayed for ligand-receptor interaction with a human embryonic lung fibroblast cell line, significantly different maximum binding (Bmax) values in the X2 allele-bearing individuals were observed. This paradoxically elevated in vitro binding and degradation of LDL from X2X2 subjects suggests that the elevated concentrations of LDL cholesterol observed with this genotype in vivo does not result from a defective ligand-receptor interaction directly related to this polymorphism.
Atherosclerosis 1992 Mar
PMID:Low density lipoprotein ligand-receptor interactions in normal healthy individuals characterized by their XbaI apolipoprotein B DNA polymorphism. 135 Jul 24

The level of lipoprotein Lp(a), one of the risk factors of atherosclerosis, was determined in 91 children and adolescents of age ranging from 3.3 to 22 years suffering from insulin-dependent diabetes. The changes in Lp(a) were analyzed in relation to the group of patients, the duration of diabetes, possible genetic factors, other factors predisposing to early onset of atherosclerosis, and occurrence of obesity in the analyzed group. The relation between the level of Lp(a) and other parameters of lipid metabolism (total cholesterol, triglycerides, phospholipids, HDL-cholesterol and apolipoprotein B) as well as a degree of metabolic normalization of diabetes (as assessed by the determination of glycosylated hemoglobin and fructosamine) was studied in addition. No relation between Lp(a) and the factors mentioned above, with exception of glycosylated hemoglobin and fructosamine concentrations, could be demonstrated. The elevated level of Lp(a) in children and adolescents during the period of poor metabolic control of diabetes may constitute an additional risk factor for early onset of atherogenic changes.
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PMID:[State of lipid metabolism in children and adolescents with insulin-dependent diabetes. I. Evaluation of lipoprotein (A) behavior in children and adolescents with insulin-dependent diabetes]. 136 93

The authors investigated selected indicators of the lipid metabolism in 31 children with insulin-dependent diabetes for a period of 3 to 14 years. They divided the patients into two groups those with a glycosylated haemoglobin below or above 9 mumol/1 g haemoglobin. They compared the assembled results of the two groups and also with the results obtained in a control group. The total cholesterol was in both diabetic groups higher than in healthy subjects and was higher than the value which is considered from the aspect of the genesis and development of atherosclerosis as a risk value. Children with poorly compensated diabetes, i. e. with a glycosylated Hb level above 9 mumol had a higher cholesterol level as compared with well compensated diabetic children. The pre-beta fraction of lipoprotein increased in both groups of patients, however, more in those where the disease was not well compensated. There was a parallel decrease of the alpha fraction and the lipoprotein profile had a markedly atherogenic character. The apolipoprotein B concentration was in patients with well compensated diabetes lower, as compared with controls but in patients with poorly compensated diabetes after 4-5 years treatment is was significantly higher. Poor compensation of diabetes led after 4-5 years duration to a significant rise of the serum triglyceride level. As the blood lipid levels are influenced in a significantly way by diet, compensation of the disease and a low-fat diet are essential with regard to the results assembled in this investigation for prevention of ischaemic heart disease in diabetic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Variations in lipid metabolism in long-term monitoring of children treated for diabetes mellitus]. 139 53

The effect of LPSw (a lipopolysaccharide from wheat flour) on cholesterol catabolism was examined using WHHL (Watanabe heritable hyperlipidemic) rabbit, which is an experimental model of familial hyperlipidemia. The serum cholesterol level of the animal decreased by the addition of LPSw to drinking water. Following cessation of the addition of LPSw to the drinking water, the cholesterol level was decreased for 30 to 40d and then gradually elevated. The serum level of apolipoprotein B, which is a constituent of apolipoprotein of low density lipoprotein (LDL), also decreased in accord with serum cholesterol at a nearly coincident rate. Conversely, the level of apolipoprotein A-I, which is a constituent of apolipoprotein of high density lipoprotein (HDL), did not change, nor did HDL-cholesterol. Furthermore, the atherosclerosis risk factor, expressed as the ratio of apolipoprotein B to apolipoprotein A-I, was decreased by LPSw administration.
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PMID:Homeostasis as regulated by activated macrophage. VII. Suppression of serum cholesterol level by LPSw (a lipopolysaccharide from wheat flour) in WHHL (Watanabe heritable hyperlipidemic) rabbit. 139 46

Lipoprotein(a) [Lp(a)] is recognized as an independent risk factor for atherosclerosis. Lp(a) consists of a LDL-like moiety with an additional glycoprotein, apo(a), linked to apolipoprotein B-100. Apo(a) has a high homology with plasminogen (Pg). In vivo, Pg is activated on a fibrin surface by tissue Pg activator (tPA). We prepared Lp(a) from plasma by sequential ultracentrifugation followed by lysine-sepharose affinity chromatography. We found that a changing (donor dependent) fraction of the Lp(a) did not bind to lysine-sepharose. This fraction, designated Lp(a)lys-, was further purified using gel filtration. Bound Lp(a) [Lp(a)lys+] was eluted with 0.2 M EACA. Apo(a) isoforms in both fractions were identical. In contrast Lp(a)lys+ inhibited Pg activation by tPA in vitro (IC50% 20 mg/l), whereas Lp(a)lys- did not. In addition Lp(a)lys- did not bind to CNBr-digested fibrinogen whereas Lp(a)lys+ did (Kd, app = 0.2 nM). Therefore we conclude that a changing donor dependent fraction of human plasma Lp(a) does not inhibit Pg activation in vitro and does not bind to CNBr-digested fibrinogen.
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PMID:Lysine-binding heterogeneity of Lp(a): consequences for fibrin binding and inhibition of plasminogen activation. 141 65

Risk factors for atherosclerosis were investigated in a group of 17 female Type II diabetic patients with microalbuminuria-urinary albumin excretion (UAE) in the range of 30-300 mg/day, and in a control group including 15 Type II diabetic females with UAE less than 30 mg/day. Significantly increased mean concentrations of total and LDL-cholesterol were measured in the group with microalbuminuria (p less than 0.05). Also mean levels of some other cardiovascular risk factors (systolic blood pressure, fibrinogen, apolipoprotein B, triglycerides and uric acid) were higher in the group of patients with microalbuminuria, although the differences in comparison to the control group did not reach the level of statistical significance. In the multiple stepwise regression analysis log transformed UAE values correlated significantly with three independent factors--uric acid (p less than 0.01), fibrinogen (p less than 0.05), and systolic blood pressure (p less than 0.05). It is concluded that a slight increase in the levels of a number of cardiovascular risk factors observed in incipient diabetic nephropathy suggests an additive effect favouring atherogenesis.
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PMID:Risk factors for atherosclerosis in female type II diabetic patients with incipient diabetic nephropathy. 141 13

Evidence for chemical and biological heterogeneity of human plasma lipoprotein density classes has been steadily accumulating over the last 15 years. Furthermore, several recent reports have indicated potential clinical significance of certain lipoprotein subspecies as either atherogenic or antiatherogenic. It is generally accepted that lipid lowering treatments can retard or even reverse development of atherosclerotic lesions. However, very little is known about effects of various lipid lowering treatments on specific lipoprotein particles. The purpose of this study was to explore the effects of heparin induced extracorporal low density lipoprotein precipitation (HELP) on various subspecies of plasma lipoprotein particles defined primarily by their apolipoprotein composition. Using particle specific enzyme immunoassays, the immediate changes in lipoprotein particle profiles were analyzed after a single HELP treatment in 12 patients with angiographically documented coronary artery disease. In a separate group of 6 patients, particles were repeatedly measured over a period of 96 h following a HELP treatment. Single HELP treatment caused an immediate and highly significant decrease (67%) in the concentration of simple lipoprotein particles containing apolipoprotein B (apo B) as a sole apolipoprotein (LP-B). Various subspecies of complex particles containing apo B and other apolipoproteins (Lp-B-complex) were also decreased although to a lesser degree (44-53%). HELP treatment caused an insignificant, 3% decrease of lipoprotein particles containing apo A-I but no apo A-II (Lp-A-I) and a 6% decrease in the concentration of particles containing both apo A-I and apo A-II (Lp-A-I:A-II). During the 96-h period following HELP treatment various apo B containing particles recovered at different rates in different patients.(ABSTRACT TRUNCATED AT 400 WORDS)
Atherosclerosis 1992 Aug
PMID:Apolipoprotein A-I and apolipoprotein B containing lipoprotein particles in coronary patients treated with extracorporal low density lipoprotein precipitation (HELP). 141 90

Dietary intakes, anthropometric indices and plasma lipoprotein and alpha-tocopherol concentrations were measured in premenopausal vegetarian women of Indian descent (n = 22) and in white women of European descent consuming either mixed (n = 22) or vegetarian diets (n = 18). The Indian women were shorter in height than the white women and had a higher proportion of body fat. Energy intakes were lower in the Indian women, both in absolute terms and per kg body weight. The proportion of energy derived from saturated fatty acids was lower and that from polyunsaturated fatty acids was greater in both Indian and white vegetarians compared with the subjects on mixed diets. Intakes of dietary fibre and vitamins C and E were higher in the white vegetarians compared with the other groups. Plasma concentrations of total and LDL cholesterol and apolipoprotein B and the ratio of apolipoprotein B/apolipoprotein AI were lower and HDL and HDL2 cholesterol, alpha-tocopherol concentrations and the ratio of alpha-tocopherol/cholesterol were greater in the white vegetarian group than in the other groups. Total plasma cholesterol was associated with measures of truncal obesity, especially subscapular skinfold thickness and the percentage energy derived from saturated fatty acids. Plasma concentrations of apo(a) were higher and those of HDL and HDL2 cholesterol and sex hormone binding globulin (SHBG) were lower in the Indian vegetarian women compared with both groups of white women. No relationship could be found between apo(a), HDL and HDL2 cholesterol concentration and nutrient intake but HDL and HDL2 were negatively associated with the proportion of body fat and apo(a) weakly with subscapular skinfold thickness.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1992 Aug
PMID:Lipoprotein risk factors in vegetarian women of Indian descent are unrelated to dietary intake. 141 95

The clinical response to long-term reduction of the plasma LDL cholesterol concentration was studied in a man with severe coronary artery disease associated with familial defective apolipoprotein B-100 (FDB). Plasma exchange repeated at 2-week intervals, combined with lipid-lowering drugs, led to remission of angina and improved exercise test performance. A similar clinical response was achieved after LDL apheresis with dextran sulphate columns repeated once every 2 weeks in combination with drug treatment. The reduction in plasma LDL cholesterol level brought about by LDL apheresis was at least as marked in the FDB patient as in 5 patients with familial hypercholesterolaemia. We conclude that FDB patients with coronary artery disease may derive clinical benefit from prolonged reduction of their plasma cholesterol levels and that LDL containing apo B-100 in which arginine at position 3500 is replaced by glutamine is removed from plasma by dextran sulphate columns as efficiently as is normal LDL.
Atherosclerosis 1992 Aug
PMID:Effective reduction of plasma LDL levels by LDL apheresis in familial defective apolipoprotein B-100. 141 96


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