Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.6 (CAD)
4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patterns of RFLP association were studied, to identify gene regions influencing quantitative variation in lipid and lipoprotein traits (coronary artery disease [CAD] risk factors or metabolically related traits). Subjects (118 female and 229 male; age 20-59 years) were selected for health. Multiple RFLPs were used to sample variability in regions around genes for apolipoprotein (apo) B (restriction enzymes HincII, PvuII, EcoRI, and XbaI), apo AI-CIII-AIV (BamHI, XmnI, TaqI, PstI, SstI, and PvuII) and cholesterol ester transfer protein (TaqI). Separate analyses were done by gender. The sample was truncated at mean +/- 4 SD, to remove extreme outliers. There was no significant gender difference in RFLP genotype frequency distribution. After trait-level adjustment to maximize removal of concomitant variability, analysis of variance was used to estimate the percentage trait phenotypic variance explained by measured variability in the gene regions studied. Fewer gene regions were involved in men, with less influence on quantitative trait variation than in women, in whom hormone use affected association patterns. Gender differences imply that pooling genders or adjusting data for gender effects removes genetic information and should be avoided. The association patterns show that variability around the candidate genes modulates trait levels: the genes are contributors to the genetics of CAD risk variables in a healthy sample.
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PMID:Patterns of association between genetic variability in apolipoprotein (apo) B, apo AI-CIII-AIV, and cholesterol ester transfer protein gene regions and quantitative variation in lipid and lipoprotein traits: influence of gender and exogenous hormones. 134 81

Five restriction fragment length polymorphisms (RFLP) of the apo B gene and their association with serum lipids and apolipoprotein levels have been studied in 139 Chinese patients with angiographically confirmed CAD (mean age 56.2 +/- 0.8 years) and 154 healthy Chinese subjects (mean 44.0 +/- 1.0 years) of both sexes. The patient group had significantly higher levels of serum total and LDL cholesterol; and apo B (P < 0.001) and lower HDL cholesterol and apo A-I (P < 0.001 and < 0.01, respectively). The frequencies of the rarer alleles of the ins/del, XbaI and EcoRI (but not the PvuII and MspI) polymorphisms were significantly lower in the Chinese compared to those reported in Caucasians. There was no significant difference in allelic frequencies of the signal peptide region (Ins/Del), XbaI, MspI and EcoRI sites of the apo B gene between the patient and control groups. The frequency of the rarer allele of the PvuII RFLP was significantly lower in the CAD patients (P < 0.05) compared to that in the control group (0.05 vs 0.10). None of the DNA polymorphisms was associated with a significant influence on serum lipid and apolipoprotein levels in the patients with coronary artery disease.
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PMID:DNA polymorphisms of the apolipoprotein B gene in Chinese coronary artery disease patients. 135 87

The mortality rate from CAD in Indians is more than 3 times that in the Chinese and Malays in the population of Singapore. The serum total, HDL cholesterol and apolipoprotein levels (Apo A-I, Apo A-II and Apo B) were studied in a group of 344 healthy male adults from the 3 ethnic groups. Indians had a significantly lower level of HDL-cholesterol (38.4 +/- 9.8 mg/dl) than the Chinese (42.7 +/- 8.9 mg/dl) (P less than 0.005). The Apo A-I levels were higher in the Chinese (115.1 +/- 14.8 mg/dl) than in the Indians (108.6 +/- 28.8 mg/dl), but the difference was not statistically significant. The Chinese also had higher levels of Apo A-II (48.1 +/- 7.2 mg/dl) compared to those in the Indians (38.6 +/- 6.4 mg/dl) and Malays (38.0 +/- 4.9 mg/dl) (P less than 0.001). The ratio of Apo A-I/Apo B level was also higher in the Chinese (1.28) than in the Indians and Malays (1.09). Higher levels of Apo B and lower levels of HDL-cholesterol, Apo A-I and Apo A-II in Indians may partly explain the higher incidence of CAD in Indians.
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PMID:Serum high density lipoprotein cholesterol, apolipoprotein A-I, A-II and B levels in Singapore ethnic groups. 312 Jul 38

In this study we compared the relative utility of plasma lipid and apolipoprotein pattern as predictor of extent of Coronary Artery Disease as angiographically established. The lipid and apolipoprotein values were plotted in multiple stepwise analysis against coronary score determined as follows: at least 1 coronary artery system (left, anterior, descendent, circumflex, right) with a >/= 25% stenosis 1 point, number of involved vessel 1, 2, 3, .... adjunctive points; sequential lesions +1 point; < = %50% stenosis +1 point; 75-95 % +2 points; > 95% +3 points. The statistical analysis demonstrate a strong influence on extent of disease by total-cholesterol, % HDL-cholesterol on total cholesterol and by the difference between LDL and HDL-cholesterol. We conclude that, in predicting the extension of CAD, is important to know how total cholesterol is distributed in plasma apolipoprotein system.
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PMID:Serum lipid pattern as severity indicator of angiographically assessed coronary artery disease. 801 Aug 90

An oral fat-load test was carried out in patients with non-insulin-dependent diabetes mellitus (NIDDM) and angiographically verified coronary artery disease (CAD; group 1, n = 6); in patients with CAD but no diabetes (group 2, n = 6); in patients with NIDDM but no CAD (group 3, n = 4); and in healthy control subjects (group 4, n = 4). Concentrations of apolipoprotein (apo) E, apo C-II, triglyceride (TG), retinyl palmitate, and cholesterol were measured in fasting plasma and in plasma obtained after 2, 4, 6, 9, and 24 h after a meal containing 78 g of fat and 345,000 IU of vitamin A. The same measurements were carried out in the lipoprotein fractions with Svedberg flotation rates Sf 400-1100, 60-400, 20-60 and 12-20, obtained by density gradient ultracentrifugation. The postprandial apo E concentrations were highest in group 1 (NIDDM and CAD) in plasma and in the TG-rich lipoprotein fractions, with significant differences in comparison with the healthy subjects. As shown by apo E to TG ratios, the postprandial lipoproteins were enriched with apo E in the patients with NIDDM and CAD. The largest excesses of apo E in group 1 patients were observed in the atherogenic Sf 12-60 lipoproteins. Across the entire study population, there was a significant inverse correlation between the postprandial apo E responses and the postheparin lipoprotein lipase activity. The results suggest that enrichment of the remnant lipoproteins with apo E may have a role in the increased risk of CAD among patients with NIDDM.
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PMID:Enrichment with apolipoprotein E characterizes postprandial TG-rich lipoproteins in patients with non-insulin-dependent diabetes mellitus and coronary artery disease: a preliminary report. 815 85

There is evidence that the overproduction of apoB-100-containing lipoproteins by the liver is the underlying event in some forms of dyslipoproteinemia. This metabolic status is associated to an increased risk of developing premature coronary artery disease CAD. The conclusions from previous studies suggested that the availability to the hepatocytes of cholesterol that is readily esterified is an important determinant for VLDL and LDL secretion. In the present study, we set out to investigate the effect of the specific stimulation and inhibition of the rate-limiting enzyme of the cholesterol esterification, acyl-CoA:cholesterol acyltransferase (ACAT, E.C. 2.3.1.26), on the lipid and on the apoB-100 secretion rate from a human hepatoma cell line (HepG2). When the specific ACAT inhibitor FCE 27677 (10-5 M) was added to the cultures, a decrease of the cellular cholesteryl ester content and at the same time a significant reduction of the neutral lipids and of the apoB-100 secretion rate were noticed. The stimulation of ACAT by 25-hydroxycholesterol (20 microgram/ml) caused a 4-fold increase of the cellular cholesteryl ester content and a 2-fold increase of the lipoprotein secretion rate. FCE 27677 (10-5 M to 10-7 M) prevented the effects elicited by the oxysterol. On the contrary, lovastatin (10-6 M) and gemfibrozil (10-6 M) had no effect. The analysis of the lipid and of the apolipoprotein composition of the lipoproteins secreted in the medium revealed that ACAT inhibition had the dual effect of both decreasing the number of apoB-100-containing lipoproteins secreted as well as their cholesteryl ester load. Altogether, these data support the idea of a close relationship between ACAT activation, leading to increased cholesteryl ester availability, and apoB-100-containing lipoprotein secretion. It is speculated that ACAT inhibitors may prove useful for the treatment of human dyslipoproteinemias caused by the hepatic overproduction of apoB-100-containing lipoproteins.
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PMID:Inhibition of acyl-CoA: cholesterol acyltransferase decreases apolipoprotein B-100-containing lipoprotein secretion from HepG2 cells. 882 97

Because remnants of triglyceride-rich lipoproteins (TRLP) are potentially atherogenic, the postprandial lipoprotein metabolism was studied in 12 normocholesterolemic, normotriglyceridemic women, aged 60 +/- 2 years, with angiographically proven coronary artery disease (CAD+; cholesterol 5.7 +/- 0.1 (S.E.) mmol/l, triglyceride 1.35 +/- 0.10 mmol/l) and in 12 individually matched controls, aged 59 +/- 2 years, without angiographical abnormalities (CAD-; cholesterol 5.1 +/- 0.2 mmol/l and triglyceride 1.16 +/- 0.13 mmol/l). Following an oral retinyl palmitate-fat load, the CAD+ women showed a significantly higher triglyceride response in the chylomicron, or Sf > 1000, fraction (P < 0.05 vs. controls). Total plasma apolipoprotein (apo) B and retinyl palmitate concentrations were similar in both groups. Fasting apo B-48 levels in the d < 1.006 g/ml fraction were significantly higher in CAD+ cases (0.25 +/- 0.03 integrated optical density (iod) units) than CAD- controls (0.15 +/- 0.03; P < 0.05). Furthermore, after the fat load, a greater absolute and incremental apo B-48 response in the intermediate density lipoprotein (IDL) fraction (d = 1.006-1.019 g/ml) was observed in CAD+ cases (incremental area under the curve (Delta-AUC)8: 0.40 +/- 0.12 h.iod) than CAD- controls (0.01 +/- 0.06 h.iod; P = 0.01). Post-heparin hepatic lipase (HL) activities were higher in the CAD+ group: 422 +/- 22 mU/l vs 288 +/- 20 mU/ml in the CAD- group (P < 0.001) while lipoprotein lipase (LPL) activities were identical. The results provide evidence that the metabolism of intestinal TRLP is significantly different in normolipidemic women with angiographically proven CAD compared with individually matched controls without coronary disease. Fasting apo B-48 levels in d< 1.006 g/ml fractions represent a potentially useful marker in women at risk for CAD.
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PMID:Abnormal postprandial apolipoprotein B-48 and triglyceride responses in normolipidemic women with greater than 70% stenotic coronary artery disease: a case-control study. 883 Sep 35

We have examined the prevalence of clinically significant atherosclerosis in 78 patients with type III hyperlipoproteinemia (HLP) and homozygosity for apolipoprotein (apo) E2. Forty-six of these individuals (59%) had no atherosclerosis, 32 patients (41%) had atherosclerosis, i.e., atherosclerosis of the extracranial carotid arteries (CAA), coronary arteries (CAD) or/and peripheral arteries of the legs (PVD), either singly or in combination. No association could be shown with respect to the co-prevalence of atherosclerotic lesions at these different arterial sites, except for the high predictive value (pv = 0.88, P = 0.006) of CAA for the presence of PVD. Hence, documentation of atherosclerosis under clinical aspects at one of these exposed arterial territories does not allow a reliable prediction of generalised atherosclerosis or local atherosclerosis at other sites of the arterial tree in individuals with this familial lipoprotein disorder. Therefore, assessment of the extent of clinically significant atherosclerosis in type III HLP patients should include careful and thorough examination of the extracranial carotid arteries, the coronary arteries, and the peripheral arteries of the legs.
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PMID:Prevalence and association of atherosclerosis at three different arterial sites in patients with type III hyperlipoproteinemia. 892 60

We investigated the role of the apolipoprotein (Apo) E polymorphism in the prediction of CAD age of onset in a sample of unrelated living male (n = 65) and female (n = 54) Caucasian subjects diagnosed with CAD. Cumulative distributions of age at the first diagnosis of CAD were estimated for each Apo E genotype and tested for homogeneity using the log-rank test. The Apo epsilon 33 genotype was used as a reference group for all hypothesis tests. Analyses were performed separately in males and females. We found evidence suggesting that the presence of the Apo epsilon 32 genotype in males is associated with a significantly earlier CAD age of onset. These results suggest that the Apo E polymorphism may be a gender-specific predictor of CAD age of onset.
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PMID:The role of the apolipoprotein E polymorphism in the prediction of coronary artery disease age of onset. 908 29

The incidence rate and mortality of coronary heart disease (CHD) is obviously higher in men than in women, which may be related to the influence of plasma lipoprotein metabolism by endogenous sex hormones. We determined plasma testosterone (TTT), estradiol, total cholesterol (TC), triglyceride (TG), high density lipoprotein-cholesterol (HDL-C), HDL2-C, HDL3-C, apolipoprotein (Apo) AI, Apo B100 and lipoprotein (a) [Lp(a)] in 201 subjects, among them 102 patients with CHD and 99 healthy subjects. It was found that, mean plasma TTT levels in patients with CAD (252+/-125 ng/ml) was significantly lower than in the healthy subjects (412+/-309 ng/ml). There was a negative association between plasma TTT level and plasma TG level (r=-0.239; P<0.001) and Lp(a) (r=-0.163, P<0.05), and a positive association between plasma TTT level and HDL-C (r=0.301, P<0.001) and HDL3-C (r=0.328, P<0.001). The results in the present study suggest that low plasma TTT level may be a risk factor for CHD, which may relate to the influence of plasma lipoprotein metabolism by endogenous testosterone.
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PMID:The association of low plasma testosterone level with coronary artery disease in Chinese men. 951 Apr 90


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