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)

We determined the insulin response to an oral glucose ingestion and levels of serum lipoproteins in 25 untreated patients with type 2 diabetes mellitus, in 26 subjects with impaired glucose tolerance (IGT), and in 35 non-diabetic control subjects. The three groups had similar compositions with respect to age and sex distribution. The levels of VLDL triglyceride in the subjects with type 2 diabetes or IGT were higher than those in controls. Serum HDL- and HDL2 cholesterol were significantly decreased in type 2 diabetics, and the subjects with IGT showed a similar tendency. Serum apolipoprotein A-II levels were lower in the male subjects with type 2 diabetes or IGT than in controls. Insulin response, i.e., sum of immunoreactive insulin (IRI) levels at basal, 30, 60, 90 and 120 min after a 75-g oral glucose load, negatively correlated to HDL- and HDL2 cholesterol levels (r = -0.396, P less than 0.05; r = -0.482, P less than 0.001, respectively), and positively correlated to VLDL triglyceride values (r = 0.485, P less than 0.001) in the male subjects with type 2 diabetes or IGT. In the female subjects, fasting plasma IRI values significantly correlated to HDL cholesterol (r = -0.496, P less than 0.05). There was a significant negative correlation between the concentrations of HDL2 cholesterol and VLDL triglyceride. These data show that lipoprotein metabolism, not only in type 2 diabetics, but also in IGT tends to show changes such as decreased HDL2 cholesterol and increased VLDL triglyceride levels, and which might be related to the hypersecretion of endogenous insulin.
Atherosclerosis 1986 Jun
PMID:Influence of endogenous hyperinsulinism on high density lipoprotein2 level in type 2 (non-insulin-dependent) diabetes mellitus and impaired glucose tolerance. 373 47

A cross-over study using 11 male subjects and a closely controlled diet, investigated the effect of alcohol on serum high density lipoprotein (HDL) components. Smoking status and body weight remained essentially constant and exercise changes were adjusted for in the analysis. As compared to sucrose, alcohol consumption was associated with a significant elevation in serum apolipoprotein A-I (0.37 mg/dl/g/day of alcohol) with similar effects for serum HDL cholesterol (0.14 mg/dl/g/day of alcohol) and serum apolipoprotein A-II (0.11 mg/dl/g/day of alcohol) achieving borderline levels of statistical significance.
Atherosclerosis 1983 Mar
PMID:The effect of alcohol on serum high density lipoprotein (HDL). A controlled experiment. 640 57

Few papers have been devoted to the study of apolipoprotein A-II (apo A-II), one of the major peptides contained in HDL, probably because of the methodological difficulties associated with its assay. The aim of this study is to provide the clinical biochemist with a simply easy to use assay technique. We have been able to demonstrate the practical value of apo A-II assay in hepatology and in the detection of excessive drinkers. On the other hand, our results indicate that apo A-II is not a parameter of choice for the detection of coronary atherosclerosis.
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PMID:[Assay of serum apolipoprotein A-II by electro-immunodiffusion on ready-for-use plates. Clinical applications]. 643 81

This study describes a variant of hypo-alpha-lipoproteinemia in a 57-year-old male patient. The total plasma cholesterol level was 258 mg/dl with 64% in esterified form. The concentration of triglycerides was 205 mg/dl. The lipoprotein electrophoretic pattern revealed the absence of alpha-lipoproteins, whereas the other lipoproteins showed an intermediate electrophoretic mobility. The concentration of HDL cholesterol (heparin: MgCl2 precipitation) was extremely low (3 mg/dl). The activity of lecithin; cholesterol acyltransferase (LCAT) and the postheparinlipolytic activity were within the normal range. Determination of apolipoproteins revealed a marked deficiency of both apoprotein A-I (17 mg/dl) and apolipoprotein A-II (11 mg/dl). The concentration of apolipoprotein-B was elevated (186 mg/dl). Unlike the clinical manifestations of Tangier disease, our patient did not show skin lesion, abnormal tonsils, hepatosplenomegaly, peripheral neurologic abnormalities or corneal deposits. Also in contrast to Tangier disease our patient had coronary artery disease with myocardial infarction accompanied with severe occlusive peripheral arterial disease.
Atherosclerosis 1982 Mar
PMID:Hypoalpha-hyperbeta-lipoproteinemia in a patient with coronary artery disease and occlusive peripheral arterial disease. 708 13

In this study the lipoprotein and apoprotein patterns of patients with coronary artery disease were evaluated. The patient population consisted of 179 men who underwent coronary arteriography. On the basis of the results of coronary arteriography these patients were subdivided into a control group (score 0) with normal arteriograms and three groups each having coronary artery disease (CAD) of increasing severity (scores 1 to 3). The patients with coronary artery disease had significantly higher plasma concentrations of total cholesterol, LDL cholesterol, triglycerides and apolipoprotein B (apo B) than the controls. HDL cholesterol as well as apolipoprotein A-I (apo A-I) were significantly lower in patients with coronary artery disease. However, no difference was found in apolipoprotein A-II (apo A-II) values. Apo B and LDL cholesterol increased with the degree of coronary atherosclerosis. In the discriminant function analysis, apo B was the best separating parameter between control patients and CAD patients (scores 1-3).
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PMID:Lipoprotein and apoprotein values in coronary angiography patients. 746 94

A dimorphic MspI RFLP (alleles M1 and M2) in an Alu unit 528 base pairs downstream from the apolipoprotein A-II gene on chromosome 1 was investigated for associations with dyslipoproteinaemia or coronary atherosclerosis. No significant differences were observed between the allele frequencies in healthy random controls (M2 = 0.850, n = 70) and patients with primary hypertriglyceridaemia (M2 = 0.846, n = 52) or severe coronary atherosclerosis (M2 = 0.819, n = 47). The apolipoprotein A-II gene may also contribute to the regulation of plasma levels or composition of HDL in response to environmental changes. To study the effect upon apolipoprotein A-II variability, 42 monozygotic twin pairs were genotyped for the MspI RFLP. Pairs with the genotype M2M2 (n = 28) had significantly smaller within-pair differences in plasma apolipoprotein A-II levels (2.2 vs 5.8 mg/dl, P < 0.02; Mann-Whitney) than those with other genotypes (n = 14). The M2 allele may be in linkage disequilibrium with a functional mutation that restricts the variability of plasma apolipoprotein A-II in response to environmental conditions. This provides a new example of a 'variability' gene, one of an important group of loci which may alter responses to hypolipidaemic therapy and cardiovascular risk.
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PMID:Variability of plasma apolipoprotein (apo) A-II levels associated with an apo A-II gene polymorphism in monozygotic twin pairs. 767 6

Quantitative trait locus (QTL) analysis is a statistical method that can be applied to identify loci making a significant impact on a phenotype. For the phenotype of susceptibility to diet-induced atherosclerosis in the mouse, we have studied four quantitative traits: area of aortic fatty streaks and serum concentrations of high-density lipoprotein-bound cholesterol (HDL-cholesterol), apolipoprotein A-I, and apolipoprotein A-II (apo A-II). QTL analysis revealed a significant locus on chromosome 1 distal impacting serum apo A-II concentration on a high-fat diet and serum HDL-cholesterol concentration on a chow diet. This locus is presumably Apoa-2, the structural gene for apo A-II. QTL analysis of aortic fatty streaks failed to reveal a significant locus.
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PMID:Quantitative trait locus analysis of susceptibility to diet-induced atherosclerosis in recombinant inbred mice. 774 56

The inverse relationship between HDL and apolipoprotein A-I concentrations and the risk for premature atherosclerosis is well established, but the mechanism whereby apolipoprotein A-I offers protection is still somewhat elusive. Recent studies suggest that a specific subpopulation within the lipoprotein (AI) subclass may be more effective than others in promoting cholesterol efflux from cells. In addition, it appears that the lipid-free form of apolipoprotein A-I may have an important role in the antiatherosclerotic process. Unique new functions of apolipoprotein A-I-containing particles in modulating cytokines and lipid hydroperoxide transport, together with their role in antiatherogenesis, are also discussed. Current research with transgenic mice, however, indicates that apolipoprotein A-II must be taken into consideration in understanding the development of atherosclerosis, because it appears to be a potent antagonist for the protective properties of apolipoprotein A-I.
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PMID:The role of apolipoprotein A-I-containing lipoproteins in atherosclerosis. 785 10

High-density lipoprotein (HDL) contains two major proteins, apolipoprotein A-I (apoA-I) and apolipoprotein A-II (apoA-II), comprising about 70% and 20% of the total HDL protein mass, respectively. HDL exists in human plasma in two main forms, one containing apoA-I with apoA-II (AI/AII-HDL) and another containing apoA-I without apoA-II (AI-HDL). A strong inverse relationship exists between total plasma HDL concentration and atherosclerosis, but the results of studies examining the relationship between AI-HDL and AI/AII-HDL and atherosclerosis have been conflicting. To determine whether these two HDL populations have different effects on atherogenesis, human apoA-I (AI) and human apoA-I and apoA-II (AI/AII) transgenic mice were produced in an atherosclerosis-susceptible strain. Following an atherogenic diet, despite similar total cholesterol and HDL cholesterol concentrations, the area of atherogenic lesions in the AI/AII mice was 15-fold greater than in the AI animals. These studies show that the protein composition of HDL significantly affects its role in atherogenesis and that AI-HDL is more antiatherogenic than AI/AII-HDL.
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PMID:Protein composition determines the anti-atherogenic properties of HDL in transgenic mice. 841 56

The plasma concentration, particle size, and chemical composition of high density lipoproteins (HDLs) are associated with the metabolism of triglyceride-rich lipoproteins (TGRLs). During alimentary lipemia there is active exchange of lipids and apolipoproteins between HDL and apolipoprotein B-containing lipoproteins. Whereas HDL has been assigned a protective role against the development of atherosclerosis, alimentary lipemia has been proposed to represent a potentially atherogenic state. We examined plasma HDL concentration, particle size, and composition and their relations to postprandial TGRLs in 32 postinfarction patients and 10 healthy control subjects after intake of a standardized oral fat load of a mixed-meal type. All patients had undergone coronary angiographies in connection with the myocardial infarction and around 5 years thereafter. The plasma HDL cholesterol concentration decreased significantly in response to the oral fat load, particularly in hypertriglyceridemic patients, with a concomitant increase of HDL triglycerides. A limited and reversible yet consistent increase of HDL particle size (1-2%) was seen 6 hours after intake of the oral fat load on nondenaturing gradient gel electrophoresis (GGE) in both patients and control subjects. Virtually no changes in the plasma concentration of HDL GGE subclasses, lipoproteins containing apolipoprotein A-I but no apolipoprotein A-II (LpA-I), or lipoproteins containing both apolipoproteins A-I and A-II (LpA-I:A-II) were induced in the postprandial state despite massive increases of large very low density lipoprotein (VLDL) and large chylomicron remnant levels (determined as apolipoproteins B-100 and B-48 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis). Strong inverse correlations with fasting plasma HDL cholesterol and the larger HDL GGE subspecies were found for large postprandial VLDL and large chylomicron remnants, whereas the corresponding relations for small VLDL and small chylomicron remnants were weaker. The relations of both large and small VLDL and chylomicron remnants to HDL cholesterol were confined to subjects in the lower fasting plasma HDL cholesterol range (< 1.2 mmol/l). None of the HDL parameters measured, either in the fasting or in the postprandial state (HDL cholesterol, HDL triglycerides, HDL GGE subclasses, LpA-I, and LpA-I:A-II), were related to the development of coronary atherosclerosis, whereas the postprandial plasma levels of small chylomicron remnants, which showed weak negative correlations with HDL, related positively to the progression of coronary atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:HDLs and alimentary lipemia. Studies in men with previous myocardial infarction at a young age. 842 32


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