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)

Concentrations of HDL cholesterol, apolipoprotein (apo) A-I and apo A-II were found to be significantly decreased in patients with insulin-dependent diabetes (IDD) and non-insulin-dependent diabetes (NIDD) compared with carefully selected controls matched for sex, age and body weight. LDL cholesterol and apo B levels did not differ significantly between diabetics and controls. Concentrations of lipoprotein Lp(a), an independent risk factor for coronary artery disease in non-diabetics, were above 20 mg/dl in only 14% of diabetics and in 5% of controls. LCAT activity was normal in diabetics, irrespective of type of diabetes, sex and age of patients. No correlation between HbA1 and either HDL cholesterol or A-I and A-II was found in IDD and NIDD. A positive correlation between HbA1 and either triglyceride or VLDL triglyceride was noted in IDD and NIDD. There was also a positive correlation between insulin dosage in IDD and HDL cholesterol, apolipoprotein A-I and A-II.
Atherosclerosis 1983 Dec
PMID:Apolipoproteins (A-I, A-II, B), Lp(a) lipoprotein and lecithin: cholesterol acyltransferase activity in diabetes mellitus. 622 55

Lp(a) concentrations, apolipoprotein A-I and B, and various lipid parameters were measured from members of 3 families in which myocardial infarction frequently occurred. No correlation could be found between Lp(a) concentration and other lipoprotein parameters. It has been demonstrated that myocardial infarction and atherosclerotic diseases occur only in patients with Lp(a) concentrations higher than 70 mg/dl. An unfavourable Apo B/Apo A-I relation or LDL/HDL relation, associated with high Lp(a) concentration seems to play a decisive role in the development of atherosclerosis or myocardial infarction. The study suggests that subjects with Lp(a) values higher than 100 mg/dl could suffer from a special form of hyperlipoproteinemia ("Hyper-Lp(a)").
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PMID:[Lipoprotein Lp(a) as a risk factor for heart infarct--a family study]. 623 58

It has recently been suggested that polymorphisms in the human apolipoprotein A-I (apo A-I) gene locus may be related to the development of premature atherosclerosis and hypertriglyceridaemia. To understand if and how these polymorphisms affect apo A-I gene expression, we studied the genomic sequences flanking the apo A-I gene. Here we show the presence of another apolipoprotein gene, apolipoprotein C-III (apo C-III), approximately 2.6 kilobases (kb) downstream of the 3' end of the apo A-I gene. We also show that the apo A-I and apo C-III genes are convergently transcribed and that a polymorphism previously reported to be associated with hypertriglyceridaemia may be due to a single base pair substitution in the 3'-noncoding region of apo C-III mRNA.
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PMID:Linkage of human apolipoproteins A-I and C-III genes. 630 58

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

We have recently shown that an inherited polymorphism occurring in the human apolipoprotein A-I (apo A-I) gene is related to decreased high density lipoprotein and apo A-I levels in the plasma of two patients with severe premature atherosclerosis. Analysis of the molecular basis of this polymorphism and its possible effects on apo A-I gene expression requires direct comparison of both normal and polymorphic apo A-I alleles. Here we report the isolation and characterization of the normal human apo A-I gene and we show that the gene is interrupted by three intervening sequences, IVS-1, IVS-2, and IVS-3, occurring in the 5' noncoding region of apo A-I mRNA, the mRNA sequence coding for the signal peptide of apo A-I, and the sequence coding for the mature protein, respectively. In addition, the nucleotide sequence analysis of the apo A-I gene allowed determination of the complete amino acid sequence of the primary translation product of apo A-I mRNA. This amino acid sequence consists of 267 residues including a 24-residue-long amino-terminal extension (preprosegment). Finally, we show that the apo A-I gene contains six 66-base-pair-long tandemly repeated DNA segments, which suggests that the gene may have evolved by intragenic duplication events.
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PMID:Isolation and characterization of the human apolipoprotein A-I gene. 641 73

Eight subjects, belonging to a large family kindred repeatedly showing the electrophoretic pattern of the "double pre-beta lipoproteinemia", were studied. In seven of them thyroid function, serum lipids and apolipoprotein A-I were determined before and after treatment with dextro-thyroxine, preparation almost free of levo-thyroxine. In most of the patients, total-T4 levels and free-T4 Index were in the lower normal range, but basal TSH levels and the TSH response to TRH were normal. Dextro-thyroxine was effective in reducing both serum total cholesterol and triglycerides, but the percentage decrease in serum triglycerides was definitely greater than that of serum total cholesterol. This marked, unexpected hypotriglyceridemic effect is similar to that observed in a group of obese, hypertriglyceridemic hypothyroid patients treated with levo-thyroxine. Besides serum total cholesterol and triglycerides, the VLDL cholesterol/triglycerides ratio and the electrophoretic "slow moving" pre-beta component were also significantly reduced after treatment, suggesting that dextro-thyroxine can remove efficiently "remnant" VLDL particles from the plasma. Following dextro-thyroxine therapy, the relatively low pretreatment values of apolipoprotein A-I were significantly increased, being restored to normal.
Atherosclerosis 1984 Feb
PMID:Effects of dextro-thyroxine, a preparation almost free of levo-thyroxine, on thyroid function, serum lipids and apolipoprotein A-I in "double pre-beta lipoproteinemia". 642 87

The purpose of this study was to establish whether women with peripheral arterial disease can be distinguished from controls on the basis of plasma lipid and apolipoprotein profiles. One group of patients with peripheral arterial disease (n = 20) was characterized by a localized aortic stenosis referred to as the 'small aorta syndrome' (SAS). The other group of patients with peripheral arterial disease (n = 23) had a diffuse segmental pattern of stenoses referred to as the 'stenosing peripheral arterial disease' (SPAD). After correcting for the effects of age and body mass index, the SAS group had elevated plasma total cholesterol (TC) levels when compared to normal controls (P less than or equal to 0.008), while the SPAD group had triacylglycerol (TG) levels different from controls (P = 0.02). Both groups of patients were characterized by reduced levels of apolipoprotein A-I (P less than or equal to 0.04) and increased levels of apolipoprotein C-III (P less than or equal to 0.002). Apolipoproteins B and E were also elevated in both groups of patients but not significantly. Mutivariate analyses indicated that the A-I/C-III ratio correctly discriminated 97.8% of the SAS and the A-I/C-III ratio plus A-I discriminated 89.8% of the SPAD patient from the controls. In addition, multivariate analyses showed that the variables age, TC/Apo B, Apo B/C-III and TG/C-III discriminated SPAD from SAS patients with a correct classification of 93.2%. Results of this study showed that the measurement of apolipoproteins A-I, B and C-III in conjunction with TC and TG is of potential use for differentiating patients with peripheral arterial disease from normal controls as well as for distinguishing patients with SAS from those with SPAD. It seems that particular patterns of peripheral arterial disease in women may be associated with slightly different alterations in the plasma lipoprotein system.
Atherosclerosis 1984 Mar
PMID:Plasma lipid and apolipoprotein profiles of women with two types of peripheral arterial disease. 642 91

This review assesses current knowledge of the clinical, genetic, and biochemical features of familial high density lipoprotein (HDL) deficiency syndromes. The focus is on HDL deficiency states occurring in the absence of severe hypertriglyceridemia or lecithin/cholesterol acyltransferase deficiency. Specific entities falling within this category include Tangier disease, familial HDL deficiency with planar xanthomas, familial apolipoprotein A-I and C-III deficiency (formerly known as apolipoprotein A-I absence), familial deficiency of apolipoprotein A-I and C-III, fish-eye disease, familial hypoalphalipoproteinemia, and apolipoprotein A-I variants (apo A-I Milano, apo A-I Marburg, apo A-I Giessen, and apo A-I Munster 1-3). Diffuse corneal opacification and premature coronary artery disease are common features in many of these kindreds. No striking clinical abnormalities have been noted in patients with currently known apolipoprotein A-I variants, possibly because these subjects are heterozygotes for their respective defects. The HDL deficiency in many of these disorders has been associated with abnormalities or deficiencies of apolipoprotein A-I. Further research will undoubtedly define the defects in all the disorders that have been described, uncover new mutations, as well as provide additional insights into the precise relationship between HDL deficiency and atherosclerosis.
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PMID:Clinical, biochemical, and genetic features in familial disorders of high density lipoprotein deficiency. 643 53

In a prospective, controlled study, the influence of strenuous physical exercise on plasma total cholesterol, HDL cholesterol, apolipoprotein A-I, total triglycerides and fatty acid composition of adipose tissue was studied during 7 months of training in 15 senior oarsmen and 21 controls matched for age, smoking and drinking habits. Dietary intake was monitored. At the start of the study there were no differences in lipid parameters and adipose tissue composition between oarsmen and controls. A significant decrease in total cholesterol and total triglycerides and an increase in HDL cholesterol and apolipoprotein A-I was noted in the oarsmen after only 2 weeks of training. Body weight remained stable but skin-fold thickness decreased. Food consumption increased considerably but diet composition remained unchanged. Nevertheless the fatty acid pattern of adipose tissue changed significantly, as a result of altered preferential endogenous fatty acid synthesis and/or fatty acid oxidation. Since lipid parameters and adipose tissue composition were equal in oarsmen and controls before the start of the training, it is concluded that the changes induced by exercise only last for the duration of the training period.
Atherosclerosis 1984 Oct
PMID:Effect of physical exercise on blood lipids and adipose tissue composition in young healthy men. 643 18

A lipoprotein species with ultracentrifugal flotation rates (F0(1.20) 9-28) intermediate to high density lipoproteins (HDL, F0(1.20) 0-9) and low density lipoproteins (LDL, F0(1.20) 28-56) found in the plasma of certain pedigreed baboons fed an atherogenic diet was studied by gradient gel electrophoresis (GGE) and ultracentrifugal techniques. These lipoproteins were found to be heterogeneous in size (125-220 A) and hydrated density (1.028-1.080 g/ml). The major apolipoprotein in all density subfractions of the F0(1.20) 9-28 lipoproteins exhibited the molecular weight (2.8 X 10(4) daltons) and immunochemical properties of apolipoprotein A-I (apoA-I). Protein corresponding to apolipoprotein E (apoE, 3.5 X 10(4) daltons) was observed primarily in the less dense subspecies of F0(1.20) 9-28 lipoproteins. Some low molecular weight (1.8 X 10(4), 1.3 X 10(4), and 1.1 X 10(4) daltons) apolipoproteins were also detected. At low serum F0(1.20) 9-28 lipoprotein concentrations, only the smaller, more dense, protein-rich species were present; at higher F0(1.20) 9-28 concentrations, the larger, less dense species were observed in addition to the small species. The HDL of pedigreed baboons in families with and without serum F0(1.20) 9-28 lipoproteins were also characterized. The HDL of both groups of progeny consisted of a similar set of 5 subpopulations designated HDL-I through HDL-V determined by GGE. HDL-I, consisting of material 100-125 A in size, was the major HDL subpopulation. ApoA-I was the major protein moiety in all HDL subpopulations; none contained apoE. Baboons in families with F0(1.20) 9-28 lipoproteins had more HLD-I (292 +/- 80 mg/dl vs. 235 +/- 55 mg/dl) and less HDL-II (86 +/- 22 mg/dl vs. 135 +/- 34 mg/dl) than baboons in families without F0(1.20) 9-28 lipoproteins; both groups showed identical total HDL concentrations (446 +/- 90 mg/dl and 444 +/- 49 mg/dl, respectively). Among those baboons in families with F0(1.20) 9-28 lipoproteins, there was an inverse correlation between F0(1.20) 9-28 concentration and total HDL, HDL-I and HDL-II concentrations, indicating a possible metabolic relationship between these HDL subpopulations and the F0(1.20) 9-28 species.
Atherosclerosis 1984 Jul
PMID:Characterization of HDL and lipoproteins intermediate to LDL and HDL in the serum of pedigreed baboons fed an atherogenic diet. 646 14


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