Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A competitive enzyme-linked immunoassay (CELIA) technique for quantitative measurement of apolipoprotein B (Apo B) was developed. The method is a non-isotopic immunoassay that utilizes a soluble enzyme/antibody complex as a universal labeling reagent. The method was characterized according to precision, sensitivity, recovery and parallelism. The CELIA Apo B method was compared to a commercially available laser nephelometric immunoassay. We found that the nephelometric results were highly correlated with triglyceride levels and the nephelometric assay was susceptible to interference from lipemia or turbidity. The range of values obtained on 56 apparently healthy, fasting young adults was 0.35-1.25 g/l by the CELIA method and 0.40-1.00 g/l by the nephelometric immunoassay. The nephelometric method was more precise (coefficient of variation 5%) than the CELIA technique (CV 10%); however, the CELIA method seems to be less sensitive to interferences.
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PMID:Examination of a competitive enzyme-linked immunoassay (CELIA) technique and a laser nephelometric immunoassay technique for the measurement of apolipoprotein B. 636 Apr 30

Plasma low density lipoprotein (LDL) kinetics and their relation to plasma very low density lipoprotein (VLDL) and LDL composition were determined in patients with familial combined hyperlipidemia (FCHL) of varying lipoprotein phenotypes. In both Type II and IV subjects, LDL apolipoprotein B (apo B) synthesis was greater than normal. In Type IV, the VLDL triglyceride/apo B ratio was normal and almost all of the LDL apo B was derived from VLDL. LDL cholesterol/apo B ratio was diminished and LDL apo B fractional catabolic rate (FCR) was sufficiently increased to prevent a rise in plasma LDL concentration. In Type II, VLDL triglyceride/apo B was reduced and 14% to 50% of the LDL was formed by direct synthesis. LDL cholesterol/apo B was normal and LDL apo B FCR was lower than in Type IV subjects. In four patients whose plasma lipid levels became normal with carbohydrate restriction and intake of a fibric acid derivative, plasma VLDL and LDL composition and LDL kinetic measurements remained unchanged. By contrast, VLDL triglyceride-apo B decreased and direct LDL synthesis increased in four patients whose phenotype changed to Type IIa. LDL cholesterol/apo B also increased and LDL FCR declined. Among patients with FCHL, significant correlations between VLDL triglyceride/apo B, LDL apo B derived by direct synthesis, LDL cholesterol/apo B, and LDL apo B FCR were found. Thus, increased apo B synthesis is a characteristic feature of FCHL. The phenotypic expression is determined by the availability of triglyceride for hepatic coupling to apo B which could influence the source, composition, and removal rate of circulating LDL. Despite normalization of their plasma lipid levels, some patients continued to show the compositional and kinetic features of FCHL.
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PMID:Low density lipoprotein metabolism in familial combined hyperlipidemia. Mechanism of the multiple lipoprotein phenotypic expression. 650 36

Total cholesterol, total triglyceride and high density lipoprotein (HDL) cholesterol and their relation to arteriosclerotic cardiovascular disease (ASCVD) were investigated in a population of Polynesian Maoris in Rarotonga who are becoming increasingly westernized. 8.5% of the population had plasma triglyceride elevations (triglyceride greater than or equal to 200 mg/dl), and the occurrence of hypertriglyceridemia was significantly higher in males than females. 5.8% of the population had elevations of total cholesterol (cholesterol greater than or equal to 250 mg/dl), and the proportion with elevation of total cholesterol was similar for males and females. 3.2% of the population had elevations of both triglyceride and cholesterol. HDL cholesterol concentrations were relatively low, and no sex differences were observed at any age. Analysis of lipoprotein cholesterol and triglyceride in a subset of those who had hyperlipemia indicated that the elevations of total cholesterol and triglyceride were mainly due to elevations of low density lipoprotein (LDL) cholesterol and very low density lipoprotein (VLDL) triglyceride, respectively; furthermore, elevations of VLDL triglyceride and LDL cholesterol were significantly correlated with increase in VLDL apolipoprotein B (apo B) and LDL apo B, respectively. Although an appreciable prevalence of diabetes was observed in this population (male: 6.7%, female: 8.4%), the diabetes could not account for the hyperlipemia. Among 693 subjects between the ages of 30 and 59 years, approx. 3% of males and 1% of females had Q-wave changes, and 16% of females and 4% of males had ST-T changes. Among males with Q-wave abnormalities, hyperlipemia was more frequent. There was also increased frequency of hypertension in those with elevated lipids. The data indicate the occurrence of some hyperlipemia in this population which could be of the familial-combined type; the elevated plasma lipids may contribute to the increased frequency of coronary heart disease.
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PMID:Hyperlipemia and arteriosclerotic cardiovascular disease in the Polynesian population of Rarotonga. 652 46

Autologous 131I-labelled very low density lipoprotein (VLDL) and 125I-labelled low density lipoprotein (LDL) were injected into seven normal subjects and into forty-three hyperlipidaemic patients, classified into groups on the basis of family studies and clinical findings, to quantitate VLDL and LDL apolipoprotein B kinetics. In normal subjects, mean VLDL-B peptide synthetic rate was 15 . 1 mg kg-1 day-1, mean LDL-B peptide synthetic rate 7 . 7 mg kg-1 day-1 and mean LDL-B fractional catabolic rate (FCR) 0 . 31 day-1. In heterozygous familial hypercholesterolaemia (n = 14) VLDL-B peptide production was normal in patients with normal triglyceride levels; in those with high triglyceride levels there was either VLDL overproduction or a catabolic defect. LDL-B peptide synthetic rates ranged from high normal to increased (8 . 5--18 . 0 mg kg-1 day-1) and LDL-B peptide FCR values were markedly reduced (0 . 14--0 . 28 day-1) confirming the presence of a defect in LDL catabolism but indicating over-production as well. In familial combined hyperlipidaemia (n = 11) VLDL-B peptide production ranged from normal to elevated (13 . 9--44 . 4 mg kg-1 day-1, mean 23 . 8 mg kg-1 day-1) correlating with the VLDl triglyceride level (i.e. with the phenotypic expression of the disorder). LDL-B peptide production ranged from high normal to markedly increased (8 . 9--19 . 5 mg kg-1 day-1, mean 12 . 2 mg kg-1 day-1) and correlated with LDL cholesterol levels (i.e. the phenotype), (r = +0 . 66, P < 0 . 05). Three patients with unclassified hypercholesterolaemia had increased LDL-B peptide synthetic rates. One patient with remnant hyperlipoproteinaemia (type III) had a high normal VLDL-B peptide synthetic rate, 17 . 3 mg kg-1 day-1, and a strikingly low FCR of VLDL-B. In familial hypertriglyceridaemia (three patients) there was a low VLDL-B peptide FCR. In unclassified hypertriglyceridaemia VLDL over-production was the finding in seven patients but four patients appeared to have catabolic defects only. Overall there were significant hyperbolic relationships between VLCL-B peptide FCR and VLDL-B peptide concentration (r = -0 . 78, P < 0 . 001, for the log/log relationship) and between LDL-B peptide FCR and LDL cholesterol (r = -0 . 88, P < 0 . 001 for the log/log relationship.)
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PMID:Kinetic bases of the primary hyperlipidaemias: studies of apolipoprotein B turnover in genetically defined subjects. 678 Mar 64

Apolipoprotein E isomorphs in very low density lipoproteins and apolipoprotein B of low density lipoproteins were measured in the plasma of normolipidemic subjects with xanthelasmas of the eyelids and in appropriate control groups. All patients tested in the experimental group had an apolipoprotein EII to apolipoprotein EIII ratio typical of the heterozygous state for familial dysbetalipoproteinemia, a hyperapobetalipoproteinemia, or both. Some patients had concomitant atherosclerosis. This is the first report of an increased frequency of the apolipoprotein E-ND phenotype in normolipidemic xanthelasma. This condition should not be dismissed as benign; tissue lipid deposition in the absence of hyperlipidemia might be related to the presence of lipoproteins of abnormal composition with an enhanced atherogenic potential.
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PMID:Increased Frequency of Apo E-ND phenotype and hyperapobeta-lipoproteinemia in normolipidemic subjects with xanthelasmas of the eyelids. 705 63

Previous studies have suggested that exposure to heavy metals may be a risk factor in coronary atherosclerotic heart disease in humans as well as in experimental animals. Little is known however on the mechanism underlying the effect of heavy metals on the development of atherosclerosis. In this study we tried to ascertain whether exposure to lead might: (a) alter plasma lipoprotein in normally fed rabbits; and (b) aggravate the hyperlipidemia usually found in cholesterol-fed animals. Rabbits were fed a normal diet or a diet containing 1% cholesterol in the presence or in the absence of 0.5% of lead subacetate for 45 days. This produced an accumulation of lead in plasma and bone. While in cholesterol-fed rabbits, lead exposure did not modify the plasma lipoprotein pattern, in normally fed animals it induced a striking elevation of cholesterol esters. This was associated with an increased concentration of VLDL (1.006 g/ml), LDL1 (1.006-1.020 g/ml), LDL2 (1.020-1.050 g/ml) and HDL1 (1.050-1.210 g/ml). These lipoproteins had an elevated content of cholesterol esters and apolipoprotein B. It is suggested that some of these lipoproteins may be important in the development of atherosclerosis in subjects chronically exposed to lead.
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PMID:Heavy metals and experimental atherosclerosis. Effect of lead intoxication on rabbit plasma lipoproteins. 715 95

In order to investigate the known associations between hyperlipidaemia and various rheumatic complaints, immune arthritis and hyperlipidaemia have been induced concurrently in rabbits. The results obtained show that: (1) Rabbit apolipoprotein B-containing lipoproteins (LpB), which are normally virtually excluded from joint fluid, gain access to the inflamed joint in the serous effusion and serve as intrinsic indicators of altered local permeability to macromolecules. (2) Much of the LpB entering the joint space is taken up by the phagocytic cells and, following intracellular hydrolysis, leaves a lipid residue. In some chronically affected joints these residues are modified so as to give rise to crystalline cholesterol and its esters. Such crystals may serve as a chronic irritant in the joint. (3) In addition intact LpB is found sequestered in the superficial layers of intra-articular collagenous structures of the challenged joint in a distribution identical with that of similarly sequestered immune complexes and complement, suggesting altered permeability of these intra-articular structures also.
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PMID:Studies on increased vascular permeability in the pathogenesis of lesions of connective tissue diseases: I. Experimental hyperlipidaemia and immune arthropathy. 743 81

A large segment of the population gradually develops insulin resistance, and the related metabolic syndrome is one of the most frequent causes of atherosclerosis. Searching for a practical indicator of insulin resistance, we studied the correlations between fasting serum insulin level, the general manifestations of insulin resistance syndrome, and various aspects of coronary artery disease in 797 men and 322 women. After we classified patients according to the quartiles of serum insulin level, we noted in the top quartile the presence of practically all manifestations of insulin resistance syndrome in persons of both sexes (e.g., increased waist/hip ratio, body mass index, glucose, uric acid, triglycerides, apolipoprotein B and decreased high-density lipoprotein cholesterol levels as well as apolipoprotein A-I/B ratios, and so forth). We also noted a higher prevalence of hypertension, diabetes mellitus, and type IV hyperlipidemia. Significantly more women in the fourth than in the first quartile had angiographically documented significant stenosis of the coronary arteries (p = 0.0016, odds ratio 2.9, 95% confidence interval 1.5 to 5.6) and previous myocardial infarction (p = 0.0297, odds ratio 2.1, 95% confidence interval 1.1 to 4.1). Men in both the first and the fourth quartile had a more disturbed lipid profile and a higher prevalence of significant stenoses of coronary arteries and/or previous myocardial infarction than women; there was a tendency toward a lower prevalence of alcohol consumption (p = 0.0503), a higher prevalence of gout (p = 0.0634), and previous myocardial infarction (p = 0.0791) in men in the fourth than in the first quartile.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fasting hyperinsulinism, insulin resistance syndrome, and coronary artery disease in men and women. 748 1

The efficacy of pravastatin (CAS 81131-70-6) on serum lipid levels in 91 type 2 diabetic patients with mean glycosylated hemoglobin of 8.5% was investigated up to 12 weeks. Oral administration of 10 to 20 mg/d of pravastatin significantly decreased total cholesterol by 18.4 +/- 1.5% after 4 weeks. When analyzed separately in type IIa and IIb hyperlipidemia, the reduction of total cholesterol by pravastatin was more prominent in the former. Low-density lipoprotein cholesterol were also significantly decreased 22.2 +/- 2.7% after 4 weeks. The effect of pravastatin in reducing triglyceride was more prominent in patients with higher triglyceride compared to those with lower triglyceride before the administration of the drug. High-density lipoprotein cholesterol showed a slight but significant increase by 4.2 +/- 1.9% after 4 weeks. Among the apolipoproteins examined, apolipoprotein B was significantly decreased after 4 weeks. Atherogenic index and apolipoprotein B/apolipoprotein A-I ratio were also significantly decreased after 4 weeks. The efficacy of pravastatin was also observed after 12 weeks to the same extent as after 4 weeks. No major side effects or abnormalities of laboratory parameters have been observed. These data lead to the conclusion that pravastatin is useful for the treatment of hyperlipidemia in type 2 diabetic patients with poor glycemic control without major adverse effects.
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PMID:Clinical efficacy of pravastatin for hyperlipidemia in patients with type 2 diabetes mellitus. 764 75

The aim was to identify genetic determinants for the development of hyperlipidemia and/or atherosclerosis. The present set of studies demonstrates for the first time the clinical expression (phenotype) of a newly discovered monogenic disorder named Familial Defective Apolipoprotein B-100 (FDB). FDB is caused by a G to A mutation in the binding protein (apolipoprotein B-100) for the cholesterol-rich low density lipoprotein (LDL), such that the affinity of LDL to the LDL receptor is severely reduced. In all 135 individuals with FDB from 56 families and 8 different countries, including Denmark, are described. On average, the effect of the FDB mutation was to increase plasma and LDL cholesterol in both men and women by about 3 mmol/l; at age 55 the average plasma cholesterol of men and women with FDB was 9.4 mmol/l and 8.9 mmol/l, respectively. A sharp rise in frequency of coronary artery disease as a function of age in both FDB males and females was comparable to that found in Familial Hypercholesterolemia (FH). At the age of 60, about 70% of both men and women with FDB had coronary artery disease; at the same age approximately 40% had tendon xanthomas, and 35% had arcus corneae, irrespective of gender. Surprisingly, the frequencies of arcus corneae were not strikingly higher than those found in the general population sample from the Copenhagen City Heart Study. Only few patients with FDB had xanthelasmas. Finally, the frequency of this mutation was estimated at 1/500-1/700 in the general population, which is equivalent to that of clinical FH. All in all the results suggest FDB to be a severe genetic disorder with early penetrance, associated with substantial elevations in plasma and LDL cholesterol and with an increased frequency of premature coronary artery disease and of tendon xanthomas. For comparison, a number of common polymorphisms in the 5'-flanking region of the insulin gene, in the apoB gene and in the apoAI-CIII-AIV gene cluster, associated with minor effects on hyperlipidemia and/or cardiovascular disease are also examined.
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PMID:Rare and common mutations in hyperlipidemia and atherosclerosis. With special reference to familial defective apolipoprotein B-100. 765 81


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