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)

Apolipoproteins are important in the structure and metabolism of lipoproteins, and alterations in levels of apoproteins or in their interrelations occur in some forms of hyperlipemia. Pregnancy is regularly accompanied by hyperlipoproteinemia, but while data on lipoprotein lipids is available, the apopipoproteins have not been studied. To characterize the lipemia of pregnancy more completely, we studied some of the apolipoproteins in plasmas of pregnancy women. Thirty-eight normal fasting women were studied between the 18th and 39th weeks of gestation and again 23 plus or minus 17 weeks after delivery. Eight additional women were sampled every 4-6 wk during the second and third trimesters of gestation. Plasma and lipoprotein lipids were assayed by standard procedures and Apolipoprotein B (ApoB) was measured by radioimmunoassay. The interrelations of Apolipoprotein A (ApoA) in high-density lipoprotein (HDL) and of Apolipoprotein C (ApoC) in very-low-density lipoprotein (VLDL) were assessed by disc gel electrophoresis in four women during the last trimester of gestation and again 6-8 mo post partum and in four nongravid controls. Gestational triglycerides (TG) and cholesterol (Chol) were elevated in 95% of the pregnant women. TG in lipoproteins rose progressively during gestation, with VLDL-TG rising the most. Low-density lipoprotein (LDL) and HDL became enriched by TG relative to other components. Total-and VLDL-ApoB increased, while LDL-ApoB remained unchanged, resulting in a change in the density distribution of ApoB. (VLDL-ApoB X 100/total ApoB rose from 3.6% to 6.7%, P less than 0.02.) The accumulation of TG-rich LDL and the increases of VLDL-ApoB may be the result of changes in the rates of secretion or intravascular catabolism of VLDL. Which process is altered remains to be determined. The relative amounts of ApoC-II and ApoC-III in VLDL and the ApoA-I/ApoA-II ratios in HDL were unchanged in pregnancy. These results differ from those seen following high-carbohydrate diets.
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PMID:Apolipoproteins in human pregnancy. 16 66

Apolipoprotein B XbaI polymorphism and apolipoprotein AI/CIII SstI polymorphism have been found to be associated with variations in serum lipoprotein levels. We investigated whether these gene polymorphisms are involved in determining the lipid-modulating action of gemfibrozil. Of the 221 male subjects with hyperlipidemia studied, 121 responded well to the treatment with more than a 25% reduction in the non-high-density lipoprotein cholesterol level, whereas 100 were nonresponders. Among responders, but not nonresponders, homozygosity for the apolipoprotein B X2 allele (XbaI site present) and heterozygosity for the apolipoprotein AI/CIII S2 allele (SstI site present) were associated with elevated baseline serum low-density lipoprotein cholesterol and triglyceride levels, respectively. However, the hypolipidemic effect of gemfibrozil among the responders was independent of these gene polymorphisms. These data indicate that common polymorphisms of the apolipoprotein B and apolipoprotein AI/CIII gene loci influence serum lipid levels by mechanisms that are amenable to an intervention with gemfibrozil.
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PMID:DNA polymorphisms of apolipoprotein B and AI/CIII genes and response to gemfibrozil treatment. 167 24

Hemodialysis (HD) patients have a high incidence of hyperlipidemia. Hypertriglyceridemia is the most frequent abnormality encountered. It results mainly from a defect in the degradation of triglycerides. The aim of this study was to evaluate the efficacy of a fish oil (Max-EPA) rich in polyunsaturated fatty acids (PUFA), such as eicosapantenoic acid (EPA), on lipid abnormalities of hemodialysis patients. Thirteen hyperlipidemic HD patients were investigated (7 males, 6 females; mean age 57 years; mean duration of HD 72 months). None were diabetic or treated with antihypertensive drugs. All patients had hypertriglyceridemia (greater than 200 mg/dl) and an increase (greater than 1) in the ratio of serum apolipoprotein B to serum apolipoprotein A1 (ApoB/ApoA1). They received for one month, 6 g/day of Max-EPA providing 1 g of EPA. After treatment, serum triglyceride levels fell by 38% from 231 +/- 40 (SD) mg/dl to 140 +/- 38 mg/dl (P less than 0.01). Total cholesterol did not change significantly (before therapy 241 +/- 33 mg/dl, after therapy 249 +/- 38 mg/dl). Apolipoprotein A1 levels (116 +/- 17 mg/dl) were not modified after therapy, 117 +/- 11 mg/dl. Apolipoprotein B decreased significantly from 182 +/- 26 mg/dl to 150 +/- 21 mg/dl after treatment (P less than 0.01). The ApoB/ApoA1 ratio showed a significant decrease from 1.56 +/- 0.26 to 1.3 +/- 0.16 after therapy (P less than 0.01). Also, the greatest reductions were found in the patients who had both the highest serum triglyceride levels and the highest ApoB/ApoA1 ratios. No side effects were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of fish oil rich in polyunsaturated fatty acids on hyperlipidemia of hemodialysis patients. 251 75

Plasma lipids and haemostasis were investigated in 17 patients with hyperlipidaemia before and after 6 weeks supplementation with 6 g n-3 fatty acids. Nine of the patients had type IIa and 8 had type IV hyperlipidaemia. No effect on plasma cholesterol, LDL- or HDL-cholesterol were seen, but plasma triglycerides decreased after n-3 supplementation. Apolipoprotein B increased and apolipoprotein A1 decreased after the oil supplement. The bleeding time was prolonged, but platelet aggregation was unaltered by n-3 fatty acids. Protein C activity increased in type IIa and decreased in type IV after the supplement. Fibrinolysis was markedly depressed while von Willebrand factor antigen was reduced after intake of n-3 fatty acids.
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PMID:The effect of n-3 fatty acids on lipids and haemostasis in patients with type IIa and type IV hyperlipidaemia. 281 27

The appearance and accumulation of apolipoprotein B and unesterified cholesterol in the lesion-prone areas of the aorta in rabbits with diet-induced hyperlipidemia were investigated by histo-, and cytochemical techniques. Apolipoprotein B was detected by an indirect immunoperoxidase procedure both in the light and electron microscopy. Unesterified cholesterol was revealed using filipin and tomatine as specific probes. In the prelesional stages of atherogenesis, before the appearance of any structurally detectable lesions, as demonstrated by bright-field and fluorescence microscopy, apolipoprotein B and free cholesterol accumulated progressively in the extracellular matrix of the subendothelial space. At ultrastructural level, extracellular phospholipid liposomes, unesterified cholesterol and apolipoprotein B concomitantly appeared and accumulated focally in the same areas. Apolipoprotein B was preferentially located on the outer surface of the free cholesterol-containing phospholipid lamellae of the extracellular liposomes. In the lesional stages leading to fatty streak formation, the extracellular liposomes, apolipoprotein B and unesterified cholesterol had also topographically a superimposed localization pattern. Intracellular apolipoprotein B and unesterified cholesterol were also colocalized in some intimal lipid-laden cells. In the prelesional stages of hyperlipidemia the prevalent localization of apolipoprotein B around individual unesterified cholesterol-rich extracellular phospholipid liposomes, progressively accumulating in the subendothelial space, suggests their possible origin from serum-derived lipoproteins.
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PMID:Prelesional events in atherogenesis. Colocalization of apolipoprotein B, unesterified cholesterol and extracellular phospholipid liposomes in the aorta of hyperlipidemic rabbit. 331 87

Lipoprotein metabolism was studied in eleven patients with Type III hyperlipoproteinaemia, one with normolipidaemic dysbetalipoproteinaemia and eight controls. Apolipoprotein B kinetics in very low density, intermediate density and low density lipoproteins (VLDL, IDL and LDL) was investigated. Fractional catabolic rates (FCRs) of VLDL-apo B and IDL-apo B were lower (P less than 0.005 and P less than 0.001) in the patients: 0.064 +/- 0.018 and 0.059 +/- 0.006 h-1 respectively, (mean +/- SEM), compared with 0.219 +/- 0.035 and 0.243 +/- 0.028 h-1. Synthetic rates (SRs) of IDL-apo B varied widely from 1.5 mg kg-1 day-1 in the subject with normolipidaemic dysbetalipoproteinaemia to 2.8-25.2 mg kg-1 day-1 in Type III. The mean time for conversion of IDL-apo B to LDL-apo B was prolonged, 18.7 h compared with 3.8 h in the controls (P less than 0.001). LDL-apo B pool size and SR were lower in the patients (P less than 0.05 for both). Two patients treated with gemfibrozil showed reduced hyperlipidaemia and decreased SR of VLDL-apo B and IDL-apo B. Dysbetalipoproteinaemia is associated with pronounced impairment of IDL and VLDL-remnant catabolism, lipoprotein levels reflecting an interaction between this defect and SR of these lipoproteins.
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PMID:Plasma apolipoprotein B metabolism in familial type III dysbetalipoproteinaemia. 392 66

It is well known that coronary heart disease (CHD) is multifactorial, with environmental and inherited risk factors both playing a role. Apolipoprotein B (apo B) is of major importance in lipoprotein metabolism and might play a central role in atherogenesis. The apo B gene is the obvious candidate gene to study the relations between lipid concentrations and CHD. Some rare mutations in the apo B gene affect plasma cholesterol levels, leading to either familial hypobetalipoproteinemia or familial defective apolipoprotein B100. Other frequent polymorphisms have little biological effect but, because of their high frequency, might contribute to the development of CHD in a given population. Many apo B gene polymorphisms are associated with variations in plasma lipid concentrations, including the response of plasma lipids to dietary intervention, and peripheral and coronary atherosclerosis. Age, body mass index and gender affect the degree and nature of the association between apo B genetic markers and normal lipid and lipoprotein levels. However, negative and contradictory results have also been reported. One likely explanation is differences between studies, including populations of different geographic origin, arbitrary definition of cases and controls and multiple criteria for CHD. Future work on the effect of the apo B locus on hyperlipidaemia and atherosclerosis must involve large numbers of patients belonging to carefully defined populations. Prospective studies using a combination of genetic markers in well-defined populations should lead to firm conclusions on the role of apo B in atherogenesis and coronary heart disease.
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PMID:[Genetic variation in the apolipoprotein B gene]. 862 6

Apolipoprotein B (apo B) plays a dominant role in cholesterol homeostasis. Several polymorphic sites within or adjacent to the gene locus for apo B have been detected. The X+ allele (XbaI restriction site present) of the XbaI restriction fragment polymorphism on the apo B gene has been found in some studies to be associated with higher serum cholesterol and/or triglyceride levels and with greater dietary response. The present study was designed to evaluate whether the apo B XbaI polymorphism was associated with the interindividual variability observed during postprandial lipemia. Fifty-one healthy young male volunteers [20 X-/X- (X-), and 31 X+/X- or X+/X+ (X+)], homozygotes for the apo E3 allele, were subjected to a vitamin A-fat load test. Subjects with the X- genotype had significantly greater retinyl palmitate (RP) and apo B-48 postprandial responses on both the large and the small TRL lipoprotein fractions compared with X+ subjects. In summary, subjects with the X-/X- genotype at the apo B locus have a greater postprandial response than X+ subjects. These differences observed in postprandial lipoprotein metabolism could explain some of the reported associations of this polymorphism to coronary heart disease risk.
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PMID:Dietary fat clearance in normal subjects is modulated by genetic variation at the apolipoprotein B gene locus. 932 75

Hyperlipidemia is a striking feature of nephrotic syndrome (NS) and the lipid profile seen in NS is accepted as atherogenic. Both low density lipoprotein (LDL) and very low density lipoprotein (VLDL) are apolipoprotein B-containing lipoproteins which are accepted as atherogenic. Oxidized-LDL (ox-LDL) has been suggested to play a fundamental role in atherogenesis. In this study, male Sprague-Dawley rats were made nephrotic by a single intraperitoneal injection of puromycin aminonucleoside (100 mg/kg body weight). We found significant elevation in serum triglycerides, total cholesterol, malondialdehyde, vitamin E levels and total cholesterol/vitamin E ratio and decrease in total protein and albumin levels in the NS group (n:8) compared with the control group (n:9). High density lipoprotein (HDL)-cholesterol and free fatty acid levels were not significantly different between these two groups. Apolipoprotein B-containing lipoproteins (non-HDL fraction) were separated by precipitation and amount of thiobarbituric acid-reactive substances (TBARS) of non-HDL fraction were measured after 60, 90, 120, 180 minutes of incubation with copper sulphate. TBARS levels of non-HDL fraction were significantly higher in the NS group compared with the control group at all of the time periods above. In nephrotic animals, the increased lipid peroxidation was influenced by serum lipids.
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PMID:Susceptibility of non-HDL fraction to oxidation in experimental nephrotic syndrome. 1040 Dec 26

Low-glycemic index diets are associated with a wide range of benefits when followed on a chronic basis. The chronic effects, however, of the substitution of 1 meal per day are not well known in diabetic subjects. Therefore, we aimed to evaluate whether the chronic use of a low-glycemic index breakfast (low-GIB) rich in low-GI carbohydrates and a modest amount of soluble fibers could have an effect on lipemia at a subsequent lunch, and improve glucose and lipid metabolism in men with type 2 diabetes. A total of 13 men with type 2 diabetes were randomly allocated in a double-blind cross-over design to a 4-week daily intake of a low-GI versus a high-GI breakfast separated by a 15-day washout interval. The low-GI breakfast was composed of whole grain bread and muesli containing 3 g beta-glucan from oats. Low-GIB induced lower postprandial plasma glucose peaks than the high-GIB at the beginning (baseline, P <.001) and after the 4-week intake (P <.001). The incremental area under the plasma glucose curve was also lower (P <.001, P <.01, baseline, and 4 weeks, respectively). There was no effect on fasting plasma glucose, insulin, fructosamine, or glycosylated hemoglobin (HbA(1c)). Fasting plasma cholesterol, as well as the incremental area under the cholesterol curve, were lower (P <.03, P <.02) after the 4-week low-GIB period than after the high-GIB period. Apolipoprotein B (apo B) was also decreased by the 4-week low-GIB. There was no effect of the low-GI breakfast on triacylglycerol excursions or glucose and insulin responses at the second meal. The high-GIB, however, tended to decrease the amount of mRNA of leptin in abdominal adipose tissue, but had no effect on peroxisome proliferator-activated receptor gamma (PPARgamma) and cholesterylester transfer protein (CETP) mRNA amounts. In conclusion, the intake of a low-GI breakfast containing a modest amount (3 g) of beta-glucan for 4 weeks allowed good glycemic control and induced low plasma cholesterol levels in men with type 2 diabetes. The decrease in plasma cholesterol associated with low-GI breakfast intake may reduce the risk of developing cardiovascular complications in subjects with type 2 diabetes.
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PMID:Four-week low-glycemic index breakfast with a modest amount of soluble fibers in type 2 diabetic men. 1207 24


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