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)

The results of plasma lipid and lipoprotein analysis in two related patients, brother (R.U.) and sister (R.R.) with analbuminemia, and three first-degree relatives (parents and sister) are reported. Both patients showed a remarkable increase in cholesterol and phospholipid levels, and there was a corresponding increase in serum apo B and apo A-I. This hyperlipidemia is due to a selective increase in LDL and HDL concentrations. R.U. showed an increase in both HDL2- and HDL3-cholesterol, R.R. only in HDL3-cholesterol. VLDL concentration was reduced in R.U. and normal in R.R. The plasma lipoprotein electrophoretic pattern did not correspond to any of the phenotypes in Fredrickson's classification. Composition of the different lipoprotein fractions was normal in the patients and family members. Serum FFA level in R.R. was very low. An increase in the plasma protein fractions, particularly the transport fractions, was confirmed in both patients. The possible pathophysiology of the hypercholesterolemia in these patients is discussed. Unlike other reported cases, clinical signs of atherosclerotic complications were absent.
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PMID:Characterization of hyperlipidemia in two patients with analbuminemia. 685 Nov 39

The effects of gemfibrozil on serum lipids and apolipoproteins were investigated in 60 male survivors of myocardial infarction (MI) (age range 29-48 years, mean 44). Fifteen had normal serum cholesterol (less than or equal to 7.0 mmol/l) and triglyceride (less than or equal to 1.7 mmol/l) levels, but most had low levels of high density lipoprotein (HDL) cholesterol (less than 1.00 mmol/l). Ten had type II A, 27 type II B and 8 type IV hyperlipidaemia. A double-blind placebo-controlled cross-over design was used with 3-month treatment periods. Gemfibrozil was given in daily doses of 1200 mg. The drug was well tolerated and there were no drop-outs attributable to its use. In all subjects, gemfibrozil reduced the mean serum total cholesterol by 17% and triglycerides by 54% and increased HDL cholesterol by 16%. The percentage HDL cholesterol of total cholesterol increased from 14 to 19%. The changes were similar in patients with normal serum cholesterol and triglyceride values and in those with classical hyperlipidaemias. In contrast, the changes during placebo treatment corresponded to those in healthy male untreated controls who were followed simultaneously. Apoprotein A-I remained unchanged, but A-II increased by 20% during gemfibrozil treatment. It is concluded that gemfibrozil corrects effectively dyslipidaemias in male MI patients but further long-term studies are warranted.
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PMID:Gemfibrozil in the treatment of dyslipidaemias in middle-aged male survivors of myocardial infarction. 701 Sep 29

The hyperlipidemia associated with aging was characterized in the rat by comparing the plasma lipid, lipoprotein, and apolipoprotein profiles of adult (12 weeks old) and old (96 weeks old) male rats. Compared with those of the adult rats, the VLDL concentrations of the old rats were reduced, but IDL, LDL, and HDL concentrations were elevated. Despite a reduced VLDL concentration, concentrations of triglycerides in the plasma of the old rats were elevated. This phenomenon was attributed to an enrichment of triglyceride in the other lipoprotein fractions. In the old rats, hypercholesterolemia was the result of elevated IDL- and HDL-cholesterol whereas elevated plasma concentrations of apolipoproteins B and E were attributed to elevated LDL and HDL concentrations, respectively. Although concentrations of apolipoproteins A-I and A-IV did not change significantly in the plasma of the old rats, the distribution pattern of the apoA-IV was altered dramatically. Compared with the adult rats, a shift of apoA-IV in the HDL to the "lipoprotein-free" fraction was observed in the old rats, as measured by agarose gel chromatography. The data demonstrate that the hyperlipidemia in the old rats is associated with selective changes in the apolipoprotein profile.
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PMID:Changes in the concentrations and distributions of apolipoproteins of the aging rat. 717 76

The significance of high density lipoproteins in the etiology of clinical complications to atherosclerosis has recently received increased attention. The levels of the major apolipoprotein in high density lipoproteins, apoA-I, have been determined in patients who had had an acute myocardial infarction, and compared with a cholesterol-matched and a randomly selected control group. ApoA-I levels were lower in the patients than in the control groups. ApoA-I levels were also lower in smokers than in non-smokers. The difference between patients and control groups persisted even when the groups were stratified according to smoking habits. This suggests that low levels of apo-A-I as well as alphalipoprotein cholesterol are additional characteristics of the infarction patients, even when the established risk factors, smoking and hyperlipidemia are taken into account.
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PMID:Serum apolipoprotein levels in relation to acute myocardial infarction and its risk factors. Apolipoprotein A-I levels in male survivors of myocardial infarction. 738 77

The relationship of VLDL-, LDL-, HDL-cholesterol, VLDL-triglycerides and of apolipoproteins A-I, A-II and apo-D has been studied in 89 survivors of myocardial infarction and in 80 age- and sex-matched controls. The two groups as a whole were analysed as well as sub-groups of subjects divided according to their lipid phenotype (normolipidaemic, IIA, IIB and IV). The data support the view that plasma levels of apo-B and apoA-I as well as their ratio and the TC/apo-B and LDL-C/apo-B ratios are better indicators of lipid derangement in survivors of myocardial infarction than the levels of LDL-cholesterol and HDL-cholesterol. Total cholesterol, total triglycerides, VLDL-cholesterol and VLDL-triglycerides are of no help in discriminating between the two series. The VLDL-C/VLDL-TG ratio in survivors is, however, very close to the ratio thought to be peculiar to type III hyperlipidaemia.
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PMID:Relationship between apolipoproteins and chemical components of lipoproteins in survivors of myocardial infarction. 742 89

The accelerated atherosclerosis in diseases associated with elevated remnant lipoprotein levels has directed interest toward the response of this lipoprotein species to lipid-lowering treatment. The effect of fluvastatin--a synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor--was compared with that of placebo on parameters of remnant metabolism in 57 patients with moderate hypercholesterolemia, but not heterozygous familial hypercholesterolemia, type III hyperlipidemia, or endogenous hypertriglyceridemia. Fluvastatin therapy resulted in decreases versus baseline in plasma total cholesterol, low density lipoprotein cholesterol (LDL-C) and LDL apolipoprotein (apo) B levels of 18%, 20%, and 18%, respectively (p < 0.01). Plasma parameters related to remnant metabolism were also significantly decreased: intermediate density lipoprotein by 43% and apo E by 22% (p < 0.01). The percent decrease in plasma intermediate density lipoprotein cholesterol level was twice that of LDL-C and 50% greater than the decrease seen in very low density lipoprotein cholesterol (VLDL-C), which was decreased by 28%. Total triglycerides were reduced by 11% and VLDL apo B by 24%, whereas high density lipoprotein cholesterol (HDL-C) rose significantly by 8%, HDL2-C by 24%, and HDL3-C by 3%. There were no increases in apo A-I levels compared with placebo nor any significant change in plasma lipoprotein(a) levels. The composition of LDL and VLDL particles did not appear to be altered by therapy, as assessed by the LDL-C:LDL-B, VLDL-C:VLDL-B, or triglyceride:VLDL-B ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of fluvastatin on intermediate density lipoprotein (remnants) and other lipoprotein levels in hypercholesterolemia. 760 88

The present report describes a competitive enzyme immunoassay for rabbit apolipoprotein A-IV (apo A-IV). This assay was applied to the determination of its concentration and distribution in sera from normolipidemic and hyperlipidemic rabbits. The assay was sufficiently sensitive to study this 42-kDa protein in lipoproteins fractionated from 200 microliters of serum by FPLC gel filtration. In normolipidemic sera (n = 8), apo A-IV concentration was 5.32 +/- 0.76 mg/dl. A diet rich in cholesterol (0.5%), which induced an 18-fold increase in serum cholesterol, did not significantly alter apo A-IV concentration (6.65 +/- 1.52 mg/dl, n = 8). By contrast, genetically induced hypercholesterolemia (Watanabe heritable hyperlipidemia, WHHL mutation) caused a significantly reduced level of apo A-IV (3.8 +/- 1.14 mg/dl, n = 7). In each of the groups studied, apo A-IV was distributed in two distinct pools; a high-density lipoprotein-(HDL) associated pool and a lipoprotein-free pool. However, compared to normal, the distribution of apo A-IV in WHHL rabbit sera was shifted towards the lipoprotein-free pool. Consistent with previously reported observations on apo A-I, these results are compatible with the hypothesis of an impaired reverse transport of cholesterol in WHHL rabbits, an animal model for familial hypercholesterolemia.
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PMID:Genetic but not diet-induced hypercholesterolemia causes low apolipoprotein A-IV level in rabbit sera. 760 56

The nephrotic syndrome is characterized by reduced plasma albumin and colloid osmotic pressure (pi), urinary protein loss and hyperlipidemia. High-density lipoprotein (HDL) and the level of apo A-I, the principal apolipoprotein in HDL, is increased in nephrotic rats and rats with hereditary analbuminemia (NAR)--animals with virtually no albumin in plasma and reduced plasma pi, but without proteinuria, suggesting that urinary protein loss is not responsible for increased plasma apo A-I levels. We conducted these studies to determine the mechanism responsible for increased plasma apo A-I levels in the nephrotic syndrome and NAR and to determine whether reduced plasma pi or albumin was responsible for increased apo A-I. We first measured the clearance of 125I apo A-I HDL in NAR and rats with passive Heymann nephritis (HN) compared with normal Sprague Dawley (SD) control. Both the clearance of apo A-I and fractional apo A-I turnover rate (FTR) were significantly reduced both in HN (7.40 +/- 2.18% plasma pool/hr) and NAR (5.63 +/- 1.12) compared with SD (9.87 +/- 0.75). Total apo A-I turnover rate, which in steady state equals apo A-I synthesis rate, was also significantly increased in both HN (487 +/- 127 micrograms/100 g body weight/hr) and NAR (253 +/- 16), compared with SD (216 +/- 19). Thus decreased apo A-I catabolism and increased synthesis both contributed to increased apo A-I levels in HN and NAR. We then infused either f3p4roncotic human albumin or ficoll into two additional groups of HN for days in quantities sufficient to maintain plasma pi within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oncotic pressure on apolipoprotein A-I metabolism in the rat. 761 Dec 50

Previous studies with a number of selective acylcoenzyme A:cholesterol acyltransferase (ACAT) inhibitors in several animal models have demonstrated significant reductions in plasma cholesterol and, in some studies, triglyceride levels. This study was conducted to examine the effects of two ACAT inhibitors, CL 283,546 and CL 283,796, in cholesterol-high fat diet fed African green monkeys, a relevant primate model of hyperlipidemia and coronary artery atherosclerosis. Treatment with CL 283,546 or CL 283,796 resulted in significant reductions (ca. 25-30%) in total plasma cholesterol at both 10 and 30 mg/kg per day doses. This reduction in plasma cholesterol was due almost entirely to reduction in low density lipoprotein (LDL) cholesterol (ca. 45%) without significantly affecting high density lipoprotein (HDL) cholesterol, very low density lipoprotein + intermediate density lipoprotein (VLDL + IDL) cholesterol, or triglyceride concentrations. There were no significant effects on plasma concentrations of apolipoproteins A-I, E, or B and, thus, the reduction seen in LDL cholesterol appears to be due to a diminished cholesterol content of LDL particles. Our studies revealed that treatment with these compounds did not reduce cholesterol absorption, which was somewhat surprising as ACAT inhibitors are generally thought to exert their hypolipidemic effects, at least in part, by inhibition of intestinal cholesterol absorption. Our data are consistent with a principal activity of these drugs on the liver to reduce cholesteryl ester secretion in VLDL, leading to a diminished LDL-cholesterol content, and, presumably, enhanced biliary cholesterol-bile acid excretion.
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PMID:ACAT inhibitors CL 283,546 and CL 283,796 reduce LDL cholesterol without affecting cholesterol absorption in African green monkeys. 766 98

Hypertensive patients with hyperlipidemia are at high risk to develop coronary heart disease (CHD). Chemotherapeutic correction of hyperlipidemia seems most reliable modality to prevent CHD. Hypolipidemic effect and tolerance of leskol (fluvastatin) in dietotherapy-resistant hypercholesterolemia were studied in 74 patients with essential hypertension treated with hypotensive drugs. The patients were included in a multicenter trial. A 12-week course reduced total cholesterol level under 6.2 mmol/l in 59% of the patients, under 5.2 mmol/l in 29% of them. LDLP cholesterol lowered to 3.5% in 34% of the patients. Mean apo B diminished by 23%. There was a 27% decrease in the proportion of atherogenic fraction apo B to antiatherogenic fraction of transport proteins apo A-I. Leskol is well tolerated and effective against hypercholesterolemia, it is safe in relation to side effects and blood biochemistry.
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PMID:[The hypolipidemic effect of and tolerance for Lescol in treating hypercholesterolemia in hypertension patients (an analysis of the data from a multicenter study)]. 770 57


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