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 present study investigated the effect of serum lipoproteins on sterol synthesis by isolated rat hepatocytes. These cells were maintained in culture medium for 24 hr and incubated for the same period of time with increasing concentrations of serum lipoproteins (5-150 microgram of lipoprotein-protein per ml) isolated from different animal species. The viability of the cells was ascertained by their ability to synthesize cholesterol and protein and to secrete serum proteins into the medium. Rat VLDL and LDL did not alter sterol synthesis, which was stimulated instead by HDL. Rat serum chylomicrons were also ineffective. Human LDL significantly reduced the synthesis of sterols from both acetate and tritiated water; this effect was also induced by human VLDL to a reduced extent. VLDL isolated from hypercholesterolemic rabbit (VLDLC) strongly inhibited sterol synthesis from acetate but not from mevalonate. Cholesteryl-ester-rich VLDL isolated from a patient with type III hyperlipidemia (type III VLDL) were more effective than normal VLDL in suppressing sterol synthesis from acetate. The implications of these findings are discussed with regard to the possible role of cholesteryl-ester-rich lipoproteins on the in vivo regulation of sterol synthesis in the liver.
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PMID:Cholesterol synthesis in isolated rat hepatocytes: effect of homologous and heterologous serum lipoproteins. 45 21

HDL cholesterol in 53 hemodialysed patients is significantly reduced (p less than 0,001) in front of 34 healthy people. The decrease is more pronounced in male but does not seem influenced by age or ethnical origin of subjects. There is no correlation between alpha cholesterol levels and hyperlipidemia which are in 50% of cases of type IV and more frequent in caucasian than in african: the beta cholesterol is correlated with total cholesterol and increased in type IV (p less than 0,001) but alpha cholesterol negatively correlated with triglyceridemia (p less than 0,001) is in comparable levels in dialysed with type IV or without hyperlipidemia. If for normal value triglyceridemia is correlated with caloric and carbohydrate intake (p less than 0,001), the diet does not seem to influence either the frequence of type IV nor the level of alpha cholesterol. However we found a positive correlation (p less than 0,05) between nervous conduction velocity and HDL cholesterol, this fact can let us hope a decrease in the cardiovascular complication associated with amelioration of the adequacy of dialysis.
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PMID:[Vascular risk factors in chronic haemodialysis: the role of HDL cholesterol. Correlation with dietary intake and the quality of dialysis (author's transl)]. 47 22

A general linear model is presented here for biological and cultural inheritance involving ten parameters to be estimated from 16 correlations in nuclear families, providing ample degrees of freedom to test goodness of fit. Applied to six lipoprotein traits the model fits acceptably to all, although there is evidence of transient maternal effects for cholesterol and lipemia. Genetic heritability in children ranges from 0.175 for triglyceride to 0.562 for total cholesterol. Cultural heritability in children ranges from 0.012 for VLDL to 0.149 for HDL-cholesterol.
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PMID:Cultural and biological determinants of lipoprotein concentrations. 47 34

Investigations performed in a patient with myeloma, hyperlipidemia, and xanthomatosis demonstrated the antilipoprotein activity of the monoclonal IgA directed against an antigenic site--called Ra.--different from those previously described. A complex IgA beta-lipoprotein has been firstly characterized. After isolation and purification of the IgA, it has been shown that the association between IgA and lipoprotein was immunologically mediated. The antibody is an IgA lambda bound via its Fab portion and in fixed combining ratio to an antigenic determinant shared only by LDL and VLDL of humans and some other mammalians to the exclusion of any other serum proteins. The results obtained with passive hemagglutination and inhibition of hemagglutination suggest that the antigenic site Ra. is not located on apoprotein B (major proteic moiety of LDL and VLDL), since the antigenic determinants of apolipoproteins are different in humans and in animals and since IgA Ra. fails to react with apolipoprotein B obtained by delipidation of LDL. On the other hand, the lack of reaction between IgA Ra. and HDL suggests that the antigenic determinant is not only present on the lipid hapten such as in the case of PG and AS determinants which are located on VLDL, LDL, and HDL from humans and animals. So the antigenic determinant revealed by IgA Ra. seems to be different from those previously described.
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PMID:[Monoclonal myelomatous IgA with antilipoprotein antibody activity of Ra specificity (author's transl)]. 51 6

Purified rat lymph chylomicrons were incubated with chylomicron-free rat plasma and examined for changes in lipid and apoprotein constituents. Upon incubation there was a five-fold increase in the arginine rich apoprotein and a concomitant reduction in chylomicron Apo A-I to less than one-sixth its preincubation mass. These apoprotein changes were most faithfully reproduced when chylomicrons were incubated with the rat HDL fraction, although incubations of chylomicrons with rat lipoprotein-free plasma showed that arginine-rich apoprotein could readily associate with chylomicrons without concomitant changes in chylomicron lipid constituents. The gain in chylomicron apoprotein paralleled an increased affinity of the incubated chylomicron for heparin, when examined by heparin affinity chromatography. The apoprotein alterations were consistent in incubations in which the triglyceride concentrations varied from 330 mg/dl to 4200 mg/dl, and were not affected by inhibition of the Lecithin:Cholesterol Acyl Transferase (LCAT) reaction in the incubation mixture. The demonstration that in vivo alimentary lipemia chylomicrons have an apoprotein pattern identical to that of chylomicrons following in vitro plasma incubation suggests that these apoprotein alterations occur physiologically in alimentary lipemia.
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PMID:Chylomicron apoprotein alteration after plasma exposure. 66 31

In more than 500 families of Japanese ancestry, selected in part through fathers with hyperlipemia or coronary heart disease, a major locus for hyper-beta-cholesterolemia (hyperlipoproteinemia type IIa) is highly significant (chi22 = 24.02), with an allele frequency .002 in the general population. This gene is revealed with about the same power by fasting levels of LDL (low density lipoprotein) cholesterol and total cholesterol. However, VLDL (very low density lipoprotein) cholesterol, HDL (high density lipoprotein) cholesterol, and triglyceride give no convincing evidence for a major locus in this population, nor was a gene for combined hyperlipoproteinemia detected.
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PMID:Major loci for lipoprotein concentrations. 74 86

Autoimmune hyperlipidemia (AIH) may be induced a variety of antibodies which inhibit different stages of the lipolytic process by which the lipid load is removed from the circulating lipoproteins. In a patient having a monoclonal gammopathy and a nephrotic syndrome with a glomerulonephritis and a marked hypertriglyceridemia, it was found previously that the monoclonal IgG gamma Lac. reacted with human VLDL as well as with human serum albumin. Here it is demonstrated that the purified IgG gamma inhibits the lipolysis of triglyceride substrates by reacting with a substance (Lac. S) necessary for lipoprotein lipase activity. The interaction of IgG lambda Lac. with serum or HDL-activated triglyceride substrates inhibits the lipolytic activity of human and rat plasma post heparin and also adipose tissue lipases. It slightly inhibits the activity of swine pancreatic lipases. The Lac S. which reacts with IgG Lac. is associated to whole and delipidated VLDL and HDL and not to LDL or purified APo-A. It may be an Apo-C or a non-peptidic co-factor of the lipases which remains bound to the apoprotein core after delipidation. Its lack of species specificity and its presence as traces in HSA preparations favors the latter hypothesis. The Lac. substances is different from the Pg and As substances which were found to react with IgA anti-Pg and IgG anti-As antibodies in previously reported antilipoprotein AIH.
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PMID:Inhibition of lipoprotein lipase activity by a monoclonal immunoglobulin in autoimmune hyperlipidemia. 83 49

The fasting concentration of cholesterol and triglycerides in serum and in very low (VLDL), low (LDL) and high (HDL) density lipoproteins (LP) was determined 3 months after a myocardial infarction (MI) in 54 men, and the values obtained were compared to those in 61 healthy male control subjects. The mean triglyceride concentration in MI patients was significantly increased in serum, VLDL, LDL and HDL by 74%, 110%, 30% and 12% respectively, compared to controls. The mean cholesterol concentration was significantly raised by 16%, 120% and 14% in serum, VLDL and LDL but decreased by 22% in HDL. Hypertriglyceridaemia occurred in 58% of MI patients. Of these patients, two-fifths had hypertriglyceridaemia only and three-fifths had combined hyperlipidaemia. The hypertriglyceridaemia was caused by elevation of only VLDL triglycerides in 26%, only LDL triglycerides in 19%, VLDL and LDL triglycerides in 23% and by various other combinations of raised LP triglyceride levels in 25% of cases. Hypercholesterolaemia was found in 41% of MI subjects. Of these, one-sixth had elevation of cholesterol levels, while five-sixths had combined hyperlipidaemia. The LP abnormalities underlying hypercholesterolaemia were increased of only VLDL cholesterol levels in 36%, only LDL cholesterol in 14% and both VLDL and LDL cholesterol in 50% of cases. The low HDL cholesterol values in comparison to controls were related to higher VLDL triglyceride values in MI patients, since HDL cholesterol fell significantly with increasing VLDL triglyceride levels. When HDL cholesterol was related to similar VLDL triglyceride levels, there were no major differences between controls and MI.
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PMID:Quantitative and qualitative serum lipoprotein analysis. Part 2. Studies in male survivors of myocardial infarction. 114 36

We examined the distribution of beta-carotene in plasma lipoprotein fractions. In healthy children and adults, LDL contained more beta-carotene than did HDL, but in cord blood more beta-carotene was found in HDL than in LDL. After the oral administration of beta-carotene, its plasma level rose although its distribution in the individual lipoprotein fractions did not change. Among disease conditions associated with hyperlipidemia, the ratio of beta-carotene to plasma lipids was highest in anorexia nervosa, while nephrotic syndrome and diabetes mellitus had similar ratios to each other.
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PMID:Distribution of circulating beta-carotene in human plasma lipoproteins. 129 1

The role of triglycerides in cardiovascular disease is a controversial subject. Despite differences of opinion, present data allow a certain number of conclusions to be drawn. Hyperchylomicronemia is not associated with atherosclerosis, whereas type III hyperlipidemia is very atherogenic. These two abnormalities are, however, rare, and the majority of hypertriglyceridemias are, in practice, associated with increased very low density lipoproteins. Many epidemiological trials do not identify hypertriglyceridemia as an independent risk factor when the cholesterol and, in particular, the HDL cholesterol levels, are taken into consideration. Nevertheless, these results must be interpreted with caution as hypertriglyceridemia represents a very heterogeneous entity which is closely related to many factors which affect coronary risk (hypertension, insulin resistance, sedentarity, and even tobacco consumption). Therefore, hypertriglyceridemia and hypo-HDL-emia may be the result of the same primary abnormality; as the HDL-cholesterol level is more stable, it is the parameter which will be identified as a protective factor in epidemiological trials. The available data is insufficient to affirm that therapeutic lowering of triglycerides is accompanied by a reduced coronary risk because none of the large scale trials were designed to analyse this problem. Despite these epidemiological data, the measurement of serum triglyceride levels remains important in patients with hyperlipidemia.
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PMID:[Role of triglycerides in cardiovascular diseases]. 129 43


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