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)

Retrospective analysis of ulcer healing trials utilizing enprostil, a synthetic dehydroprostaglandin E2 analogue, has demonstrated a 10% or greater reduction in total serum cholesterol in 64%, 64% and 67%, respectively, of hypercholesterolemic subjects receiving the drug in doses of 70 micrograms, 35 micrograms, and 7 micrograms bid, respectively. Only 16% of subjects receiving placebo exhibited a similar reduction (P less than 0.05). The median percent changes for hypercholesterolemic patients receiving enprostil 70 micrograms, 35 micrograms, or 7 micrograms bid, and placebo were -17%, -13%, -11%, respectively, while the median percent change for those on placebo was 0% (P less than 0.05). Eight normocholesterolemic subjects participated in a double-blind crossover study comparing enprostil 70 micrograms/d with its placebo. Nine days of enprostil administration was associated with reductions in total serum cholesterol (-16%) and apolipoprotein B (-16%) and with significant reductions from baseline for LDL-cholesterol (-22%), the LDL/HDL-cholesterol ratio (-13%), and the ratio of serum apolipoprotein B to apolipoprotein A-1 (-12%). Relative to placebo, mean HDL-cholesterol, total triglycerides, and apolipoprotein A-1 concentrations remained unchanged. Daily oral administration of microgram quantities of enprostil is associated with reductions in total cholesterol, LDL-cholesterol, and apolipoprotein B suggesting therapeutic potential of this synthetic prostaglandin for the treatment of hyperlipidemia.
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PMID:Reduction of serum lipoproteins in man by the oral administration of a prostaglandin analogue (enprostil). 313 81

Familial dysbetalipoproteinemia is characterized by hyperlipidemia, increases in beta-migrating, very low density lipoproteins (beta-VLDL), and homozygosity for apolipoprotein E2 (apo E2). In this study, 3 patients with familial dysbetalipoproteinemia were treated with lovastatin, and kinetics for apolipoprotein B (apo B) were determined in control and drug treatment periods. Multicompartmental analyses of apo B kinetics in VLDL and in low density lipoproteins (LDL) were carried out. Lovastatin therapy generally lowered plasma concentrations of apo B and cholesterol in VLDL and LDL. The reductions in concentrations were due mainly to a decrease in transport (production) rates for these fractions. Indeed, the fractional clearance rate (FCR) for LDL-apo B was reduced during lovastatin therapy. The decreased transport rate for VLDL-apo B and LDL-apo B could have been due to an inhibition of the synthesis of lipoproteins containing apo B. An alternate explanation is that lovastatin promoted direct removal of a rapidly-catabolized fraction of VLDL-apo B that is a precursor for longer-lived lipoproteins in the circulation; this mechanism could decrease input rates of identifiable lipoprotein species and retard their clearance because of "saturation" of LDL receptors by more rapidly removed lipoproteins. Finally, both mechanisms, i.e., decreased production and increased clearance of lipoproteins, may have contributed to the fall in VLDL-apo B and LDL-apo B concentrations during lovastatin therapy.
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PMID:Lovastatin therapy in familial dysbetalipoproteinemia: effects on kinetics of apolipoprotein B. 316 80

The plasma lipoprotein and liver lipid composition, and the lipid, cholesterol and apolipoprotein synthesis have been studied in normal and diet-induced hyperlipidemic rats, receiving ciprofibrate (2.5 mg/kg body weight) or fenofibrate (50 mg/kg b.w.) for 8 days. Ciprofibrate is about 25-fold more active than fenofibrate in reducing plasma triglyceride and cholesterol concentrations both in normolipemic and in hyperlipemic rats. In normolipemic rats ciprofibrate reduced the concentration and the lipid content of all lipoprotein classes. The incorporation of [14C]palmitate and [3H]leucine into the lipoproteins was reduced by ciprofibrate and fenofibrate. The reduction in lipoprotein production was confirmed by prevention of Triton-induced hyperlipemia. Liver and plasma cholesterol synthesis estimated by 3H2O and [14C]mevalonate incorporation indicated an inhibitory effect on HMG-CoA reductase. Administration of ciprofibrate or fenofibrate to rats fed a fat and cholesterol-rich diet partially prevented liver steatosis and hyperlipemia. Both drugs reduced the overproduction of lower density lipoproteins. The ratio of (VLDL + LDL)-cholesterol/HDL-cholesterol which was increased by the diet alone from 0.4 (normal) to 11 remained close to the normal value in the animals receiving ciprofibrate. In the hyperlipemic animals, ciprofibrate reduced the incorporation of [3H]oleate into the liver and plasma glycerolipid and increased cholesterol esterification. Ciprofibrate efficiently reduces plasma levels of cholesterol, triglyceride and phospholipid. Cholesterol and glycerolipid synthesis in the liver were significantly reduced leading to a lower lipoprotein secretion rate in both normolipidemic and diet-induced hyperlipidemic rats.
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PMID:Effects of ciprofibrate and fenofibrate on liver lipids and lipoprotein synthesis in normo- and hyperlipidemic rats. 324 Mar 33

Patients treated with corticosteroids often have a dyslipoproteinemia characterized by elevated plasma levels of triglyceride and low density lipoprotein cholesterol and/or decreased levels of the high density lipoprotein2 fraction of high density lipoprotein cholesterol. This study was undertaken to determine if such patients also have elevated apolipoprotein-B (apoB) levels and/or abnormalities of the activities of the triglyceride lipases in postheparin plasma. Plasma lipoprotein levels and the postheparin activities of hepatic lipase and lipoprotein lipase were measured in 28 women with systemic lupus erythematosus (SLE) who were treated with prednisone, 10 women with SLE not treated with prednisone, and 15 normal women. The prednisone-treated group had higher mean plasma levels of triglyceride [2.06 +/- 1.3 (+/- SD) vs. 1.15 +/- 0.35 and 0.95 +/- 0.46 mmol/L; P less than 0.01], low density lipoprotein cholesterol [3.41 +/- 1.4 (+/- SD) vs. 2.79 +/- 0.67 and 2.84 +/- 0.70 mmol/L; P less than 0.01], and apoB [1.16 +/- 0.35 (+/- SD) vs. 0.82 +/- 0.13 and 0.76 +/- 0.22 g/L] than the other 2 groups. Forty-three percent of the prednisone-treated group had apoB levels of 1.20 g/L or more compared to 7% of normal subjects and none of the untreated SLE group (P less than 0.05). However, of the 12 prednisone-treated patients with elevated plasma apoB levels 5 had normal plasma lipid levels. There were no differences in the postheparin lipase activities among the 3 groups. These data indicate that corticosteroid-treated patients have elevations in apoB as well as hyperlipidemia. The lipoprotein abnormalities may explain the increased risk of atherosclerosis reported in these patients.
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PMID:Elevated apolipoprotein-B levels in corticosteroid-treated patients with systemic lupus erythematosus. 341 Sep 32

The effects of labetalol on plasma lipoprotein metabolism were evaluated in a 3-month double-blind drug versus placebo study conducted on 30 consenting hypertensive patients, 15 of whom had normal plasma lipid levels and 15, minor type II hyperlipoproteinaemia; 20 patients received labetalol 400 mg/day and 10 the placebo. All patients remained in stable nutritional status throughout the study. Full clinical examination and blood sampling were carried out 30 days before, and on days 0, 30 and 90 of treatment. Whole blood was collected after 12 hours' fasting and immediately centrifuged prior to determination of plasma lipids (total cholesterol and triglycerides, by enzymatic assay), lipoprotein lipids (HDL, HDL2, HDL3, LDL, VLDL separated by ultracentrifugation in density gradient), apoproteins A1 and B (by laser immunonephelometry) and post-heparin lipoprotein lipase activity (PHLA). Significant changes in heart rate and systolic and diastolic blood pressures were noted in patients under labetalol but not in patients under placebo. Lipid and apolipoprotein levels were similar in both groups on day 0, and no significant variation in lipids, lipoprotein lipids and apolipoproteins were observed after 30 and 90 days of treatment with either labetalol or the placebo. At the end of treatment PHLA was unmodified in the group under placebo and raised in the group under labetalol (p = 0.05). The absence of changes in blood lipid values was found both in patients with normal lipidemia and in those with hyperlipidaemia. This study confirms that labetalol in doses of 400 mg/day has notable anti-hypertensive activity and, as previously reported and in contrast with other beta-blocking agents, is devoid of any adverse effect on lipid metabolism.
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PMID:[Effect on lipids, lipoproteins and apoproteins of labetalol prescribed in doses of 400 mg/day in hypertensive patients. Double-blind versus placebo study]. 352

Lipoprotein lipase (LPL) activity in postheparin plasma of 38 normolipidemic volunteers was related to the magnitude of postprandial lipemia after a fat meal, to triglyceride content of high density lipoprotein2 (HDL2), to hepatic lipase (HL) activity, and to HDL2 levels. LPL activity correlated indirectly with lipemia, triglyceride content of HDL2, HL activity, and levels of HDL2 but not of HDL3. HL activity correlated directly with lipemia and indirectly with HDL2 levels. Triglyceride content of HDL2 correlated directly with lipemia and indirectly with HDL2 levels. In HDL2, abundance of apolipoprotein (apo) A-II and the apoA-I/apoA-II ratio varied widely. The latter correlated positively with LPL activity and HDL2 levels, and, inversely, with HL activity, lipemia, and triglyceride content of HDL2. The study suggests that HDL-cholesterol is not an independent parameter of lipid transport, but is strongly affected by triglyceride metabolism through lipolytic enzymes, as exemplified by postprandial lipemia that affect both composition and plasma levels of HDL2.
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PMID:High density lipoprotein2. Relationship of the plasma levels of this lipoprotein species to its composition, to the magnitude of postprandial lipemia, and to the activities of lipoprotein lipase and hepatic lipase. 361 51

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.
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PMID:Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia. 372 96

A case of familial hyperlipidemia incidentally found through a 16 year-old high school girl with type V hyperlipoproteinemia and abdominal bouts consistent with this type of hyperlipemia is reported for the first time in Japan. The laboratory findings of the plasma of her father revealed typical hyperlipoproteinemia of type IIa. Nineteen of her 26 kindred were investigated. Type V was seen only in the proband, type IIa in father, paternal grandmother, two paternal aunts, and two paternal cousins, type IV in three paternal cousins. The serum apolipoprotein (apo A-I, A-II, B, C-II, C-III, and E) concentrations were determined by the single radial immunodiffusion technique. The apolipoprotein concentrations were not different from those of normolipidemic control subjects except for apo B, which was higher in the hyperlipidemic members, and apo C-II, C-III, and E, which were higher in the proband.
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PMID:A kindred of familial combined hyperlipidemia (FCHL) with proband showing type V hyperlipoproteinemia. 377 23

We have isolated an isoform of the protein activator of lipoprotein lipase, apolipoprotein C-II, from the very low density lipoproteins of four patients of African ancestry with hypertriglyceridemia and eruptive or pedunculated xanthomata. This protein, which we designate apolipoprotein C-II2, differs from the previously recognized species, which we denote apolipoprotein C-II1, by substitution of glutamine for lysine at residue 55, a mutation which would require only a single-base substitution in the structural gene for apolipoprotein C-II1. Each of the patients in whom apolipoprotein C-II2 was found had approximately equal amounts of apolipoprotein C-II1 and apolipoprotein C-II2 among the apoproteins of the very low density lipoproteins, suggesting that the structural genes for these proteins are allelic. Two additional apparent heterozygotes were found among the first-degree relatives of each of two of the patients in patterns compatible with monogenic autosomal transmission. Approximately equal amounts of apolipoproteins C-II2 and C-II1 were also found by isoelectric focusing in 6 of a casual series of 50 normolipidemic blacks, but none or only trace amounts of apolipoprotein C-II2 were found in 500 samples from Caucasian subjects with hyperlipidemia. These findings suggest that this polymorphism is distributed primarily among blacks, possibly reflecting some positive Darwinian selection pressure. Whether this polymorphism has a modifying effect upon the development of hyperlipemia remains to be determined.
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PMID:A variant primary structure of apolipoprotein C-II in individuals of African descent. 394 71

Alterations in plasma lipoprotein lipid and apoprotein accompanying the hyperlipidemia of rats bearing Morris hepatoma 7288C were characterized. In tumor-bearing animals all plasma lipid classes except cholesterol ester (CE) were elevated, particularly free cholesterol (FC) and triglyceride (TG), which increased by 57 and 63%, respectively. Fasting only partially reduced the tumor-induced hyperlipidemia and had no effect on the ratios of FC/CE and TG/CE. Analysis of plasma lipoproteins revealed an elevation of VLDL, IDL, and LDL in host rats, with more than a 2-fold increase in both lipid and protein of VLDL. In contrast, the three high density fractions, HDL2, HDL3, and d greater than 1.21 g/ml, were reduced. The inverse changes in concentration of host lipoproteins of lower versus higher density indicate a defective catabolism of TG-rich lipoprotein. This possibility is supported by the analysis of apolipoprotein. The percentage of total apoprotein contributed by apo C-I and C-II was reduced in all host fractions except HDL2, while the C-IIIs remained unchanged except for a small decrease in C-III-3 of host VLDL and a slight increase in the combined C-IIIs of HDL2. These changes were reflected in the decreased C-I+C-II/C-III ratios of all host lipoprotein fractions. Apo E levels remained similar to control values except for a significant decrease in HDL2. Host VLDL showed increased apo A-IV and A-I content, while A-IV was decreased in HDL2. Changes in apo B profiles were also observed.
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PMID:Characterization of alterations in plasma lipoprotein lipid and apoprotein profiles accompanying hepatoma-induced hyperlipidemia in rats. 394 72


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