Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of integrated estimations of a complex of lipid indices are presented. Their abnormalities are considered to be atherosclerosis risk factors in the evolution of glomerulonephritis and its different variants, types and stages. The quantitative and qualitative peculiarities of the indicated abnormalities are revealed, in particular, their major expressiveness in chronic form, nephrotic variant and in the stage of renal failure. Two aspects of correction of actual abnormalities are singled out: 1. indirect, i.e. treatment of the renal pathologic process with preparation of pathogenetic therapy (glucocorticoids, indomethacin), and 2. direct, i.e. with medications exerting a corrective influence on lipid metabolism (clofibrate, nicotinic acid, curantil). The selection of corrective methods is determined by the stage of disease and by the character of the changes in lipid metabolism.
 ...
PMID:Abnormalities of lipid metabolism and methods of their correction in patients with glomerulonephritis. 653 84

The efficacy of clofibrate (CPIB) and nicotinic acid (NA) in the treatment of type III hyperlipoproteinemia was evaluated in 5 male subjects in a randomized cross-over study with clofibrate 1 g b.i.d. and NA 3 g/day (given either b.i.d. or t.i.d.). Following a baseline period of 6 weeks, each drug was given for 12 weeks with samples for lipid and lipoprotein determinations obtained at 6, 9, and 12 weeks. Both clofibrate and NA resulted in a significant reduction from baseline of total cholesterol (23% and 28%), VLDL cholesterol (49% and 56%), total triglycerides (40% and 43%), and VLDL triglycerides (46% and 48%), as well as a significant increase in HDL cholesterol (22% and 28%) and HDL/LDL ratio (31% and 62%). The HDL/LDL ratio was higher on NA than clofibrate (0.47 +/- 0.19 vs. 0.38 +/- 0.09, P less than 0.05). Four subjects were continued in the study and treated sequentially with NA 3.0 g/day (alternate to the previous schedule) and gemfibrozil 1.2 g/d in divided doses. Each of the 4 regimens resulted in a significant change from baseline of each of the measured lipid and lipoprotein determinations except LDL cholesterol. Comparison among the treatment regimens revealed no differences except for significantly higher HDL cholesterol and HDL/LDL ratio with NA given t.i.d.
Atherosclerosis
PMID:Treatment of type III hyperlipoproteinemia with four different treatment regimens. 658 75

The effect of AY-25,712 (2-methyl-2-phenyl-3(2H)-furanone-5-carboxylic acid) on serum lipids, hepatic lipogenesis and biliary cholesterol was investigated in male rats. Based on one-week treatment, the minimal effective dose of AY-25,712 which lowered serum triglycerides was 1 mg/kg/day, and LDL-cholesterol, 5 mg/kg/day. Nicotinic acid produced a similar lipid-lowering profile albeit at 5 times higher doses. AY-25,712 at doses of 2 mg/kg/day and higher significantly increased the ratio of HDL to total cholesterol. Unlike clofibrate, AY-25,712 did not increase liver weight or liver mitochondrial alpha-glycerophosphate dehydrogenase, nor increase biliary cholesterol levels in rats fed a diet containing 2% cholesterol and 0.5% cholic acid. AY-25,712 lowered serum cholesterol, triglycerides and phospholipids in rats rendered hyperlipidemic with Triton WR-1339 and decreased the elevated serum triglycerides in streptozotocin-diabetic rats. [14C]Acetate incorporation into cholesterol by liver homogenate was suppressed in rats given AY-25,712 p.o. for 1 week. The results show that AY-25,712 is a potent LDL-cholesterol- and triglyceride-lowering agent in rats, and that its lipid-lowering profile differs from that of clofibrate but resembles that of nicotinic acid.
Atherosclerosis 1982 Dec
PMID:Evaluation of the lipid-lowering activity of AY-25,712 in rats. 681 76

The fatty acid composition of the plasma lipid esters has been studied during lipid-lowering treatment of 95 patients with atherosclerotic disease. During the first two months of the trial only a diet was prescribed. During the ensuing two months either clofibrate or niceritrol, a nicotinic acid ester, was added in a randomized order. During the last two months the second drug was added. The combined treatment with diet, clofibrate and niceritrol caused highly significant serum lipid reductions. The fatty acid composition in the plasma lipid esters was determined in samples from each trial period to measure the degree of dietary adherence. During dietary treatment the relative content of saturated and monounsaturated fatty acids secreased and the polyunsaturated fatty acids increased with an increasing ratio between pulyunsaturated and saturated fatty acids (P/S ratio) in the cholesterol esters and triglycerides. Only minor changes were seen in the phospholipids. The changes caused by the diet were partly reversed by clofibrate while niceritrol did not cause any major changes of the fatty acid composition. Clofibrate treatment coincided with increasing amounts of monounsaturated fatty acids, especially oleate (18 : 1), in the cholesterol esters, triglycerides and phospholipids while there were significant reductions of the content of linoleic (18 : 2) acid in both the cholesterol esters and triglycerides. The 18 : 2/18 : 1 ratio decreased significantly in all the lipid esters analyzed. However, the P/S ratio was not significantly affected, partly because the relative content of saturated fatty acids also tended to decrease during clofibrate treatment. It is concluded that addition of clofibrate treatment to patients who are on a diet enriched with polyunsaturated fats is associated with a change from polyunsaturated to monounsaturated fatty acids in the plasma lipid esters but does not significantly effect the ratio between polyunsaturated and saturated fatty acids. The fatty acid changes caused by clofibrate treatment and counteracted by an increased amount of polyunsaturated fat in the diet.
Atherosclerosis 1980 Jan
PMID:Changes in the fatty acid composition of the plasma lipid esters during lipid-lowering treatment with diet, clofibrate and niceritrol. Reduction of the proportion of linoleate by clofibrate but not by niceritrol. 698 77

The effect of AY-25,712 [2-methyl-2-phenyl-3(2H)-furanone-5-carboxylic acid] on various aspects of free fatty acid (FFA) and triglyceride metabolism was studied in male rats. Serum triglycerides were lowered by a single oral dose of AY-25,712 or nicotinic acid, but not of clofibrate. Unlike with clofibrate, when AY-25,712 or nicotinic acid was given in the diet, serum triglycerides were not affected. In vitro, both AY-25,712 and nicotinic acid suppressed the theophylline-induced FFA release by epididymal fat pads, but had no effect on lipolysis induced by norepinephrine. Both AY-25,712 and nicotinic acid enhanced the activity of adipose tissue lipoprotein lipase. The initial decrease in plasma FFA and triglycerides, and in liver triglycerides after a single oral dose of nicotinic acid was followed by a rebound to levels which, at later time intervals, wee significantly higher than in controls. AY-25,712 was more potent than nicotinic acid in lowering plasma FFA and triglycerides as well as liver triglycerides, but produced no such rebound effect. The data show that, except for the absence of this rebound effect, the mode of action of AY-25,712 in rats resembles that of nicotinic acid and differs from that of clofibrate.
Atherosclerosis 1982 Dec
PMID:Effect of AY-25,712 on fatty acid metabolism in rats. 715 99

The present investigations were performed in conscious rabbits with the aim of determining the effects of an atherogenic diet (AD) on the cerebral blood flow (CBF) and of a nicotinic acid derivative (SN) on the CBF alterations induced by the diet. Experimental atherosclerosis reduces the blood flow in the rapidly exchanging cerebrovascular compartment; SN largely counteracts this effect. The experimental data suggest that the effect of this antiatherogenic drug is not due to vasoactive properties.
 ...
PMID:Effects of experimental atherosclerosis on cerebral blood flow in rabbits. Reversal by sorbinicate. 717 22

Eight males with hypertriglyceridaemia were treated with a combination of procetofene (400 mg/day) and nicotinic acid (4 g/day) for 6 weeks. Previous therapy with only procetofene (400 mg/day) had given a certain, but not complete degree of normalisation. The combined treatment lowered the VLDL TG concentration values from 3.21 to 1.11 mmol/l and increased the HDL cholesterol concentration from 1.04 to 1.43 mmol/l (P less than 0.05 for both). The significant LDL cholesterol increase from 4.45 to 5.27 mmol/l, observed during treatment with procetofene only, reverted to 4.05 mmol/l when combined therapy was given. This drug combination may be a valuable tool to obtain maximum reduction of elevated TG in the therapy of hypertriglyceridaemia.
Atherosclerosis 1980 Apr
PMID:Effects of combined procetofene--nicotinic acid therapy in treatment of hypertriglyceridaemia. 737 21

In rabbits kept on a diet containing 1 g/day cholesterol for 12 weeks, the nicotinic acid derivative sorbinicate displayed greater hypolipemic and antiatherogenic activity than an equidose of plain nicotinic acid at much lower and more constant plasma nicotinic acid levels. In normocholesterolemic rats, nicotinic acid given at a level of 300 mg/kg per dose for 3 weeks induced plasma FFA and triglyceride rebound and triglyceride accumulation in the liver and possibly in the heart (all parameters determined 24 h after the last dosing), whereas an equidose of sorbinicate was free from these effects, potentially the two most dangerous side effects of nicotinic acid. By modulating the bioavailability of nicotinic acid, sorbinicate maintains and in some cases enhances the pharmacological activity of the acid, avoiding at least some of its major side effects.
Atherosclerosis 1980 May
PMID:Comparative evaluation of some pharmacological properties and side effects of D-glucitol hexanicotinate (sorbinicate) and nicotinic acid correlated with the plasma concentration of nicotinic acid. 738 73

The effect of 50 mg/kg body weight Xantinol-nicotinate (XN) on serum lipids and on non-esterified fatty acids (NEFA) was tested in 94 out-patients with hyperlipoproteinemia Types IIa, IIb, IV and V. The lipids were measured before treatment, during a 3-week period of drug administration and 10 days after rejection. In each group of hyperlipoproteinemic patients the lipid lowering effect of XN was accompanied by a constant fall in serum NEFA levels. The time dependent course of NEFA showed that the higher the initial level, the longer the time span required to achieve the lowest values. In the context of the partially conflicting data on the hypolipidemic action of nicotinic acid and its derivatives, it is suggested that the constant decrease in NEFA induced by XN treatment might contribute significantly to the lipid lowering effect of this drug.
Atherosclerosis 1980 Sep
PMID:Serum profile of non-esterified fatty acids (NEFA) in patients with hyperlipoproteinemia under xantinol--nicotinate (XN) medication. 742 90

The effects of niceritrol, a nicotinic acid derivative, on the levels of HDL-cholesterol (HDL-Ch) and a mixture of VLDL- and LDL-Ch (VLDL- + LDL-Ch) were studied in hyperlipidemic patients. Serum total cholesterol (sTC) and serum triglyceride (sTG) were significantly reduced during niceritrol administration. Lipoprotein electrophoresis showed that niceritrol increased the alpha:beta ratio. HDL-Ch showed a significant increase of 12.5% by the 16th week of therapy. This increase was more marked in patients with lower pre-treatment HDL-Ch levels and significant in patients whose pre-treatment sTG levels were in excess of 200 mg/dl. Females displayed higher pre-treatment HDL-Ch levels (38.5 mg/dl) than males (30.6 mg/dl). However, niceritrol increased HDL-Ch significantly in both groups. At 16 weeks, the VLDL- + LDL-Ch level showed a significant decrease of 9.2%; the HDL-Ch:VLDL + LDL-Ch and HDL-CH:sTC ratios were significantly increased throughout niceritrol administration. Niceritrol is thought to be effective in preventing the development and progression of atherosclerosis because it raises the level of anti-atherogenic HDL-Ch and lowers the level of atherogenic VLDL- + LDL-Ch.
Atherosclerosis 1980 Nov
PMID:Clinical study of niceritrol on serum lipids in the treatment of hyperlipidemia. 745 80


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>