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

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.
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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

The Prevenzione Aterosclerosi Studio Torino (P.A.S.T.) was a prospective, randomized trial testing the effect on carotid and femoral atherosclerotic lesions of lipid-lowering therapy, as assessed by duplex scanning (DS) technique, in 85 patients (12 women, 73 men), forty-five to fifty-five years old, with ischemic heart disease (IHD), and randomly assigned to a hypolipidemic diet or diet + 250 mg acipimox (a nicotinic acid compound) two to three times/day. Forty-one patients, without inclusion criteria, were compared with the randomized groups as a reference population. All three groups were submitted to DS and to hematic monitoring of lipid levels at the beginning and at the end of the study. During three years of treatment, there was a significant reduction (-6.5%) in total plasma cholesterol in the diet + drug group (P = 0.04) and a simultaneous elevation of high-density lipoprotein cholesterol, significant in the treatment groups (respectively, +15% P = 0.02 in the diet and +16% P = 0.016 in the diet + drug group). Every group showed a trend toward the increasing number of lesions in all explored areas and toward the progression in size of the already existing ones. Whereas in the initial DS the prevalence of lesions was significantly lower in the nonrandomized group in every site, at the end of the study the total number of lesions did not differ among groups, and there was a significant increase of plaques in carotid area in the nonrandomized group in comparison with the treatment groups. The final number of stable plaques was greater in the treatment groups as compared with the nonrandomized group (P = 0.01 diet vs nonrandomized, P = 0.03 diet + drug vs nonrandomized). In conclusion, lipid-lowering treatment, with diet and with diet + drug, was useful in slowing the natural progression of atherosclerosis; particularly, it reduced the development of new lesions in the carotid and femoral arteries and increased the stability of the already existing ones. In these patients, diet was equivalent to diet + drug in regard to progression of lesions. The most favorable results in the treatment groups seem to correlate with high-density lipoprotein cholesterol, significantly increased in comparison with the nonrandomized group.
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PMID:Effect of lipid-lowering treatment on progression of atherosclerotic lesions--a duplex ultrasonographic investigation. 772 47

Lipoprotein (a) has been implicated with an increased risk of atherosclerosis and cardiovascular disease. Recently, considerable progress has been made toward understanding the importance of genetics in the regulation of plasma levels of lipoprotein (a). However, the issue as to whether lipoprotein (a) levels should be treated is still debated and furthermore the possibilities to influence lipoprotein (a) levels remain limited. The potential clinical importance of lipoprotein (a) has stimulated interest in the dietary and pharmacologic agents that affect this lipoprotein. At present, only a few of the existing therapeutic tools, such as nicotinic acid and estrogens, have been found to consistently affect lipoprotein (a).
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PMID:Diet and drug therapy for lipoprotein (a). 773 16

Lipid-lowering therapy ameliorates coronary atherosclerosis in patients with raised concentrations of low-density-lipoprotein (LDL) cholesterol. We have investigated whether a similar benefit can be obtained in normocholesterolaemic patients. We studied 79 normocholesterolaemic patients with coronary heart disease (70 male, 9 female), mean age 58 years, all non-smokers, with mean total cholesterol concentration 5.5 mmol/L. All patients received diet therapy and were randomly assigned placebo (39) or active treatment (40) with pravastatin, nicotinic acid, cholestyramine, and gemfibrozil stepwise as needed to reach the specified goal (total cholesterol < or = 4.1 mmol/L, ratio of LDL/high-density-lipoprotein [HDL] cholesterol < or = 2.0). Coronary angiograms at baseline and after 2.5 years of treatment were analysed by computer-assisted quantitative techniques. There was no significant difference in coronary atherosclerosis during follow-up between the active treatment and placebo groups; the mean minimum diameter narrowed significantly but to the same extent in both groups (change baseline to 2.5 years 0.14 [SD 0.42] and 0.15 [0.42] mm, respectively, both p < 0.001). Similarly, the change in percentage stenosis did not differ between the groups (2.1 [10.6] vs 2.4 [10.3]%). By multiple regression analysis, the adjusted difference between the groups was a 0.04 mm (95% CI -0.04 to 0.12 mm) increase in minimum diameter and a 0% (-1.7 to 1.7) change in percentage stenosis. The groups differed significantly in plasma lipids (% change in active minus % change in placebo group: -28% total cholesterol, -41% LDL-cholesterol, 13% HDL-cholesterol, -26% triglycerides, -31% apolipoprotein B, all p < 0.001). Thus, intensive pharmacological treatment of normocholesterolaemic patients has significant effects on plasma lipid concentrations but no angiographically measurable benefit on the coronary arteries.
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PMID:Effect on coronary atherosclerosis of decrease in plasma cholesterol concentrations in normocholesterolaemic patients. Harvard Atherosclerosis Reversibility Project (HARP) Group. 799 16

This study examines the effect of nicotinic acid (1 g t.d.s.) on serum Lp(a) concentration in a group of patients with type II hyperlipidaemia selected on the basis of a plasma Lp(a) concentration greater than 30 mg/dl. Reductions in total cholesterol, triglyceride, LDL-cholesterol and Lp(a) were 16.3%, 25.5%, 23.7% and 36.4%, respectively, with an increase in HDL cholesterol of 37.3%. The reduction in Lp(a) concentration did not correlate with any other lipoprotein changes. In order to establish the mechanism of the fall in Lp(a) concentration, in vivo turnover of autologous Lp(a) was studied in three subjects before and whilst taking nicotinic acid. The fractional catabolic rate in Lp(a) was unaltered in the subjects on therapy, indicating that nicotinic acid did not increase catabolism of Lp(a) but decreased the synthetic rate. Since nicotinic acid was poorly tolerated we examined the effect of acipimox, an analogue of nicotinic acid on lipoproteins using a placebo controlled double-blind crossover design in a group of hyperlipidaemic patients again selected with plasma Lp(a) concentration greater than 30 mg/dl. Acipimox was better tolerated than nicotinic acid but the percentage changes in lipoprotein concentrations were smaller.
Atherosclerosis 1993 Jun
PMID:The effect of nicotinic acid and acipimox on lipoprotein(a) concentration and turnover. 821 3


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