Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NICOTINIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed1988

Hypocholesterolemic effects of nicotinic acid and chromium supplementation.

During the course of a study of the hypoglycemic effects of nicotinic acid and chromium on humans, two hypercholesterolemic subjects were found to experience clinically significant decreases in serum cholesterol levels. These subjects have now been followed for one year. The first subject had a cholesterol level of 10.33 mmol/L (399 mg/dL). Daily supplementation for four weeks with 100 mg of nicotinic acid (niacin) and 200 micrograms of chromium chloride led to a decrease in serum cholesterol to 8.86 mmol/L (342 mg/dL). Further supplementation for four months led to a further decrease in serum cholesterol to 7.25 mmol/L (280 mg/dL). The second subject had a cholesterol level of 8.73 mmol/L (337 mg/dL). Four weeks of supplementation lowered the level to 6.73 mmol/L (260 mg/dL). When supplementation was discontinued, the cholesterol level rose slightly. When supplementation was reinstituted, the cholesterol level decreased to 6.68 mmol/L (258 mg/dL).

Cholesterol↗
PubMed1981

Effect of nicotinic acid and dipyridamole on tissue blood flow in peripheral vascular disease.

The effect of 2-weeks' treatment with daily doses of 150 mg nicotinic acid, 300 mg dipyridamole and placebo, in random order, on muscle blood flow and skin temperature gradient in the legs was measured in 6 patients with advanced arteriosclerotic peripheral vascular disease. Mean resting skin temperature gradient and muscle blood flow were uninfluenced by any of these treatments. Dipyridamole, but not nicotinic acid, caused a significant increase in exercise muscle blood flow compared to placebo (p less than 0.01). This improvement was maintained after 2-months' continuous treatment at the end of the trial. It is concluded that dipyridamole may be of value in the medical management of peripheral vascular disease.

Adult↗
PubMed1981

The use of nicotinic acid and pyridoxine in the treatment of schizophrenia.

As part of the Canadian Mental Health Association Collaborative Study, the hypothesis that combined administration of nicotinic acid and pyridoxine has greater therapeutic effects than the component drugs in chronic schizophrenic patients was tested. This could not be substantiated in a 48-week study in which supplementation of neuroleptic treatment with a single vitamin, i.e., nicotinic acid or pyridoxine, produced significant therapeutic changes, while supplementation with both vitamins did not.

Adult↗
PubMed1970

Nicotinic acid as adjuvant therapy in newly admitted schizophrenic patients.

A placebo-controlled, comparative clinical study was conducted to test the hypothesis that nicotinic acid as an adjuvant medication has a beneficial therapeutic effect over and above the effect which can be achieved by the administration of phenothiazine drugs alone, over a six-month period, in newly (recently) admitted schizophrenic patients.The most important single finding was that no statistically significant therapeutic difference was seen between the active treatment and the placebo groups; i.e., the addition of nicotinic acid or nicotinamide to the regular phenothiazine treatment regimen did not have any measurable therapeutic effect in this sample of patients. It was shown that patients in the placebo group received a lower total daily amount of phenothiazine drugs than those on either of the active substances. Furthermore, it was noted that the addition of the active substances did not reduce the number of days of hospitalization.

Adult↗
PubMed1995

Effects of nicotinic acid and lovastatin in renal transplant patients: a prospective, randomized, open-labeled crossover trial.

Lipid abnormalities are seen frequently in renal transplant patients. Cardiovascular disease is an important cause of morbidity and mortality in these patients. We assessed the efficacy and safety of the lipid-lowering drugs, nicotinic acid (short acting) and lovastatin, the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Twelve renal transplant patients who had persistent hyperlipidemia despite 6 weeks of dietary treatment participated in this prospective, randomized, open-labeled crossover trial. At 16 weeks, when compared with control values, nicotinic acid (> or = 1.5 g twice a day) significantly reduced the total cholesterol (from 312 +/- 18 [+/- SEM] mg/dL to 229 +/- 19 mg/dL; P = 0.03) and the low-density lipoprotein cholesterol (from 218 +/- 15 mg/dL to 142 +/- 13 mg/dL; P = 0.03) and significantly increased the high-density lipoprotein cholesterol (from 44 +/- 3 mg/dL to 58 +/- 5 mg/dL; P = 0.03). The triglyceride level was reduced from 255 +/- 40 mg/dL to 150 +/- 23 mg/dL (P = 0.09). At 16 weeks, lovastatin therapy (40 mg/d) significantly reduced the total cholesterol (from 285 +/- 13 mg/dL to 233 +/- 10 mg/dL; P = 0.005) and the low-density lipoprotein cholesterol (from 201 +/- 11 mg/dL to 147 +/- 7 mg/dL; P = 0.001). There were no significant changes in the triglyceride and high-density lipoprotein cholesterol levels. Although flushing developed in 67% of patients treated with nicotinic acid, this was not a reason for any of the study dropouts. During this short-term study period no adverse biochemical effects were noted with either of the drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Raising high-density lipoprotein cholesterol with reduction of cardiovascular risk: the role of nicotinic acid--a position paper developed by the European Consensus Panel on HDL-C.

Reduction of low-density lipoprotein cholesterol (LDL-C) is presently the primary focus of lipid-lowering therapy for prevention and treatment of coronary heart disease (CHD). However, the high level of residual risk among statin-treated patients in recent coronary prevention studies indicates the need for modification of other major components of the atherogenic lipid profile. There is overwhelming evidence that a low plasma level of high-density lipoprotein cholesterol (HDL-C) is an important independent risk factor for CHD. Moreover, a substantial proportion of patients with or at risk of developing premature CHD typically exhibit distinct lipid abnormalities, including low HDL-C levels. Thus, therapeutic intervention aimed at raising HDL-C, within the context of reducing global cardiovascular risk, would benefit such patients, a viewpoint increasingly adopted by international treatment guidelines. Therapeutic options for patients with low HDL-C include treatment with statins, fibrates and nicotinic acid, either as monotherapy or in combination. Of these options, nicotinic acid is not only the most potent agent for raising HDL-C but is also effective in reducing key atherogenic lipid components including triglyceride-rich lipoproteins (mainly very low-density lipoproteins [VLDL] and VLDL remnants), LDL-C, and lipoprotein(a). The principal features of the atherogenic lipid profile in type 2 diabetes and the metabolic syndrome make them logical targets for nicotinic acid therapy, either alone or in combination with a statin. The lack of comprehensive European data on the prevalence of low HDL-C levels highlights a critical need for education on the importance of raising HDL-C in CHD prevention and treatment. The development of a reliable and accurate assay for HDL-C, as well as clarification of criteria for low and optimal levels of HDL-C in both men and women, constitute critical factors in the reliable identification and treatment of patients at elevated risk of CHD due to low HDL-C. Based on the available evidence, the European Consensus Panel recommends that the minimum target for HDL-C should be 40 mg/dL (1.03 mmol/L) in patients with CHD or with a high level of risk for CHD, including patients at high global risk with type 2 diabetes or the metabolic syndrome.

Cholesterol, HDL↗
PubMed1993

Quantitative efficacy of niacin sources for chicks: nicotinic acid, nicotinamide, NAD and tryptophan.

A niacin-deficient diet based upon corn and casein was used to establish growth-promoting efficacy of various sources of niacin activity. In the presence of excess dietary nicotinamide, chicks fed the corn-casein diet achieved maximal weight gain when 100 mg/kg of L-tryptophan was supplemented. The basal diet for efficacy studies therefore contained 100 mg/kg of added tryptophan and no supplemental nicotinic acid. Weight gain in the linear response surface of the growth curve proved to be a far better measure of niacin bioactivity than tissue accumulation of NAD(P). Slope-ratio growth efficacy studies indicated that excess dietary tryptophan was 1.94 +/- 0.14% as efficient as nicotinic acid in furnishing bioavailable niacin activity (52:1, wt:wt). Relative to nicotinic acid used as a standard (100%), nicotinamide bioactivity was 124%. Nicotinamide in NAD was utilized with an efficiency of 95% relative to nicotinamide per se.

Analysis of Variance↗
PubMed1976

Metabolic response of humans to ingestion of nicotinic acid and nicotinamide.

The identification of nicotinamide-N1-oxide as a metabolite in the urine of a schizophrenic patient prompted a study of the relative metabolism of nicotinic acid and nicotinamide in mental patients and healthy volunteers. Metabolites quantified included N1-methyl-2-pyridone-5-carboxamide, N1-methyl-4-pyridone-3-carboxamide, N1-methylnicotinamide, nicotinuric acid, and nicotinamide-N1-oxide. More of most of these metabolites evidently was excreted after nicotinamide ingestion than after nicotinic acid. At the highest doses (3000 mg/day), the relative proportions of these metabolites in the urine were changed. There were only slight difference between healthy individuals and mental patients in the quantities of metabolites excreted, and no statistically significant trends were noted.

Adult↗
PubMedDate not supplied

Reduction of fluid-loss in cholera by nicotinic acid: a randomised controlled trial.

A randomised controlled clinical trial was conducted to investigate the ability of nicotinic acid to reduce intestinal secretion in patients with severe cholera. Of the 62 adults investigated, 29 received either 1 or 2 g of nicotinic acid given orally in divided doses and 33 served as controls. Patients who received the 2 g dose had less fluid loss than did their controls during the first (p less than 0.01) and second (p less than 0.05) 8 h post-treatment periods. During the third and fourth 8 h periods, the rates were lower in the treatment groups, but not significantly so. The drug-specific stool reduction was 31%-47% during the first 16 h. Patients receiving 1 g consistently had lower rates of purging than had their controls during each 8 h observation period, but the differences were not significant. The effect of the 2 g dose was significantly better than that with the 1 g dose. The peak inhibition occurred 8-16 h after start of therapy. The drug was well tolerated, the only side-effect being transient flushing of the body in 1 patient.

Adult↗
PubMed1993

Urinary solute transport by ileal segments. I. Effects of nicotinic acid.

This study was conducted to quantify urinary solute transport by the ileum, using an in vivo human model, and to determine the effect of nicotinic acid on this process. Patients were studied under both basal conditions and niacin therapy. The rates of solute transport were established by analysis of excretion indexes for each solute. Potassium and ammonium were absorbed by the ileum, while phosphorus, sodium and bicarbonate were secreted. The percentage excretion index of sodium and bicarbonate increased by approximately 100 and 600% respectively, causing a significant rise in urinary pH. Although not statistically significant, there was a tendency for chloride to be absorbed and for water to pass into the bowel lumen. Nicotinic acid 3 g/day had no significant effect on urinary solute transport.

Ammonia↗
PubMed1988

Microviscosity in lecithin liposomes: effect of nicotinic acid.

We have studied the effect of nicotinic acid, a drug commonly used as a vasodilatory agent and also for the treatment of hypercholesterolemia, on the fluidity profile of liposomes of egg lecithin and dipalmitoyl lecithin, using a fluorescent polarization probe. In both cases the drug decreases the membrane fluidity and for cholesterol-probed liposomes, it disrupts the "intermediate fluid condition" induced by cholesterol. The drug also affects the activation energy for diffusion in the hydrophobic region of the liposomes.

Algorithms↗
PubMed1997

Caged nicotinic acid adenine dinucleotide phosphate. Synthesis and use.

Nicotinic acid adenine dinucleotide phosphate (NAADP) is a metabolite of NADP with Ca2+ mobilizing activity. The Ca2+ release mechanism activated by NAADP as well as the Ca2+ stores that it acts on are different from those activated by either cyclic ADP-ribose or inositol 1,4,5-trisphosphate (IP3) (Lee, H. C., and Aarhus, R. (1995) J. Biol. Chem. 270, 2152-2157). In order to demonstrate unambiguously that NAADP can mobilize Ca2+ stores in live cells, a caged analog was synthesized by reacting NAADP with 1-(2-nitrophenyl)diazoethane. Anion exchange high pressure liquid chromatography (HPLC) was used to purify one particular caged form from the mixture of products. Phosphate analyses following specific enzymatic cleavage indicate that the caging group is on the 2'-phosphate. This is confirmed by 31P NMR spectroscopy, showing that the 2'-phosphate of the caged compound exhibits an altered chemical shift of -2.6 ppm as compared with 2.3 ppm determined for the 2'-phosphate of NAADP. Caged NAADP had no Ca2+ releasing activity at a concentration as high as 1 micro;M when tested on sea urchin egg microsomes. After photolysis, it released Ca2+, was effective in nanomolar range, and was indistinguishable from authentic NAADP. The regeneration of NAADP after photolysis was also confirmed by HPLC analyses. The analog is particularly susceptible to UV and can be efficiently photolyzed using a spectrofluorimeter. To demonstrate its utility in live cells, caged NAADP was microinjected into sea urchin eggs. Photolysis effectively regenerated NAADP and activated Ca2+ oscillations in the eggs. Removal of external Ca2+ did not prevent the Ca2+ oscillations but only delayed the second Ca2+ peak by about 45 s, indicating that the oscillations are due to release from internal stores and not caused by Ca2+ influx. A mechanism based on sensitization of the Ca2+ release by Ca2+ loading is proposed to account for the Ca2+ oscillation observed.

Animals↗
PubMed2000

Widespread distribution of binding sites for the novel Ca2+-mobilizing messenger, nicotinic acid adenine dinucleotide phosphate, in the brain.

Nicotinic acid adenine dinucleotide phosphate (NAADP) is a potent Ca(2+)-mobilizing agent in invertebrate eggs that has recently been shown to be active in certain mammalian and plant systems. Little, however, is known concerning the properties of putative NAADP receptors. Here, for the first time, we report binding sites for NAADP in brain. In contrast to sea urchin egg homogenates, [(32)P]NAADP bound reversibly to multiple sites in brain membranes. The rank order of potency of NAADP, 2',3'-cyclic NAADP and 3'-NAADP in displacing [(32)P]NAADP was, however, the same in the two systems and in agreement with their ability to mobilize Ca(2+) from homogenates. These data indicate that [(32)P]NAADP likely binds to receptors mediating Ca(2+) mobilization. Autoradiography revealed striking heterogeneity in the distribution of [(32)P]NAADP binding sites throughout the brain. Our data strongly support a role for NAADP-induced Ca(2+) signaling in the brain.

Animals↗
PubMed1987

Hypersideremic and hyperbilirubinemic effect of nicotinic acid in patients with Gilbert's syndrome.

Nicotinic acid test (NA) administration is followed by a rise in unconjugated bilirubin and serum total iron in healthy man. A similar concomitant effect has never been investigated in Gilbert's syndrome (GS) patients, who by definition have a hyperbilirubinemia higher than that of controls. The aim of this study was to verify whether, in addition to the hyperbilirubinemic action, NA could induce parallel hypersideremia in GS subjects. The data we obtained confirm in GS patients: 1. the well-known hyperbilirubinemia; 2. a delayed NA plasma concentration curve, and document that in GS the hypersideremic effect is comparable to that of controls. Previous investigators reported that NA produces an equimolar rise of bilirubin and iron levels in healthy man. In our study the extent of the sideremic response to NA occurring in GS patients is comparable to that seen in controls, and appears unrelated to the bilirubinemic values. If the NA effects are based on the documented hemolytic properties of NA, a disturbance in bilirubin handling by the liver of GS subjects appears to be plausible in the presence of almost normal behavior of NA-induced hypersideremia.

Adolescent↗
PubMedDate not supplied

[Action mechanism of nicotinic acid on fibrinolysis in vitro and in vivo].

Action of nicotinic acid (NA) on components of fibrinolysis in vitro and in vivo and on fibrinolytic activity in vivo was studied. It is shown that NA represses action of inhibitors as well as of fibrinolysis activators. Interaction of NA with plasma in vitro is associated with enhanced fibrinolytic activity on account of inhibition of antiplasmins. Action of NA of fibrinolytic activity of blood during intravenous administration depends on dose. Small doses of NA induce slight activation of fibrinolysis due to binding of antiplasmins. Administration of high doses of NA induces activation of fibrinolysis through thrombogenesis involving central nervous system.

Animals↗
PubMed1978

Metabolic abnormalities of tryptophan and nicotinic acid in patients with rheumatoid arthritis.

The mean plasma total tryptophan concentration of 13 long-standing rheumatoid arthritis patients was found to be lower than that of seven nonrheumatoid control subjects, but the plasma nicotinic acid concentration was unchanged. In the rheumatoid patients the urinary excretion of the tryptophan metabolites, kynurenine, xanthurenic acid and 3-hydroxyanthranilic acid, was increased several fold, but the excretion of N-methylnicotinamide was normal. These findings are discussed in relationship to the dietary intakes of tryptophan, nicotinic acid and pyridoxine, the effect of antirheumatoid drugs on plasma tryptophan and liver tryptophan pyrrolase, and requirement of rheumatoid patients for pyridoxine.

3-Hydroxyanthranilic Acid↗