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At least 415 records · Page 23Linked to original sources
PubMed1976

Modification of nicotinic acid and prostaglandin E1 antilipolytic action in vitro.

In epididymal adipose tissue from rats, human serum antagonizes inhibition of basal lipolysis by nicotinic acid in vitro. Under similar conditions caffeine-stimulated lipolysis was unaffected by the presence of human serum. Very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins were all found to antagonize the action of nicotinic acid on basal lipolysis. VLDL also antagonized prostaglandin E1 (PGE1)-inhibition of basal lipolysis in vitro. The fat cell membrane was suggested as the site at which human serum lipoproteins antagonize nicotinic acid or PGE1 antilipolytic action on basal lipolysis in vitro.

Adipose Tissue↗
PubMed1989

Effect of nicotinic acid supplementation in vivo on oxygen radical-induced genetic damage in human lymphocytes.

The ability of nicotinic acid to protect human lymphocytes in vivo against oxygen radical-induced DNA strand breakage was tested. NAD+ concentrations rose progressively in lymphocytes to nearly 5 times baseline levels in human volunteers ingesting nicotinic acid (100 mg/day) for 8 weeks. Strand breaks decreased proportionately to NAD+ concentrations over this time period in lymphocytes exposed to oxygen radicals. After 8 weeks of supplementation with nicotinic acid, radical-treated lymphocytes incubated for 24 h evidenced significantly less DNA damage compared to controls.

DNA↗
PubMed1984

Effect of nicotinic acid associated with retinol and tocopherols on plasma lipids in hyperlipoproteinaemic patients.

Twelve hypercholesterolaemic patients, with or without hypertriglyceridaemia, were treated sequentially with 600 mg nicotinic acid alone per day and 300 mg nicotinic acid plus 60,000 U retinol and 140 mg tocopherols per day, each treatment being given for 30 days in random order sequence. Plasma concentrations of lipid fractions were determined before the start of the study and at the end of each treatment period. Both treatments resulted in a significant decrease in total cholesterol and LDL-cholesterol; HDL-cholesterol showed a small but significant increase and plasma triglycerides presented a variable behaviour pattern of change. The difference between the hypolipidaemic effects of nicotinic acid alone and the lower dose given with Vitamins A and E was small but the combination seemed to be more effective. No side-effects were reported with either treatment.

Cholesterol, HDL↗
PubMed1984

Determination of nicotinic acid in serum by high-performance liquid chromatography with fluorescence detection.

A sensitive method for the determination of nicotinic acid in serum is described which employs high-performance liquid chromatography with fluorescence detection. Nicotinic acid and 2-chloronicotinic acid as an internal standard in deproteinized serum are reacted with N,N'-dicyclohexyl-O-(7-methoxycoumarin-4-yl)methylisourea in acetone to give the corresponding fluorescent 4-hydroxymethyl-7-methoxycoumarin esters. The compounds are separated by reversed-phase chromatography on LiChrosorb RP-18 with isocratic elution using aqueous acetonitrile containing a small amount of sodium 1-hexanesulphonate as a mobile phase. The detection limit of nicotinic acid in serum was 0.2 nmol/ml. The method requires only 100 microliters of serum.

Chromatography, High Pressure Liquid↗
PubMed1986

Evaluation of the effects of forskolin and the antilipolytic agents insulin and nicotinic acid on cyclic AMP levels in rat epididymal adipocytes.

The effects of forskolin and the antilipolytic agents nicotinic acid and insulin on cAMP accumulation in rat epididymal adipocytes were evaluated. Forskolin markedly stimulated cAMP accumulation in adipocytes of the rat. Addition of epinephrine to cells treated with forskolin acted synergistically to increase the cAMP accumulation 4-fold when compared with cells treated with forskolin alone. Analysis of the forskolin dose-response kinetics indicated a dose-dependent increase in the accumulation of cAMP. The presence of 1-methyl-3-isobutylxanthine caused a shift in the forskolin dose-response to lower concentrations. In contrast, addition of nicotinic acid to cells treated with 1-methyl-3-isobutylxanthine caused a shift in the forskolin dose-response to higher concentrations. Preincubation of cells with adenosine deaminase did not alter the forskolin dose-response curve but potentiated its effect. Forskolin stimulation of cAMP accumulation in adipocytes was inhibited by the antilipolytic agents nicotinic acid and insulin.

1-Methyl-3-isobutylxanthine↗
PubMed1978

Stimulation of ketogénesis after glycogen depletion by nicotinic acid in perfused rat liver.

Treatment with nicotinic acid produced an enhancement of ketone bodies production from endogenous, substrates, either oleate or octanotate. The enhancement was accounted for by an increase of acetoacetate synthesis. These results suggest that the increase of acetoacetate production may be due to the enhancement of extramitochondrial ketogenesis as a consequence of the inhibition of lipogenesis.

Animals↗
PubMed1982

Effects of nicotinic acid therapy on plasma lipoproteins and very low density lipoprotein apoprotein C subspecies in hyperlipoproteinemia.

The effects of long term treatment with nicotinic acid on lipids, lipoproteins, and the plasma distribution of very low density lipoproteins (VLDL) apoprotein C (ApoC) subspecies were studied in 33 patients with types IIa (n = 9), IIb (n = 11), and IV (n = 13) hyperlipidemias. After 6 months of treatment, a significant decrease in triglyceride, total cholesterol, and low density lipoprotein (LDL) cholesterol levels occurred. High density lipoprotein (HDL) cholesterol increased significantly by 31.1%, 41.8%, and 32.0% in types IIa, IIb, and IV, respectively (P less than 0.01 for all). A significant negative correlation existed between changes in HDL cholesterol and triglycerides (r = -0.613; P less than 0.02) in all groups studied. Therapy also produced changes in VLDL, LDL, and HDL protein concentrations. VLDL protein decreased from 20.9 +/- 3.9 to 15.2 +/- 1.0 mg/dl (P less than 0.05) in type IIa. In types IIb and IV, mean VLDL protein decreased from 44.7 +/- 8.2 to 27.1 +/- 3.9 mg/dl (P less than 0.001) and from 46.3 +/- 7.1 to 30.6 +/- 4.9 mg/dl (P less than 0.001), respectively. LDL protein decreased significantly, and HDL protein increased in type IIa only. Gel isoelectric focusing of VLDL before and after nicotinic acid in types IIb and IV hyperlipidemia produced a significant increase in the VLDL ApoC-II component with simultaneous decreases in the total VLDL ApoC-III subspecies. This resulted in increases in the ApoC-II to ApoC-III area ratio from 0.50 +/- 0.1 to 1.02 +/- 0.2 (P less than 0.001) in type IIb and from 0.62 +/- 0.07 to 0.88 +/- 0.13 (P less than 0.01) in type IV, respectively. The ApoE subspecies and the ApoE-III to ApoE-II area ratio did not change significantly. Our results show that nicotinic acid produces a significant improvement in the lipoprotein profiles of these patients.

Adult↗
PubMed1977

Metabolism of nicotinic acid in children with burns and scalds.

The excretions of two metabolites of nicotinic acid, N1-methylnicotinamide and N1-methyl-2-pyridone-5-carboxamide have been measured at varying times after injury in a group of 27 burned or scalded children. Compared with control patients the excretions of both of these metabolites were significantly raised after injury, which suggests that the utilisation of nicotinic acid is increased.

Burns↗
PubMed2005

Mass spectrometric decompositions of copper complexes with esters and amides of nicotinic acid.

Mass spectrometric decompositions of complexes of nicotinic acid esters and amides with copper are discussed. Liquid secondary ion mass spectrometry (LSIMS) was used as an ionisation technique and metastable ion spectra were recorded by using B/E linked scans. The fragmentation pathways consist mainly of the loss of one ligand molecule and also the cleavage of amide or ester bonds. It may be possible, on the basis of cleaved neutral fragments, to determine the site of coordination in the gas phase. It was also found that the presence of a chlorine atom affects the fragmentation pathways of complexes.

Amides↗
PubMed1992

Percutaneous absorption of nicotinic acid, phenol, benzoic acid and triclopyr butoxyethyl ester through rat and human skin in vitro: further validation of an in vitro model by comparison with in vivo data.

The in vitro percutaneous absorption of three model compounds, nicotinic acid, phenol and benzoic acid, and the herbicide triclopyr butoxyethyl ester (triclopyr BEE) has been investigated in flow-through diffusion cells using skin from male Fischer 344 rats and humans. After the application of the four chemicals to the epidermal surface of unoccluded full-thickness rat skin, the absorption of each compound across the skin and into the receptor fluid at 72 hr reached 3.7 +/- 0.3, 5.7 +/- 0.6, 26.7 +/- 3.7 and 48.3 +/- 1.2% (mean +/- SD, n = 2-7) of the applied dose for triclopyr BEE, nicotinic acid, phenol and benzoic acid, respectively. After the application of the four chemicals to the epidermal surface of unoccluded full-thickness human skin, the absorption of each compound across the skin and into the receptor fluid at 72 hr was significantly (P < 0.05) less than through rat skin, reaching 0.7 +/- 0.1, 0.7 +/- 0.2, 18.8 +/- 1.3 and 37.8 +/- 6.9% (mean +/- SD, n = 2-7) of the applied dose for triclopyr BEE, nicotinic acid, phenol and benzoic acid, respectively. Occlusion of the skin surface with teflon caps often significantly (P < 0.05) enhanced the percutaneous absorption of the model compounds, although this effect was not uniform, varying with the compound under study and the skin (rat or human) used. When rat skin was occluded with teflon caps, the extent of absorption at 72 hr reached 8.6 +/- 0.8, 36.2 +/- 1.7 and 51.8 +/- 3.3% (mean +/- SD, n = 3-4) for nicotinic acid, phenol and benzoic acid, respectively. Corresponding values for human skin occluded with teflon caps were 3.3 +/- 1.6, 47.1 +/- 0.5 and 65.5 +/- 7.1% (mean +/- SD, n = 3-4). The experiments on the absorption of each model compound through rat and human skin were repeated and there was generally good agreement between the results from the two sets of experiments. The in vitro data reported compare favourably with data obtained by other workers using both in vitro and in vivo methodologies. The in vitro: in vivo correlation supports the use of the flow-through diffusion cell system as a model for the prediction of percutaneous absorption in vivo in the rat and in humans.

Absorption↗
PubMed1985

Nicotinic acid: treatment for the hyperchloremic acidosis following urinary diversion through intestinal segments.

The syndrome of hyperchloremic metabolic acidosis following urinary diversion through intestinal segments has posed a problem for urologists for more than 50 years. Recent work demonstrates that chlorpromazine, an intestinal cyclic-AMP inhibitor, partially corrects the metabolic derangements associated with this syndrome. Nicotinic acid has also been shown to be a potent inhibitor of intestinal cyclic-AMP. The present investigation employs nicotinic acid in a rat vesico-cecostomy model to examine its efficacy in the management of this syndrome. Rats with vesico-cecostomies treated with nicotinic acid are compared to untreated rats, rats with intestinal but not urinary diversions and non-operative controls. Nicotinic acid in a dose of 50 mg./kg./day corrects the hyperchloremia (p less than 0.02), elevated serum osmolality (p less than 0.0001), hyperammoniumemia (p less than 0.05) and acidosis (p less than 0.001). Results compare favorably to those obtained in an identical model with the use of chlorpromazine.

Acidosis↗
PubMed2006

Extended release nicotinic acid - a novel oral agent for phosphate control.

BACKGROUND: Hyperphosphatemia is common in hemodialysis patients. Recent animal studies show that nicotinamide inhibits the sodium dependent phosphate co-transport in the small intestine and thereby reduces serum phosphorus levels. Nicotinic acid which is the prodrug of nicotinamide is widely used as antihyperlipidemic agent. We examined in a prospective study whether it reduces serum phosphorus levels in hemodialysis patients. METHODS: Patients who were on maintenance hemodialysis were enrolled in to the study if their predialysis serum phosphorus was more than 6 mg/dl. During the pre-trial run in period of 1 week all phosphate binders were stopped. A single dose of extended release nicotinic acid (375 mg) tablet was given with meal. Repeat measurements of serum calcium, phosphorus and alkaline phosphatase were carried out after 8 weeks. Then the drug was stopped in a subgroup of patients and serum phosphorus remeasured after 2 weeks. RESULTS: There were 34 patients with varied etiological spectrum of end stage renal disease. They were on hemodialysis for a mean period of 8.7 months. Serum phosphorus levels changed significantly from a pre treatment level of 7.7 +/- 1.5 mg/dl to post treatment level of 5.6 +/-1 mg/dl (p < 0.001). There was no significant variance across age groups, sex, disease categories and dialysis duration. The calcium level increased from 8.1 +/- 1.0 to 8.5 +/- 1.0 mg/dl (p < 0.015). The serum alkaline phosphatase level decreased significantly from 107+/-66 IU/l to 82+/-46 IU/l (p < 0.001 ). There was a significant reduction of calcium phosphate product from 63.1 + 15.1 mg2 to 48.7 +/- 10.9 mg2/dl2 (p < 0.001). Oral nicotinic acid was well tolerated. Mild pruritus was encountered in 2 patients. CONCLUSION: Oral nicotinic acid may emerge as a safe, low cost yet powerful agent for phosphorus control in dialysis patients.

Adult↗
PubMed1982

[Inhibition of prostaglandin synthesis by (phenylthio-4 phenylamino)-2 nicotinic acids].

In the rat, (phenylthio-4 phenylamino)-2 nicotinic and [(chloro-4 phenylthio)-4 phenylamino]-2 nicotinic acids inhibit the hypotensive prostaglandin-mediated action of arachidonic acid. They inhibit also the formation from arachidonic acid, of prostaglandin-like substances by chopped rat lungs and of malonaldehyde by rat platelets. They are prostaglandin synthetase inhibitors, three to ten times less active as indomethacin.

Animals↗
PubMed1990

Supplemental nicotinic acid or nicotinamide for lactating dairy cows.

In two experiments with multiparous Holstein cows, the effects of feeding supplemental nicotinic acid or nicotinamide on milk production and metabolite changes associated with early lactation were measured. In Experiment 1, 30 cows were assigned to three groups. The treatment groups received 6 g nicotinic acid or 6 g nicotinamide per head per day beginning 2 wk prepartum to 12 wk postpartum. Control group received no treatment. Cows receiving nicotinamide produced more milk (wk 9, 11, and 12) and had higher milk fat test (wk 1 and 4) than did controls. Concentrations of beta-hydroxybutyrate in blood serum (wk 4) were lower for cows receiving nicotinic acid or nicotinamide. Serum glucose concentration (wk 4 to 6) was higher and FFA (wk 4) were lower for cows receiving nicotinamide than for controls. In Experiment 2 with six multiparous Holstein cows, the effects of feeding nicotinamide on metabolic changes associated before, during, and after a 48-h period without feed initiated at 4 wk postpartum were studied. The treatment groups received 12 g nicotinamide per head per day beginning 2 wk prepartum to 4 wk postpartum. The control group received no treatment. Supplementing nicotinamide to lactating cows had no effect on serum glucose, beta-hydroxybutyrate, or free fatty acids before, during, or after 48-h period without feed.

3-Hydroxybutyric Acid↗
PubMed2003

Optical coherence tomography findings in nicotinic acid maculopathy.

PURPOSE: To report optical coherence tomography findings in nicotinic acid maculopathy. DESIGN: Observational case report. METHOD: The patient was examined with ophthalmoscopy, fluorescein angiography, and optical coherence tomography. RESULTS: A 71-year-old man presented with bilateral decreased visual acuity with metamorphopsia. Optical coherence tomography demonstrated cystoid spaces in the outer plexiform layer and inner nuclear layer. Fluorescein angiography did not show leakage. Two weeks after stopping the nicotinic acid, the cystoid spaces resolved. CONCLUSIONS: Niacin maculopathy causes cystoid spaces in the inner nuclear and outer plexiform layers that resolve with discontinuation of the drug.

Aged↗
PubMed1996

Effect of chromium nicotinic acid supplementation on selected cardiovascular disease risk factors.

The effects of daily supplemental chromium (200 micrograms) complexed with 1.8 mg nicotinic acid on plasma glucose and lipids, including total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides, were assessed in 14 healthy adults and 5 adults with noninsulin-dependent diabetes mellitus (NIDDM) using a double-blind crossover study with 8-wk experimental periods. Eight of the 14 healthy subjects and all 5 subjects with NIDDM also underwent an oral glucose tolerance test with assessment of 90 min postprandial plasma glucose and insulin concentrations. No statistically significant effects of chromium nicotinic acid supplementation were found on plasma insulin, glucose, or lipid concentrations, although chromium nicotinic acid supplementation slightly lowered fasting plasma total and LDL cholesterol, triglycerides, and glucose concentrations, and 90-min postprandial glucose concentrations in individuals with NIDDM.

Administration, Oral↗
PubMed1988

Effects of fenofibrate, gemfibrozil and nicotinic acid on plasma lipoprotein levels in normal and hyperlipidemic mice. A proposed model for drug screening.

These studies examine the effects of a hypercholesterolemic diet (with butter and cholesterol added), or a hypertriglyceridemic diet (30% sucrose (w/v) in drinking water), on murine plasma lipids and lipoproteins prepared either by sequential ultracentrifugation or gel exclusion chromatography. The hypercholesterolemic diet increased plasma cholesterol (186%), particularly that associated with very low (VLDL) and low (LDL) density lipoproteins. In addition, the cholesterol/triglyceride ratio in the VLDL fraction rose significantly from 0.10 to 4.0. The hypertriglyceridemic diet raised markedly plasma triglyceride levels (46%) by expanding the circulating VLDL pool (+39%). These dietary modifications were used to provide a model for the examination of 3 classical hypolipidemic drugs (fenofibrate, gemfibrozil and nicotinic acid). In animals receiving the standard diet, fenofibrate, gemfibrozil and nicotinic acid decreased the triglyceride (TG) level (-28%, -31%, and -38%) by lowering VLDL-TG (-37%, -42%, and -49%), fenofibrate and gemfibrozil increased HDL-cholesterol by 18% and 31%, respectively. In animals receiving the hypercholesterolemic diet fenofibrate lowered the total plasma cholesterol level by 40%, at the same time increasing HDL-cholesterol by 23%. In animals fed sucrose, on the other hand, fenofibrate (100 mg/kg per day) and nicotinic acid (900 and 600 mg/kg per day) reduced plasma triglyceride levels (-20%, -40% and -33%), and nicotinic acid (900 mg/kg per day) decreased VLDL-TG by 58%. These results are in good agreement with clinical data from studies in man and suggest that this animal model may provide a useful and rapid screening system for testing new lipid lowering drugs.

Animals↗
PubMed1980

Kinetic studies of the reaction of ferric soybean leghemoglobins with hydrogen peroxide, cyanide and nicotinic acid.

A kinetic study of the reaction of two soybean leghemoglobins (components a and c) with hydrogen peroxide to form the oxidized compound (leghemoglobin IV) has been carried out over the pH range 2.5--10. Three different ionization processes of leghemoglobins with pKa values of 3,4.7 +/- 0.2 and 8.2 +/- 0.1 are required to explain the rate/pH profiles. Protonation of the former group and ionization of the latter cause a decrease in the rate of reaction of the hemoproteins with H2O2. The results are compared to those obtained for the reactions of plant peroxidases and myoglobin with H2O2. The results obtained from the kinetic study of cyanide binding to soybean leghemoglobins indicate that CN- is the reactive species. Two ionization processes of leghemoglobins with pKa values of 4.7 +/- 0.2 and 8.2 +/- 0.1 affect the reaction rates. The association and dissociation rate constants corresponding to nicotinic acid binding to leghemoglobins a and c have been measured over the pH range 2.5--7. The dissociation rate constant is affected by ionization of a group with pKa less than 2.5 for both leghemoglobin-nicotinate complexes. In this pH range the association rate constant is only affected by ionization of a group with pKa value of 4.7 +/- 0.2. The analysis of these results shows that both ionization processes corresponding to ring nitrogen atom of the ligand (pKa approximately equal to 4.9) and to a heme-linked group (pKa approximately equal to 4.7 +/- 0.2) influence the association rate constant. Furthermore, it appears that in the binding site of leghemoglobins the pKa value corresponding to ionization of the ring nitrogen atom of nicotinic acid is shifted from the normal value of 4.9 to a value of less than 2.5. This pecularity might explain the exceptional reactivity of leghemoglobins for nicotinic acid, over a large pH range. For both cyanide and nicotinic acid binding reactions, the ionizable group of leghemoglobins with pKa value of 4.7 +/- 0.2 seems to act as an electrostatic gate. When the group is deprotonated, it restricts the access of anion ligands to the heme pocket. For all the three reactions studied, leghemoglobin a reacts about twice as fast as leghemoglobin c.

Cyanides↗