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At least 19 recordsLinked to original sources
PubMed1981

Studies on the riboflavin, pantothenic acid, nicotinic acid, and choline requirements of young Embden geese.

Four experiments were conducted to examine the riboflavin, pantothenic acid, nicotinic acid, and choline requirements of young Embden geese fed purified diets. Goslings fed diets deficient in either riboflavin, pantothenic acid, nicotinic acid, or choline grew poorly. Feeding a pantothenic acid-deficient diet resulted in 100% mortality. Goslings fed diets containing 530 mg/kg of choline or less developed perosis. Under the conditions of these experiments it was found that: 1) goslings require no more than 3.84 mg/kg of riboflavin and 31.2 mg/kg of nicotinic acid in the diet for rapid growth and normal development, 2) the pantothenic acid requirement of goslings is no more than 12.6 mg/kg of diet, and 3) a dietary choline level of 1530 mg/kg is adequate for both the prevention of perosis and rapid growth of goslings. The levels of vitamins found to support normal growth and development of goslings appear to be similar to requirements of other species that have been examined.

Animal Feed↗
PubMed1996

Relative activity of N-(beta-D-glucopyranosyl)nicotinic acid to nicotinic acid as a niacin nutrient in rats and in Lactobacillus plantarum ATCC 8014.

We investigated the relative activity of N-(beta-D-glucopyranosyl)-nicotinic acid as a niacin nutrient in rats and in Lactobacillus plantarum ATCC 8014. N-(beta-D-Glucopyranosyl)-nicotinic acid is a detoxified product or storage form of nicotinic acid that is found in plants. The relative activity of N-(beta-D-glucopyranosyl)nicotinic acid to nicotinic acid in rats was 1/2.3, 1/2.2, 1/1.0, and 1/1.7 as indices of the body weight gain, food intake, blood NAD content, and the increased urinary excretion of niacin and its metabolites, respectively. N-(beta-D-Glucopyranosyl)nicotinic acid had no niacin activity in Lactobacillus plantarum ATCC 8014.

Animals↗
PubMed2001

Characterization of a G protein-coupled receptor for nicotinic acid.

Nicotinic acid is a lipid-lowering agent widely used to treat hypertriglyceridemia and to elevate low high density lipoprotein levels. However, the underlying mechanisms are poorly understood. In this study, G protein activation by nicotinic acid and derivatives was assessed as stimulation of guanosine 5'-(gamma-[(35)S]-thio)triphosphate ([(35)S]GTPgammaS) binding, and [(3)H]nicotinic acid was used for specific labeling of binding sites. Nicotinic acid (EC(50) approximately 1 microM) stimulated [(35)S]GTPgammaS binding in membranes from rat adipocytes and spleen, but not from other tissues. G protein activation in adipocyte membranes in the presence of maximally activating concentrations of the selective A(1) adenosine receptor agonist 2-chloro-N(6)-cyclopentyladenosine and nicotinic acid was almost additive, indicating that G proteins of mostly distinct pools were activated by these agonists. G protein activation by nicotinic acid and related substances in spleen and adipocytes revealed identical pharmacological profiles. [(3)H]Nicotinic acid specifically detected guanine nucleotide-sensitive binding sites of identical pharmacology in adipocyte and spleen membranes. The site of action of nicotinic acid is distinct from other G protein-coupled receptors. These data indicate that nicotinic acid most probably acts on a specific G protein-coupled receptor.

Adenylyl Cyclase Inhibitors↗
PubMed1975

Renal mechanisms for the excretion of nicotinic acid.

Nicotinic acid, an essential endogenous organic acid, was studied in free-flow clearance experiments in the dog at plasma concentrations ranging from 1.2 to 600 mug/ml. At all concentrations, net reabsorption was observed. At concentrations of 1.2 mug/ml, the clearance of nicotinic acid as compared to the clearance of insulin was approximately 0.50. As nicotinic acid plasma concentrations were increased to 90 mug/ml, the clearance ratio declined to 0.22. The clearance ratio then steadily increased to 0.75 as plasma concentrations reached 600 mug/ml. Plasma levels of nicotinic acid in excess of 600 mug/ml resulted in renal toxicity as indicated by a marked decrease in the glomerular filtration rate. The decline in the clearance ratio in the presence of 90 mug/ml of nicotinic acid suggested saturation of a secretory system and hence cyanine 863 and probenecid were used to observe their effects on the clearance ratio. The base transport inhibitor was without effect; probenecid decreased the clearance. Alkalinization of the urine had no noticeable effect on nicotinic acid clearance. Protein binding did not occur. The data indicate two important points. First, nicotinic acid is secreted to a limited degree by the organic anion secretory system and is simultaneously reabsorbed. Second, a homeostatic mechanism for conservation of nicotinic acid at low plasma levels does not seem to exist.

Animals↗
PubMed1976

Pyruvate kinase activity and gluconeogenesis in rat liver after glycogen depletion with nicotinic acid.

Nicotinic acid administration, which depletes liver glycogen, leads to an increase of both pyruvate kinase L and phosphoenolypyruvate carboxykinase in liver by a factor of nearly two. The former is not prevented by either cycloheximide or actinomycin D. L-Cysteine, an allosteric inhibitor of pyruvate kinase L, favors gluconeogenesis from lactate in both nicotinic acid treated and starved animals.

Animals↗
PubMed1989

Release of markedly increased quantities of prostaglandin D2 in vivo in humans following the administration of nicotinic acid.

Nicotinic acid (niacin) is a B vitamin which is also a potent hypolipidemic agent. However, intense flushing occurs following ingestion of pharmacologic doses of niacin which greatly limits its usefulness in treating hyperlipidemias. Previous studies have demonstrated that niacin-induced flushing can be substantially attenuated by pre-treatment with cyclooxygenase inhibitors, suggesting that the vasodilation is mediated by a prostaglandin. However, the prostaglandin that presumably mediates the flush has not been conclusively determined. In this study we report the finding that ingestion of niacin evokes the release of markedly increased quantities of PGD2 in vivo in humans. PGD2 release was assessed by quantification of the PGD2 metabolite, 9 alpha, 11 beta-PGF2, in plasma by gas chromatography mass spectrometry. Following ingestion of 500 mg of niacin in three normal volunteers, intense flushing occurred and plasma levels of 9 alpha, 11 beta-PGF2 were found to increase dramatically by 800, 430, and 535-fold. Levels of 9 alpha, 11 beta-PGF2 reached a maximum between 12 and 45 min. after ingesting niacin and subsequently declined to near normal levels by 2-4 hours. Levels of 9 alpha, 11 beta-PGF2 in plasma correlated with the intensity and duration of flushing that occurred in the 3 volunteers. Release of PGD2 was not accompanied by a release of histamine which was assessed by quantification of plasma levels of the histamine metabolite, N tau-methylhistamine. This suggests that the origin of the PGD2 release is not the mast cell. Only a modest increase (approximately 2-fold) in the urinary excretion of the prostacyclin metabolite, 2,3-dinor-6-keto-PGF1 alpha, occurred following ingestion of niacin and no increase in the excretion of the major urinary metabolite of PGE2 was found. These results indicate that the major vasodilatory PG released following ingestion of niacin is PGD2. The fact that markedly increased quantities of PGD2 are released suggests that PGD2 is the mediator of niacin-induced vasodilation in humans.

Adult↗
PubMedDate not supplied

[Citrate influence on acetyl-CoA-carboxylase activation and phosphorylation in chicken liver with lipogenesis inhibited by nicotinic acid].

Nicotinic acid in vivo affects the citrate demand for acetyl-CoA-carboxylase activation in the chicken liver under conditions of alimentary lipogenesis stimulation. Stoichiometry of the citrate binding with the dissociation constant of the enzyme-allosteric activator complex is determined under experimental conditions. Endogenic phosphorylation of acetyl-CoA-carboxylase completely correlates with its inactivation and depends on the citrate level. cAMP is established to have an activating effect on phosphorylation of acetyl-CoA-carboxylase of test animals.

Acetyl-CoA Carboxylase↗
PubMedDate not supplied

[Role of pyruvate dehydrogenase and ATP-citrate (pro-3S)lyase in inhibition of the biosynthesis of fatty acids by nicotinic acid].

The pyruvate dehydrogenase and ATP-citrate(pro-3S)lyase activity in the liver after administration of nicotinic acid to chickens against a background of stimulated lypogenesis is shown to increase in the period of maximum fall of the acetyl-CoA-carboxylase activity. Affinity of ATP-citrate (pro-3S)-lyase to citrate at this time is lowered, the content of citrate and isocitrate is elevated and CoASac is decreased to some extent. A conclusion is made on the absence of substrate limitation of acetyl-CoA-carboxylase with administration of nicotinic acid to chickens under conditions of the fatty acid biosynthesis intensification.

ATP Citrate (pro-S)-Lyase↗
PubMed1982

[Effect of combination therapy of clofibric acid and nicotinic acid derivatives on fatty acid metabolism in hyperlipoproteinemia].

71 patients (42 males and 29 females at the age of 45-76 years) with primary hyperlipoproteinaemia were treated with clofibrin acid and derivatives of nicotinic acid during 3 years. Gas-chromatographic analyses of the composition of fatty acids of their serum cholesterol ester and triglyceride fractions showed an increase of linoleic, linolenic, arachidonic, eicosapentaenic acid as well as a decrease of palmitinic, palmitoleinic, stearic, oleic and eicosatrienic acid under treatment. The changes were more efficient than under monotherapy. Selective competitive inhibition of unesterified fatty acid, blocking of lipolysis, influence on the hepatogenic metabolism of fatty acids and on the LCAT as well as better utilization of the alimentary repeatedly unsaturated fatty acids were discussed as possible mechanism. The increase of the polyunsaturated fatty acids with their interrelations to the prostaglandin metabolism must be seen in the sense of a vasoprotective effect.

Aged↗
PubMed1985

The effects of nicotinic acid and xanthinol nicotinate on human memory in different categories of age. A double blind study.

The treatment effect of nicotinic acid and xanthinol nicotinate on human memory was compared with placebo in 96 healthy subjects. Forty-three subjects were young (35-45 years), 30 subjects middle aged (55-65 years) and 23 subjects were old aged (75-85 years). Pre- and post-treatment scores were measured on a battery of memory tasks, covering sensory register, short-term memory and long-term memory. The treatment regime was 1 dragee t.i.d. for 8 weeks. The administration of xanthinol nicotinate (500 mg, containing 141.7 mg nicotinic acid), nicotinic acid (141.7 mg) and placebo (lactose) was double-blind. Pre- and post-treatment scores were analysed by means of a multivariate covariance technique, the pre-treatment score serving as covariate. Nicotinic acid treatment resulted in improvement of sensory register and short-term memory, while xanthinol nicotinate improved sensory register, short-term memory and long-term memory. In comparison with placebo, both active compounds yielded improvements of 10-40%, depending on type of task. Treatment effects of nicotinic acid were predominantly found in the young and middle-aged, whereas treatment effects of xanthinol nicotinate were predominantly found in the old. These results are interpreted by the supposed activity of nicotinic acid at the cell membrane, improving neuronal transmission, and of xanthinol nicotinate inside the cell, enhancing cell metabolism and oxygen supply in the brain.

Adult↗