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Results for “NICOTINIC ACID”

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PubMed1980

Effects of administration of nicotinic acid on glucose, insulin, and glucose tolerance in ruminants.

Effects of nicotinic acid on glucose metabolism were studied in a series of experiments with goats. Oral administration of single doses of nicotinic acid (6.5 to 17.0 g) elevated blood glucose, impaired glucose tolerance, and elevated insulin. The magnitude of the effects was related positively to nicotinic acid dosage. Maximum effect occurred 2 to 3 days after administration. Blood glucose was elevated, with or without glucose administration, despite markedly elevated insulin. However, exogenous insulin given 48 h after nicotinic acid still reduced blood glucose although the response was delayed and was less than in control animals. A lactating cow given 160 g nicotinic acid exhibited alterations in glucose metabolism similar to control animals. These studies demonstrate that nicotinic acid, in addition to previously reported effects on lipid metabolism, also has significant effects on carbohydrate metabolism.

Animals↗
PubMed1979

The sensitivity of Staphylococcus aureus 79 and 80, and Escherichia coli 95 to sodium salicylate, nicotinaldehyde singly, and in combination with nicotinic acid or nicotinamide.

Minimum bactericidal concentrations of salicylate, nicotinaldehyde singly, and in combination with nicotinic acid, or nicotinamide were determined for Staphylococcus aureus 79 and 80, and Escherichia coli 95, at inocula of 10(7)--10(2). The bactericidal dose of salicylate was affected markedly by the inoculum size. The bactericidal dose of nicotinic acid, or nicotinamide was affected only slightly by the size of the inoculum. Escherichia coli 95 was least affected by the inoculum size. Nicotinaldehyde is a far more bactericidal agent than is nicotinic acid, or nicotinamide; its bactericidal dose was approximately a tenth that of nicotinic acid, or nicotinamide. S. aureus 79 and 80 were affected synergistically by the combinations of nicotinic acid, or nicotinamide with salicylate. Nicotinaldehyde reduced the effectiveness of nicotinic acid, at all inoculum sizes, of S. aureus 79, while the reduction of effectiveness of nicotinamide was only found with inocula of 10(7)--10(5). At low inocula, 10(4)--10(2), an additive effect was demonstrated. S. aureus 80 was antagonistically affected, at all inoculum sizes, by the combination of nicotinaldehyde with nicotinamide, while with nicotinic acid a slight synergy was noted. In contrast, Escherichia coli 95 was antagonistically affected, at all inoculum sizes, by combinations of nicotinic acid, nicotinamide with salicylate, or nicotinaldehyde.

Aldehydes↗
PubMed1997

Influence of duodenal infusion of nicotinic acid on the milk fat composition of dairy cows.

Two experiments I and II, with 2 and 4 lactating dairy cows respectively, each fistulated with ruminal and duodenal cannulae, were carried out. The effects on milk composition and milk fat fatty acids' pattern through a continuous daily infusion into the duodenum with 6 g nicotinic acid were investigated. Treatments were nicotinic acid (NA) infusion in experiment I, and nicotinic acid infusion plus feeding 270 g of stearic acid in experiment II. No application of NA and stearic acid in experiments I and II respectively, acted as controls. Nicotinic acid infusion did not significantly influence protein, fat and lactose contents of milk. In both experiments, infusion of nicotinic acid decreased the proportion of short and middle chain fatty acids in milk fat and increased significantly the percentage of oleic acid from 19.0 to 25.4%. The addition of stearic acid alone had no effect on milk composition and fatty acids' pattern. Additional infusion of nicotinic acid infusion significantly increased nicotinamid concentration in the milk from 49.7 to 87.2 micrograms/100 ml.

Administration, Oral↗
PubMed1978

Effect of nicotinic acid on catecholamine synthesis in rat brain.

Effect of nicotinic acid on the formation of catecholamine has been studied. Norepinephrine and dopamine concentrations in brain were 30 per cent higher and brain catecholamine formation was 50 per cent higher in the nicotinic acid-supplemented rats than the nicotinic acid-deficient rats. However, these catecholamine levels of the nicotinic acid-deficient rats were recovered by the administration of nicotinic acid. The concentration of brain tyrosine was unaltered after administration of nicotinic acid to the nicotinic acid-deficient rats. Therefore, the changes catecholamine formation by the nicotinic acid supplementation were not due to the difference of tyrosine concentration in the brain which is the precursor for catecholamine biosynthesis. As the difference of catecholamine concentration between the nicotinic acid deficient and the nicotinic acid supplemented group was smaller than that of catecholamine formation of these groups, the turnover of catecholamine was supposed to be decreased in nicotinic acid deficiency.

Animals↗
PubMed1985

Nicotinic acid transport in Escherichia coli.

The uptake of nicotinic acid by Escherichia coli is dependent on the presence of the enzyme nicotinic acid phosphoribosyl transferase and a source of energy. Glucose concentrations between 0.1 and 0.5%, a temperature of 46 degrees C and an external concentration of 2.5 X 10(-5) were optimal conditions for nicotinic acid uptake. Saturation kinetics occur with a Km of 1.75 microM and a Vmax of 0.116 nmoles/min/mg dry weight. The intracellular molarity of the accumulated pyridine compounds is 44-fold that of the initial concentration. Inhibitors of respiration and anaerobiosis do not significantly inhibit uptake rate. However, an inhibitor of glycolysis, uncouplers of ATP production and sodium arsenate reduce vitamin transport. A mutant defective in ATPase does not accumulate exogenously supplied nicotinic acid when lactate is used as an energy source, although L-proline, the transport of which is independent of ATP production, is accumulated.

Adenosine Triphosphatases↗
PubMed1995

Enzymic method for the amperometric determination of nicotinic acid in meat products.

An enzymic method for the determination of nicotinic acid is described, based on the indirect electrochemical monitoring of nicotinic acid via its reaction with oxygen in the presence of nicotinic acid hydroxylase. Derivative amperometric signals due to oxygen depletion enable a one-point kinetic analysis to be carried out. Nicotinic acid hydroxylase catalyses the hydroxylation of nicotinic acid to produce 6-hydroxynicotinic acid, which is accompanied by a stoichiometric consumption of oxygen. The method was applied successfully to the analysis of real samples.

Catalysis↗
PubMed1997

Isolation of new 6-methylnicotinic-acid-degrading bacteria, one of which catalyses the regioselective hydroxylation of nicotinic acid at position C2.

2-Hydroxynicotinic acid is an important building block for herbicides and pharmaceuticals. Enrichment strategies to increase the chances of finding microorganisms capable of hydroxylating at the C2 position and to avoid the degradation of nicotinic acid via the usual intermediate, 6-hydroxynicotinic acid, were used. Three bacterial strains (Mena 23/3-3c, Mena 25/4-1, and Mena 25/ 4-3) were isolated from enrichment cultures with 6-methylnicotinic acid as the sole source of carbon and energy. Partial characterization of these strains indicated that they represent new bacterial species. All three strains completely degraded 6-methylnicotinic acid, and evidence is presented that the first step in the degradation pathway of strain Mena 23/3-3c is hydroxylation at the C2 position. Resting cells of this strain grown on 6-methylnicotinic acid also hydroxylated nicotinic acid at the C2 position, but did not further degrade the product. Strain Mena 23/ 3-3c showed the highest degree of 16S rRNA sequence similarity to members of the genera Ralstonia and Burkholderia.

Bacillus↗
PubMed1994

[Nicotinic acid and derivatives for therapy of hyperlipoproteinemia].

Nicotinic acid and derivatives are effective in numerous forms of hyperlipoproteinemia. Its primary mode of action is to inhibit lipolysis in adipose tissue and to prevent the utilization of free fatty acids for TG-rich lipoprotein synthesis in the liver. Consequently, it decreases the plasma lipoproteins which are considered to be atherogenic--VLDL, LDL and Lp(a), while it increases the antiatherogenic lipoprotein--HDL. A gradual administration of nicotinic acid or derivatives is useful to reduce the side effects such as flushing and itching. In the secondary prevention trials, nicotinic acid therapy with other hypolipidemic drugs asserted protective effects on the development/progression of cardiovascular disease.

Adipose Tissue↗
PubMedDate not supplied

[Influence of nicotinic acid on the methylation of phospholipids in various tissues of rats].

The content and methylation of total phospholipids in the brain, liver and muscles and some of their fractions obtained by the method of thin-layer chromatography on silicic acid were studied as affected by nicotinic acid. It is established that nicotinic acid in a dose of 20 mg/kg 4 hrs after subcutaneous injection evokes an increase in the content of phosphatidyl ethanol amine in the liver and sphyngomyelin in the muscles. The intensity of methylation of choline-containing phospholipids under the effect of nicotinic acid lowers in all the tissues under study.

Animals↗
PubMed1993

[Hemostasis-regulating role of nicotinic acid and its analogs].

Nicotine acid and especially its analogs nicomorpholine and azethylnicotinate have ability to inhibit the thrombocytes' aggregation, inhibit thromboxane A2 biosynthesis, stimulate prostacyclin generative function of vascular wall, increase the cycle nucleotide level, have the features of calcium antagonists. This features predetermine their use for correction and healing of thromboembolic diseases and improvement of microcirculation, cerebral as well.

Animals↗
PubMedDate not supplied

Loss of cholesterol from muscle and skin of monkeys treated with nicotinic acid.

In Rhesus monkeys, nicotinic acid given daily by subcutaneous injection for 5 weeks brought about a reversible decrease in total cholesterol concentration in skeletal muscle and skin to about half the normal value. The decrease in cholesterol concentration was due to a net loss of cholesterol from muscle, since the treatment had no effect on the water content or on the percentage of DNA or protein in fresh tissue. In muscle, free cholesterol was lost in preference to esterified cholesteol, but in skin both cholesterol fraction were affected to about the same extent. Analysis of the cholesterol content of subcellular fractions of homogenates of muscle showed that loss of cholesterol occurred mainly from the soluble fraction and the 800-g sediment, with no significant loss from the mitochondrial or microsomal fractions.

Animals↗
PubMed1996

Nicotinic acid transport mediated by pH-dependent anion antiporter and proton cotransporter in rabbit intestinal brush-border membrane.

In order to determine whether the vitamin nicotinic acid is absorbed via an anion antiporter, intestinal epithelial cell membrane transport mechanisms for nicotinic acid were characterized using isolated rabbit jejunal brush-border membrane vesicles. The uptake of nicotinic acid by the membrane vesicles showed an overshoot phenomenon in the presence of an outwardly directed bicarbonate gradient or an inwardly directed proton gradient and the uptakes were two times and six times greater, respectively, than that in the absence of any ion gradient. The bicarbonate-dependent initial uptake of nicotinic acid was increased at acidic pH, showing pH-dependent transport activity. An inhibitor of anion transport, 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid, specifically reduced bicarbonate-dependent transport of nicotinic acid. The initial uptakes of nicotinic acid via the anion antiporter and the proton cotransporter were specifically inhibited by monocarboxylic acids such as acetic acid, benzoic acid, D- and L-lactic acid, pravastatin and valproic acid, but not by di- or tricarboxylic acids, bile acids or amino acids. Nicotinic acid uptake activity was, furthermore, expressed in a Xenopus laevis oocyte system after injection of messenger RNA (mRNA) derived from rabbit intestinal epithelial cells. These observations demonstrate that nicotinic acid is absorbed by two independent active transport mechanisms from small intestine, i.e. a proton cotransporter and an anion antiporter. The pH-dependence observed in the intestinal absorption of nicotinic acid might, therefore, be ascribed partly to pH-sensitive and partly to carrier-mediated transport mechanisms in the brush-border membrane.

Animals↗
PubMed1990

Variation of cofactor levels in Escherichia coli. Sequence analysis and expression of the pncB gene encoding nicotinic acid phosphoribosyltransferase.

The pncB gene from Escherichia coli, which encodes nicotinic acid phosphoribosyltransferase (EC 2.4.2.11), was cloned on a 1.5-kilobase TaqI-EcoRI fragment. Its position on the E. coli chromosome was determined at 20.8 min between the asnS and pepN loci. The nucleotide sequence of the gene and the transcription and translation initiation sites were determined. Expression of pncB on a multicopy plasmid leads to a 25-fold increase in nicotinic acid phosphoribosyltransferase activity. Growth of E. coli in the presence of nicotinic acid leads to strong repression of nicotinic acid phosphoribosyltransferase activity, indicating that the cloned pncB sequence contains its own control sequences. It is shown that increased nicotinic acid phosphoribosyltransferase activity effects a 5-fold increase in the intracellular concentration of NAD. The cloned pncB gene can therefore be used as a tool to raise intracellular cofactor levels.

Amino Acid Sequence↗
PubMed1992

Reversible adsorption of nicotinic acid onto charcoal in vitro.

The effects of various factors on the adsorption of nicotinic acid onto and desorption from activated charcoal were investigated in vitro. The affinity of nicotinic acid for charcoal was poor both in acidic and neutral media. Adsorption increased with increasing charcoal:drug ratios and decreasing incubation volume:charcoal ratios. Desorption of nicotinic acid from dried drug-charcoal complexes was investigated in a Sartorius dissolution apparatus. The rate of the rapid, initial desorption depended on the pH and the amounts of charcoal and drug. As equilibrium was reached in the dissolution chamber, the release rate of nicotinic acid decreased slowly, depending mainly on the flow of the medium. Thus, nicotinic acid preadsorbed onto charcoal was released in a sustained manner under "continuous flow" conditions. However, because of the poor affinity for nicotinic acid, charcoal may not be a suitable matrix for sustained release of nicotinic acid.

Adsorption↗
PubMed1983

Possible glucagon-mediated hypocholesterolemic activity of a nicotinic acid derivative (sorbinicate).

The antilipolytic activity of nicotinic acid was investigated in 7 patients with type II b hyperlipoproteinemia and in 7 with type IV hyperlipoproteinemia treated for two months with a nicotinic acid derivative, sorbinicate (1600 mg daily, ie 1454 mg NA). Before and after treatment the blood levels of total cholesterol and triglycerides were determined and three dynamic tests -- oral glucose tolerance test, insulin test and tolbutamide test -- were done to check in each test the variations in blood glucose, NEFA, insulin (excluding obviously the insulin test), glucagon and growth hormone levels. At the end of the treatment, there was a significant reduction of cholesterol (type IIb and type IV) and of triglycerides (type IV), a marked reduction of the glucagon response, a slight increase in the insulin response and in the basal secretion of the growth hormone. It is suggested that the antilipolytic activity of nicotinic acid (and hence of sorbinicate) is at least partly mediated by an inhibition of glucagon secretion (and/or synthesis).

Adult↗
PubMed1991

Tolerance to nicotinic acid flushing.

The mechanism of tolerance to nicotinic acid flushing was determined in subjects during a 5-day course of treatment. Objective measures of skin blood flow were used to confirm the development of tolerance. Plasma levels of nicotinic acid showed marked intraindividual variability but were not decreased with the development of tolerance. However plasma levels of 9-alpha 11-beta prostaglandin F2, a stable metabolite of prostaglandin D2, became undetectable in most subjects with the development of tolerance. Thus tolerance is not associated with decreased levels of nicotinic acid or development of tolerance to the prostaglandin mediator, but with decreased levels of the mediator.

Administration, Oral↗