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PubMedDate not supplied

[Kinetic sorption of nicotinic acid by anionites].

Studies of the kinetic sorption of nicotinic acid have demonstrated that the ionites AH-22, AH-31 and IR-45 absorb it quantitatively from water solutions. The static exchange capacity of nicotinic acid makes 3.5 mmole/g for AH-22 and IR-45 and 2.0 mmole/g for AH-31 and remains unchanged after ionite sterilization. Ionite AH-22 absorbs also quantitatively nicotinic acid from reaction mixtures used in its microbiological synthesis from 3-methyl pyridine. Formic acid (2n) desorbs entirely nicotinic acid from the above ionites. The sorption of nicotinic acid on AH-22 and IR-45 ionites is associated with diffusion processes; there is no chemical interaction between nicotinic acid and the ionites tested.

Anion Exchange Resins↗
PubMed2002

Fatty acid metabolism in liver of dairy cows fed supplemental fat and nicotinic acid during an entire lactation.

Liver biopsies from 38 multiparous Holstein cows were used to determine rates of peroxisomal beta-oxidation and total beta-oxidation of palmitate in liver homogenates and contents of total lipid, triglyceride, and glycogen during the lactation cycle. Cows were assigned to one of four diets from wk 4 through wk 42 of lactation: control, control plus nicotinic acid (12 g/d), supplemental fat, or supplemental fat plus nicotinic acid. Liver biopsies were obtained at wk 3 (covariate), 6, 12, 24, and 42 of lactation. Neither supplemental fat nor nicotinic acid affected palmitate oxidation in liver homogenates or liver composition. Peroxisomal beta-oxidation capacity and the ratio of peroxisomal to total beta-oxidation decreased from wk 3 to 12 and then increased at wk 42. Contents of total lipid and triglyceride decreased, and content of glycogen increased, from wk 3 to 12. Total oxidation capacity in liver homogenates was correlated negatively with total lipid and triglyceride in liver, yields of milk and solids-corrected milk (SCM), and plasma nonesterified fatty acids (NEFA), and was correlated positively with liver glycogen, dry matter intake (DMI), energy balance, and plasma glucose. Peroxisomal beta-oxidation was correlated negatively with yields of milk and SCM. The ratio of peroxisomal to total beta-oxidation was correlated positively with liver total lipid, liver TG, and plasma NEFA and negatively with DMI and energy balance. When only data from wk 3 postpartum were considered, both total and peroxisomal beta-oxidation were correlated negatively with hepatic concentrations of total lipid and TG. Peroxisomal beta-oxidation in liver of dairy cows is not affected by feeding supplemental fat or nicotinic acid during wk 4 to 42 of lactation but may be a part of the hepatic adaptations to negative energy balance.

Animals↗
PubMed1993

Changes in acid-base balance and calcium metabolism after urinary diversion through ileal segments. II. Treatment with nicotinic acid.

Investigations in animals have shown that nicotinic acid, an intestinal cyclic-AMP inhibitor, partially corrects the metabolic changes associated with urinary diversion through intestinal segments. Blood and serum chemistry were studied in patients before and 3 to 5 months after undergoing urinary diversion through ileal segments, both with and without nicotinic acid treatment. It was found that diverted patients had metabolic acidosis, an increased anion gap and increased levels of serum alkaline phosphatase; there were no significant changes in serum PTH and vitamin D levels, calcaemia and phosphoraemia. There was a tendency towards dehydration, hypernatraemia, hyperchloraemia and secondary hyperaldosteronism produced by ileal secretion of a hypotonic fluid. Nicotinic acid 3 g/day significantly reduced the chloraemia but did not correct the metabolic acidosis, although it reduced its severity, since blood pH decreased when treatment was suspended. Nicotinic acid cannot be recommended for routine use in the management of metabolic acidosis after urinary diversion, and patients with a marginal renal reserve should not be considered for trans-intestinal urinary diversion.

Acidosis↗
PubMed1982

Effect of nicotinic acid on cochlear blood flow.

Effects of nicotinic acid on cochlear blood flow were studied in rats by the microsphere method. One measurement was performed before drug administration and the second after i.v. injection of the nicotinic acid 25 mg/kg body weight. No measurable effect on cochlear blood flow was observed in normal animals. In one group of animals the cervical sympathetic trunks were cut and the distal part on one side was electrically stimulated during the measurements. On the unstimulated side the cochlear blood flow was significantly higher than in intact animals, but uninfluenced by nicotinic acid. On the sympathetically stimulated side a significant increase of the cochlear blood flow occurred after nicotinic acid administration.

Animals↗
PubMed1978

An automated method for the analysis of nicotinic acid in serum.

Rational antihyperlipemic therapy based on the use of nicotinic acid and its derivatives and/or combinations demands a rapid and reliable method for monitoring nicotinic acid blood levels. To this end, an automated colorimetric method for the analysis of nicotinic acid in serum has been elaborated. For serum from rats, dogs and man given p.o. nicotinic acid or 3-pyridine methanol, the method is greater than 90% specific for nicotinic acid. The limit detection for nicotinic acid is 2 microgram/ml based on 0.15 ml of serum or 0.3 microgram/ml based on 1.5 ml of serum.

Animals↗
PubMed1994

Different oxidative pathways of isonicotinic acid hydrazide and its meta-isomer, nicotinic acid hydrazide.

1. Superoxide was generated during the auto-oxidation of the antituberculous drug, isonicotinic acid hydrazide (INH), but not with its meta-isomer, nicotinic acid hydrazide (NH). During Fe(3+)-stimulated oxidation of INH and NH, aromatic hydroxylation occurred which was inhibited by the chelating agent, phytic acid. 2. A mixture of myeloperoxidase (MPO) and a hydrazide induced formation of compound III (oxyperoxidase) and aromatic hydroxylation which was stimulated by phytic acid. INH was considerably more potent than NH. 3. Co-oxidation of a hydrazide and thyroxine (T4) in the MPO system resulted in the formation of a pink-coloured product (maximum absorbance at 504 nm) which was more stable with NH than with INH. 4. The hydrazides and Cl- acted synergistically on MPO haem modification when co-oxidised in the MPO-H2O2 system. INH was more destructive than NH. 5. The different oxidative pathways of the hydrazides are consistent with the fact that an acyl intermediate of INH, unlike that of NH, is resonance stabilized.

Carcinogens↗
PubMed2002

G protein-coupled receptor for nicotinic acid in mouse macrophages.

The use of the HDL-elevating drug nicotinic acid in the treatment and prevention of atherosclerotic disease is limited by the frequent induction of skin flushing. The therapeutic effects of nicotinic acid are attributed to inhibition of lipolysis in adipose tissue via a G protein-coupled receptor, whereas the mechanism of flush induction by release of prostaglandin D(2) from macrophages is not understood. In this study, we investigated if macrophages contain nicotinic acid receptors. Specific guanine nucleotide sensitive binding sites for [(3)H]nicotinic acid were detected in membranes from mouse RAW 264.7 macrophages. Nicotinic acid and related heterocycles stimulated activation of pertussis toxin-sensitive G proteins. The rank orders of potency in macrophage membranes were identical for inhibition of [(3)H]nicotinic acid binding and G protein activation, and were pharmacologically indistinguishable from that of the G protein-coupled nicotinic acid receptor in spleen membranes. These results indicate that the effects of nicotinic acid on macrophages, spleen and probably adipocytes are mediated via an identical, unique G protein-coupled receptor.

Animals↗
PubMed1950

Tissue culture studies. V. Analogues for nicotinic acid.

The use of acetyl-3-pyridine and pyridine-3-sulfonic acid as analogues for nicotinic acid has been tested with tissue cultures of embryonic chick heart. Both roller tube and Carrel flask cultures were employed. Cell migration, appearance of the cells, and the uptake of tracer P(32) were used as criteria for the action of the analogues. Migration of the cells could be inhibited by both compounds, but at different levels. Both produced abnormal types of cells, but not the same type of abnormality. Uptake of P(32) was inhibited by both compounds. Addition of nicotinic acid failed to reverse the effects of the analogues at the concentrations used.

Niacin↗
PubMed1981

Nicotinic acid transport by brush border membrane vesicles from rabbit kidney.

The transport of nicotinic acid was investigated in brush border membrane vesicles isolated from rabbit kidney. The imposition of a Na+ gradient (out to in) induced a transient stimulation of nicotinic acid uptake above its final equilibrium value. This stimulation was specific for Na+. The uptake of nicotinic acid by the brush border membranes represented transport into an internal space and occurred in the absence of significant nicotinic acid degradation. The Na+ gradient-dependent uptake of nicotinic acid was saturable, apparent Km = 0.3 mM. Uptake of nicotinic acid was inhibited by its two isomers: picolinic and isonicotinic acid. In contrast, pyridine derivatives with two carboxyl groups or an amide group in addition to the carboxyl group were without inhibitory effect. Evaluation of changes in membrane potential using the lipophilic cation triphenylmethylphosphonium demonstrated that conditions that transiently generated either an interior-positive or an interior-negative membrane potential failed to affect the Na+-dependent transport of nicotinic acid. These findings provide evidence of the existence on the luminal membrane of a Na+ gradient-dependent and electroneutral transport system for nicotinic acid.

Absorption↗
PubMed2003

Varying cost and free nicotinic acid content in over-the-counter niacin preparations for dyslipidemia.

BACKGROUND: Nicotinic acid is an effective treatment for dyslipidemia, but the content of over-the-counter niacin is not federally regulated. As a result, patients may use preparations of over-the-counter niacin that do not contain free nicotinic acid. OBJECTIVE: To characterize the types, costs, and free nicotinic acid content of over-the-counter niacin preparations and to review literature on the use of over-the-counter niacin for dyslipidemia. DATA SOURCES: Commonly used over-the-counter niacin preparations (500-mg tablets or capsules) from the 3 categories of immediate-release, sustained-release, and no-flush were purchased at health food stores and pharmacies and from Internet-based vitamin companies. Pertinent literature on the use of over-the-counter niacin was obtained by searching PubMed. MEASUREMENTS: For each preparation studied, the monthly cost of therapy (at 2000 mg/d) and the free nicotinic acid content (quantified by high-performance liquid chromatography) were reported. DATA SYNTHESIS: On average, immediate-release niacin preparations cost 7.10 dollars per month, sustained-release preparations cost 9.75 dollars per month, and no-flush preparations cost 21.70 dollars per month. The average content of free nicotinic acid was 520.4 mg for immediate-release niacin, 502.6 mg for sustained-release niacin, and 0 for no-flush niacin. CONCLUSIONS: No-flush preparations of over-the-counter niacin contain no free nicotinic acid and should not be used to treat dyslipidemia. Over-the-counter sustained-release niacin contains free nicotinic acid, but some brands are hepatotoxic. Immediate-release niacin contains free nicotinic acid and is the least expensive form of over-the-counter niacin.

Chromatography, High Pressure Liquid↗
PubMed1977

Study of blood pyruvic acid levels in pellagrins with and without neurological manifestations and response to nicotinic acid therapy.

In 25 cases of pellagra and 10 healthy controls, the blood pyruvic acid levels in the fasting stage and after 60 and 90 minutes of glucose load were estimated by the technique of Friedmann & Haugen (1943). The blood pyruvic acid levels after 60 and 90 minutes of glucose load were significantly higher in pellagrins as compared to controls. The following conclusions were drawn from this study: (i) that there is impairment of pyruvic acid metabolism in cases of pellagra, which is more marked in pellagrins with neurological manifestations than in those without; (ii) that after administration of nicotinic acid alone for 15 days the pyruvic acid levels returned to normal, thereby indicating that nicotinic acid deficiency is the cause of deranged pyruvate metabolism; (iii) that there is significant improvement in neurological status after nicotinic acid therapy.

Adolescent↗
PubMed2005

Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review.

Nicotinic acid has, like the Roman God Janus, two faces. One is the vitamin. The other is the broad-spectrum lipid drug. The Canadian pathologist Rudolf Altschul discovered 50 years ago that nicotinic acid in gram doses lowered plasma levels of cholesterol. From the point of view of treatment of the dyslipidaemias that are risk factors for clinical atherosclerosis nicotinic acid is a miracle drug. It lowers the levels of all atherogenic lipoproteins--VLDL and LDL with subclasses as well as Lp(a)--and in addition it raises more than any other drug the levels of the protective HDL lipoproteins. Trials have shown that treatment with nicotinic acid reduces progression of atherosclerosis, and clinical events and mortality from coronary heart disease. The new combination treatment with statin-lowering LDL and nicotinic acid-raising HDL is reviewed. A basic effect of nicotinic acid is the inhibition of fat-mobilizing lipolysis in adipose tissue leading to a lowering of plasma free fatty acids, which has many metabolic implications which are reviewed. The very recent discovery of a nicotinic acid receptor and the finding that the drug stimulates the expression of the ABCA 1 membrane cholesterol transporter have paved the way for exciting and promising new 50 years in the history of nicotinic acid.

Adipose Tissue↗
PubMed1978

High-performance liquid-chromatographic determination of free nicotinic acid and its metabolite, nicotinuric acid, in plasma and urine.

We report a liquid-chromatographic procedure for determining free nicotinic acid and a metabolite, nicotinuric acid, in plasma and urine. Five-tenths milliliter of urine or deproteinized plasma is evaporated and the residue analyzed isocratically by reversed-phase ion-pair chromatography, with measurement of the eluted nicotinic acid and nicotinuric acid at 254 nm. Nicotinic acid, nicotinuric acid, and the internal standard (isonicotinic acid) have retention times of 7.8, 8.4, and 6.8 min, respectively, in plasma, and 12.3, 13.1, and 10.8 min in urine, because of double column length. Day-to-day reproducibilities (CV) for nicotinic acid and nicotinuric acid within 7.5% are attainable for the concentration ranges 0.1--20 mg/liter, equivalent to 0.81--162 micromol of nicotinic acid and 0.55--11 micromol of nicotinuric acid per liter for plasma; in urine for the range 0.5--100 mg/liter, equivalent to 4--810 micromol of nicotinic acid and 2.8--555 micromol of nicotinuric acid per liter. Metabolites of nicotinic acid such as nicotinamide, N-methylnicotinamide, 2-hydroxypyridine-5-carboxylic acid, and other structurally related substances do not interfere.

Chromatography, Liquid↗