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At least 631 records · Page 35Linked to original sources
PubMed1991

Percutaneous absorption of nicotinic acid derivatives in vitro.

The permeation rates through isolated epidermis of a homologous series of glycol, polyglycol, and alkyl esters of nicotinic acid were measured in vitro in a two-compartment diffusion cell assembly, using an isotonic buffered solution as the receiving phase. The esters were applied from aqueous solutions and also as the pure liquids. The results were consistent with those reported by other using compounds of equal or different structures either in vitro or in vivo. The experiments are compared in terms of partition equilibrium between vehicle and tissue and distribution from tissue to the receiving phase. It was demonstrated that the plateau observed in skin permeabilities of the compounds beyond a certain degree of lipophilicity is the result of the effect of water when used as the vehicle in the laboratory models.

Chromatography, High Pressure Liquid↗
PubMed1991

Transport of the new quinolone antibacterial agents of lomefloxacin and ofloxacin by rat erythrocytes, and its relation to the nicotinic acid transport system.

Transport mechanism of quinolonecarboxylic acid derivatives (quinolones), lomefloxacin and ofloxacin, in rat erythrocytes was investigated. The uptake of lomefloxacin by erythrocytes was apparently nonsaturable over the concentration range of 0.1-1.0 mM at 27 degrees C and pH 7.4. In the case of ofloxacin, however, the erythrocytes took up ofloxacin in a concentration dependent manner at 20 degrees C and pH 7.4, with a maximum rate (Jmax) of 28.8 +/- 0.98 pmol/10(6) cells/s and a Michaelis constant (Kt) of 0.92 +/- 0.15 mM. An increase in the medium osmolarity caused a decrease in the [14C]lomefloxacin uptake, indicating that the drug is transported into the intracellular space of erythrocytes. The uptake of [14C]lomefloxacin by the erythrocytes was independent of pH but increased above pH 6.0, and, moreover, was dependent on temperature with an activation energy of 16.6 kcal/mol. The uptake of [14C]lomefloxacin was competitively inhibited by a water-soluble vitamin, nicotinic acid, with an inhibition constant (Ki) of 16.1 mM, but not inhibited by 10 mM of L-alanine, glucose, p-aminohippuric acid (PAH), N-methyl-nicotinamide (NMN) or tetraethylammonium chloride (TEA). These lines of evidence suggest that the transport system of lomefloxacin and ofloxacin in rat erythrocytes is common with that of a water-soluble vitamin, nicotinic acid, to which quinolones are structurally analogous.

Animals↗
PubMed1976

The uptake in the pancreatic islets of nicotinamide, nicotinic acid and tryptophan and their ability to prevent streptozotocin diabetes in mice.

The uptake of the nicotinamide adenine dinucleotide (NAD)-precursors nicotinamide, nicotinic acid and tryptophan in the pancreatic islets of mice was studied by use of autoradiographic methods. The ability of these substances to prevent streptoxotocin diabetes was studied in the same species. It was found that only nicotinamide was strongly accumulated in the pancreatic islets and nicotinamide was also the only NAD-precursor which protected against the streptoxotocin diabetes. Apparently there is a relationship between the ability of the NAD-precursors to be taken up in the pancreatic islets and their ability to prevent streptoxotocin diabetes.

Animals↗
PubMed1979

Effects of noradrenaline and nicotinic acid on plasma free fatty acids and oxygen consumption in cold-adapted rats.

A 3-h noradrenaline (NA) infusion (1.5 microgram kg-1 min-1) produced a sustained enhanced oxygen consumption (O2 cons.) in cold-adapted rats. Plasma free fatty acid (FFA) levels were elevated by NA in control and in cold-adapted rats, but to lesser extent in cold-adapted rats; the increase was maintained at a plateau in both groups during the entire period of NA infusion. A 1-h nicotinic acid (Nic A) infusion (1.5 mg kg-1 min-1) added to the NA infusion inhibited the calorigenic response to NA in cold-adapted rats and reduced the elevated plasma FFA concentration in control and in cold-adapted rats to values below basal levels. However, when the Nic A infusion was stopped, the O2 cons. was increased again in cold-adapted rats by the uninterrupted NA infusion, without the simultaneous increase of the plasma FFA concentration; the plasma FFA concentration was maintained in cold-adapted rats below basal values and merely brought back to basal levels in control rats. From these results, it is suggested that plasma FFA are not an essential substrate to the calorigenic response to NA observed in cold-adapted rats, as 85% of the response can occur when the plasma FFA concentration is very low.

Adaptation, Physiological↗
PubMed1979

Oral nicotinic acid as a treatment for ketosis.

Changes in blood metabolites and milk production were measured in eight cows with subclinical or clinical ketosis following treatment with daily doses of 12 g nicotinic acid fed with the concentrate mixture. Ketotic cows displayed a positive milk ketone test, reduced milk production and feed intake, hypoglycemia, hyperketonemia, and elevated free fatty acids in plasma. The milk ketone test was negative in all cows 5 to 9 days following initiation of treatment. After 7 days of treatment, milk production and glucose in plasma were increased while there were decreases in plasma beta-hydroxybutyrate and free fatty acids. No relapses occurred.

Acidosis↗
PubMed2000

Effects of nicotinic acid on fatty acid kinetics, fuel selection, and pathways of glucose production in women.

Chronic nicotinic acid (NA) ingestion effectively lowers lipid levels, but adverse effects on glucose metabolism have been reported. Our goal was to investigate acute and chronic effects of NA on lipolysis and glucose metabolism in women. Healthy normolipidemic volunteers (n = 5) were studied twice; four-day hospital stays were separated by 1 mo, during which time subjects took increasing doses of NA to 2 g/day (500 mg, 4 times). In the second study, 500 mg of NA was given at 0800. Rates of appearance (R(a)) of free fatty acid (FFA), glycerol, and glucose were determined by isotope dilution (of [1,2,3,4-(13)C(4)]palmitate, [2-(13)C(1)]glycerol, and [U-(13)C(6)]glucose). Mass isotopomer distribution analysis was used to measure gluconeogenesis and glycogenolysis. Fasting FFA concentrations ([FFA]), R(a) FFA, and R(a) glycerol were nonsignificantly elevated after 1 mo. Acute NA induced a significant reduction followed by a rebound overshoot of [FFA], R(a) FFA, and R(a) glycerol. Whole body fat oxidation fell initially and then increased back to basal levels; endogenous glucose production (EGP) increased in parallel with carbohydrate oxidation and then returned to basal values. The increased EGP was due entirely to increased glycogenolysis, not gluconeogenesis. We conclude that chronic effects of NA on FFA metabolism are complex (acute suppression followed by overshoot of R(a) FFA and [FFA] on top of a trend toward basal elevations), that responses after NA are consistent with operation of a glucose-fatty acid cycle in peripheral tissues, and that secondary effects on EGP were through changes in glycogenolysis, not gluconeogenesis.

Adult↗
PubMed1988

Excretion and metabolism of nicotinic acid by the avian kidney.

The renal tubular transport and metabolism of nicotinic acid (NA) were investigated using the Sperber technique in unanesthetized hens. Infusion of [14C]NA into the avian renal portal circulation at 10(-10) mol/kg/min revealed that the 14C label was actively transported into urine at a rate 74% that of simultaneously infused tetraethylammonium. Increases in NA infusion rates enhanced 14C label transport so that it eventually equalled the excretion rate of tetraethylammonium. At a NA infusion rate of 10(-8) mol/kg/min, this transport was not affected by probenecid, pyrazinoic acid or p-aminohippurate. Above infusion rates of 10(-7) mol/kg/min, saturation of 14C label transport was reached. Electrophoretic analysis of the 14C label excreted in urine at NA infusion rates less than 10(-7) mol/kg/min revealed a single, unidentified metabolite. At infusion rates greater than 10(-7) mol/kg/min, both the radiolabeled metabolite and [14C]NA were found in the urine. We conclude that NA is transported by a specific mechanism into the avian tubule cell where it is metabolized. As the body's load of this vitamin increases, NA is excreted first in the form of a metabolite and then as both metabolite and unutilized NA.

Animals↗