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Results for “NICOTINIC ACID”

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PubMed1984

[Antilipolytic activity in vitro of various analogs of nicotinic acid. Structure-activity relationship].

The antilipolytic activity of a series of N aryl-nicotinamides and of alpha picolinic acid, has been tested in vitro. Lipolysis was stimulated by epinephrine (20 micrograms/ml of incubation medium) using rat's epididymal adipose tissue slices. Only N(2-carboxy methyl phenyl) nicotinamide showed antilipolytic effect comparable to that of nicotinic acid at similar concentrations (2 X 10(-5) M). Picolinic acid (10(-4) M) showed no antilipolytic effect. These results, together with those of the literature, are discussed in regard to the relations between structure and antilipolytic activity.

Adipose Tissue↗
PubMedDate not supplied

[Effect of nicotinic acid on phosphodiesterase and adenyl cyclase activities in chicken liver].

Stimulation of fatty acid biosynthesis by feeding high-carbohydrate diet to chickens after fasting induces a 38% and 23% rise in the 3':5'-cyclo-nucleotide phosphodiesterase and adenylate cyclase activities in the liver tissue, respectively. Administration of nicotinic acid (150 mg per 1 kg of weight) to chickens with stimulated biosynthesis of fatty acids leads to a sharp (70% at an average) decrease of 3':5'-cyclo-nucleotide phosphodiesterase activity, the adenylate cyclase activity under these conditions remains practically unchanged. The participation of the adenylate cyclase system in regulating the fatty acid biosynthesis under mentioned conditions, the role of phosphodiesterase are discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1971

Primitive earth synthesis of nicotinic acid derivatives.

Nicotinonitrile, 2-cyanopyridine, and 4-cyanopyridine can be synthesized under primitive earth conditions by the action of electric discharges on ethylene and ammonia. The electric discharge first synthesizes pyridine and hydrogen cyanide, which react in the discharge to form the cyanopyridines. Nicotinonitrile would have hydrolyzed in the primitive ocean to nicotinamide and nicotinic acid.

Ammonia↗
PubMed1999

Nicotinic acid adenine dinucleotide phosphate triggers Ca2+ release from brain microsomes.

Mobilization of Ca2+ from intracellular stores is an important mechanism for generating cytoplasmic Ca2+ signals [1]. Two families of intracellular Ca(2+)-release channels - the inositol-1,4, 5-trisphosphate (IP3) receptors and the ryanodine receptors (RyRs) - have been described in mammalian tissues [2]. Recently, nicotinic acid adenine dinucleotide phosphate (NAADP), a molecule derived from NADP+, has been shown to trigger Ca2+ release from intracellular stores in invertebrate eggs [3] [4] [5] [6] and pancreatic acinar cells [7]. The nature of NAADP-induced Ca2+ release is unknown but it is clearly distinct from the IP3- and cyclic ADP ribose (cADPR)-sensitive mechanisms in eggs (reviewed in [8] [9]). Furthermore, mammalian cells can synthesize and degrade NAADP, suggesting that NAADP-induced Ca2+ release may be widespread and thus contribute to the complexity of Ca2+ signalling [10] [11]. Here, we show for the first time that NAADP evokes Ca2+ release from rat brain microsomes by a mechanism that is distinct from those sensitive to IP3 or cADPR, and has a remarkably similar pharmacology to the action of NAADP in sea urchin eggs [12]. Membranes prepared from the same rat brain tissues are able to support the synthesis and degradation of NAADP. We therefore suggest that NAADP-mediated Ca2+ signalling could play an important role in neuronal Ca2+ signalling.

Animals↗
PubMed2001

Nicotinic acid adenine dinucleotide phosphate enhances quantal neurosecretion at the frog neuromuscular junction: possible action on synaptic vesicles in the releasable pool.

Inositol 1,4,5-trisphosphate (IP(3)) and cyclic adenosine diphosphate-ribose (cADPR) are second messengers that enhance neurosecretion by inducing Ca(2+) release from smooth endoplasmic reticulum (SER). The putative intracellular messenger, nicotinic acid adenine dinucleotide phosphate (NAADP), releases Ca(2+) from stores that are distinct from SER. Evidence is presented here that NAADP causes a concentration-dependent increase in quantal output that is associated with an increase in probability of transmitter release at the frog neuromuscular junction. This effect is mimicked by A23187, a Ca ionophore that promotes Ca(2+) entry at the plasmalemma. The response to NAADP is potentiated by IP(3) but antagonized by cADPR. Thapsigargin completely blocks IP(3) and cADPR responses and decreases but does not prevent the response to NAADP. We conclude that NAADP, whose receptors are widely distributed in the brain, enhances neurosecretion by releasing Ca(2+) from an internal store near the plasmalemma, possibly from synaptic vesicles in the releasable pool. These data also support the hypothesis of a two-pool model for Ca(2+) oscillations at the presynaptic site.

Adenosine Diphosphate Ribose↗
PubMed2004

Nicotinic acid controls lactate production by K1-LDH: a Saccharomyces cerevisiae strain expressing a bacterial LDH gene.

Industrial applications for lactate, such as the production of chemicals, has led to interest in producing this organic acid by metabolically engineered a yeast such as Saccharomyces cerevisiae, which is more acid tolerant than lactic acid bacteria. This paper deals with lactate production by S. cerevisiae K1-LDH, in which the Lactobacillus plantarum lactate dehydrogenase (LDH) gene is integrated into the genome of the wine yeast strain K1. We show that a vitamin, nicotinic acid (NiA), was the limiting factor for lactate production during fermentation with the K1-LDH strain. Increasing the NiA concentration in batch conditions or in the medium used to feed chemostats affected the lactate yield. Moreover, the addition of pulses of NiA or the exponential addition of NiA made it possible to control the lactate production kinetics throughout the fermentation process. The results point to the role of NiA in the regulation of metabolic pathways, but the physiological mechanisms remain poorly understood.

Culture Media↗