Nicotinamide Effects Oxidative Burst Activity of Neutrophils in Patients with Poorly Controlled Type 2 Diabetes Mellitus

NAD+ homeostasis in renal health and disease

 analogues and related nutritional precursors.

Glaucoma as a Metabolic Optic Neuropathy: Making the Case for Nicotinamide Treatment in Glaucoma

 (a decline that occurs in different genetic contexts and species).

Dependence of tumor cell lines and patient-derived tumors on the NAD salvage pathway renders them sensitive to NAMPT inhibition with GNE-618.

While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if

Supplementation of nicotinic acid with NAMPT inhibitors results in loss of in vivo efficacy in NAPRT1-deficient tumor models.

 and NAM levels in NAPRT1-deficient tumors to levels that sustained growth in vivo.

Nicotinamide, a SIRT1 inhibitor, inhibits differentiation and facilitates expansion of hematopoietic progenitor cells with enhanced bone marrow homing and engraftment.

 is a known potent inhibitor of several classes of ribosylase enzymes that require 

 for their activity, as well as sirtuin (SIRT1), class III NAD(+)-dependent-histone-deacetylase.

Niacin status, NAD distribution and ADP-ribose metabolism.

Dietary niacin deficiency, and pharmacological excesses of

 or nicotinamide, have dramatic effects on cellular 

 pools, ADP-ribose metabolism, tissue function and health.

The role of dietary niacin intake and the adenosine-5′-diphosphate-ribosyl cyclase enzyme CD38 in spatial learning ability: is cyclic adenosine diphosphate ribose the link between diet and behaviour?

In young male rats, both niacin deficiency and

 supplementation significantly altered brain 

 and cADPR, both of which were inversely correlated with spatial learning ability.

PolyADP‐ribosylation and cancer

 levels by pharmacological supplementation with 

 has also been found to exert preventive effects against cancer.

NAD+ Modulates p53 DNA Binding Specificity and Function

 (vitamin B3) increases the rate of intracellular 

 synthesis, alters radiation-induced p53 DNA binding specificity, and modulates activation of a subset of p53 transcriptional targets.

Medicinal chemistry of nicotinamide in the treatment of ischemia and reperfusion.

 can facilitate DNA repair by inhibiting poly(ADP-ribose) polymerase, increasing 

 levels and adjusting other related enzyme activities.

Nicotinamide in type 1 diabetes. Mechanism of action revisited.

, the substrate of PARP, but also has major regulatory effects on gene expression, as shown for the major histocompatibility complex class II gene.

[Nicotinamide and prevention of insulin-dependent diabetes mellitus. Rationale, effects, toxicology and clinical experiences. ENDIT Group].

 pool, thus increasing the energy supply of the cell.

Nicotinamide prolongs survival of primary cultured hepatocytes without involving loss of hepatocyte-specific functions.

These results suggest that the maintenance of the intracellular NAD level is essential for the growth and functioning of hepatocytes and that

 degradation as well as by acting as a precursor for NAD synthesis.

Biosynthesis of pyridine nucleotides in early embryos of the mouse (Mus musculus).

Growth of two-cell embryos in vitro for 24 hours in the presence of either

 or nicotinate (0.8 mm) lead to a 2.5-fold increase in 

NAD metabolites interfere with proliferation and functional properties of THP-1 cells

 and NR caused an increase in intracellular 

 concentrations and SIRT1 and PARP1 mRNA expression was found to be enhanced.

Modulating NAD+ metabolism to prevent acute kidney injury

Impaired de novo NAD+ biosynthesis predisposes to acute kidney injury, and augmenting

 supplementation may prevent acute kidney injury.

The NAD+ precursor nicotinic acid improves genomic integrity in human peripheral blood mononuclear cells after X-irradiation.

Our data reveal that even in normal primary human cells cellular NAD+ levels may be limiting under conditions of genotoxic stress and that boosting the

 levels as well as DNA repair efficiency and enhanced genomic stability evaluated by micronucleus test after x-ray treatment.

Nicotinamide: a vitamin able to shift macrophage differentiation toward macrophages with restricted inflammatory features

 concentrations; however, it did not prevent the LPS-mediated drain on NAD pools.

Changes in NAD Content Induced by Nicotinic Acid-Related Compounds in K562 Cells during Differentiation

 content was reduced by a treatment with 

NAD+ Levels Control Ca2+ Store Replenishment and Mitogen-induced Increase of Cytosolic Ca2+ by Cyclic ADP-ribose-dependent TRPM2 Channel Gating in Human T Lymphocytes*

 levels were increased by supplementing peripheral blood lymphocytes with the NAD+ precursors 

, nicotinic acid, or nicotinamide mononucleotide, the Ca2+ content of thapsigargin-sensitive Ca2+ stores as well as cell responsiveness to mitogens in terms of [Ca2+]i elevation were up-regulated.

Nicotinamide and neutrophilia

In addition to seeing increased neutrophil counts, we found that the amounts of

, CCAAT-enhancer–binding proteins and G-CSF in myeloid cells were increased, providing further evidence that 

The Role of NAD+ Depletion in the Mechanism of Sulfur Mustard–Induced Metabolic Injury

 levels at all time points, but did not prevent adverse effects on glycolysis, intracellular ATP, or viable cell number.

Mechanistic implications of the cysteine-nicotinamide adduct in aldehyde dehydrogenase based on quantum mechanical/molecular mechanical simulations.

These simulations revealed formation of the oxyanion thiohemiacetal intermediate only when the

 is oriented away from the active site, contrary to prior arguments.

Inhibition of Silencing and Accelerated Aging by Nicotinamide, a Putative Negative Regulator of Yeast Sir2 and Human SIRT1*

 inhibits deacetylation by binding to a conserved pocket adjacent to 

The effects of niacin on DNA repair after N-methyl-N'-nitro-N-nitrosoguanidine treatment in normal human lymphocytes.

When lymphocytes were incubated in culture medium with various concentrations of niacin, incubation of lymphocytes with

 at 5 microM or nicotinamide at 10 mM caused a 2-3 fold increase in 

Different basal NAD levels determine opposite effects of poly(ADP-ribosyl)polymerase inhibitors on H2O2-induced apoptosis.

 concentration could be increased in LN cells by adding 

 (5-and 25-fold increase) to the culture medium.

HIV infection decreases intracellular nicotinamide adenine dinucleotide [NAD].

ADPRT-mediated decrease of cellular NAD content and the detection of chemically induced DNA damage--development of a new short-term screening test for mutagens.

 after DNA damage could be partially or completely prevented by ADPRT inhibitors, 3-aminobenzamide or 

, which showed no influence on reduction of NAD induced by metabolic blocking agents.

Biochemical markers for assessment of niacin status in young men: levels of erythrocyte niacin coenzymes and plasma tryptophan.

The results indicate that the erythrocyte

 level may serve as a sensitive indicator for the assessment of 

Effect of nicotinic acid supplementation in vivo on oxygen radical-induced genetic damage in human lymphocytes.

 concentrations rose progressively in lymphocytes to nearly 5 times baseline levels in human volunteers ingesting 

Effects of nicotinamide on NAD and poly(ADP-ribose) metabolism in DNA-damaged human lymphocytes.

In cells treated with UV irradiation or with MNNG,

 caused a two-fold stimulation of unscheduled DNA synthesis and retarded the rate of 

Thus under conditions that it enhances unscheduled DNA synthesis,

 causes marked effects on the metabolism of 

Disruption of flavin homeostasis in isolated rat liver mitochondria.

This process is inhibited by adenosine and guanosine phosphates, as well as

Niacin protects against abdominal aortic aneurysm formation via GPR109A independent mechanisms: role of NAD+/nicotinamide

 and nicotinamide supplementation increased 

 (NAD+) levels and NAD+-dependent Sirt1 activity, which were reduced in AAA tissues.

Exogenous nicotinamide supplementation and moderate physical exercise can attenuate the aging process in skeletal muscle of rats

 (NAM) could enhance the availability of 

The therapeutic effect and mechanism of niacin on acute lung injury in a rat model of hemorrhagic shock: Down-regulation of the reactive oxygen species–dependent nuclear factor &kgr;B pathway

, nicotinamide adenine dinucleotide phosphate levels, and glutathione–glutathione disulfide ratios; decreased lung malondialdehyde levels; down-regulated the NF-&kgr;B pathway; suppressed TNF-&agr;, IL-6, and IL-8 levels in the lung tissue and serum; and attenuated histologic lung damage.

Streptozotocin–nicotinamide-induced diabetes in the rat. Characteristics of the experimental model

 serves as a precursor of NAD+ and thereby additionally increases intracellular 

 inhibits this enzyme, preventing depletion of 

Muscle type-specific responses to NAD+ salvage biosynthesis promote muscle function in Caenorhabditis elegans.

 (NAD(+)) from nicotinamide (NAM) lowers 

 levels and replenishes the critical molecule NAD(+) after it is hydrolyzed.

Identification of the Aryl Hydrocarbon Receptor Target Gene TiPARP as a Mediator of Suppression of Hepatic Gluconeogenesis by 2,3,7,8-Tetrachlorodibenzo-p-dioxin and of Nicotinamide as a Corrective Agent for This Effect*

 levels and suppression of AHR target gene induction.

Comparison of metabolic fates of nicotinamide, NAD+ and NADH administered orally and intraperitoneally; characterization of oral NADH.

 and NADH produced significant increases in urinary excretion of 

Inhibition by nicotinamide of a homologous PCA reaction and antigen-induced histamine release from isolated rat peritoneal mast cells

Synthesis and degradation of NAD in guinea pig cardiac muscle: II. Studies about the different biosynthetic pathways and the corresponding intermediates

 degrading glycohydrolase in high concentrations.

The action of nicotinamide on the release of histamine

The cytotoxicity of chrysotile asbestos fibers to pulmonary alveolar macrophages I. Effects of inhibitors of ADP-ribosyl transferase

 and 3-aminobenzamide increased the intracellular 

[Effect of nicotinamide adenine dinucleotide on the serotoninergic mediator system in the rat brain during 3-acetylpyridine administration].

Dynamics of intracellular calcium and free radical production during ischemia in pyramidal neurons.

 hydrolysis, reproduced the CsA effects on FR generation, mitochondrial calcium accumulation and cytoplasmic calcium increases.

NAD+ biosynthesis from tryptophan in the presence of nicotinic acid or vice versa by rat hepatocytes--effect of clofibrate-feeding.

 at their physiological concentrations was significantly higher than that in the control hepatocytes as a result of a large increase of NAD+ synthesized from tryptophan.

Nicotinamide as a precursor for NAD+ prevents apoptosis in the mouse brain induced by tertiary-butylhydroperoxide

 can protect against oxidative stress-induced apoptosis in the brain when used as a precursor for 

Nicotinamide inhibits cyclic ADP-ribose-mediated calcium signalling in sea urchin eggs.

, cGMP and NO strongly suggests that these agents act as modulators of cADPR synthesis rather than to sensitize calcium release channels to cADPR.

We now report that in sea urchin egg homogenates,

 inhibits the Ca(2+)-mobilizing action of 

, cGMP and NO, but has no effect on cADPR-induced Ca2+ release.

Peroxynitrite-mediated DNA strand breakage activates poly-adenosine diphosphate ribosyl synthetase and causes cellular energy depletion in macrophages stimulated with bacterial lipopolysaccharide.

Inhibition of NO synthase by NG-methyl-L-arginine or S-methyl-isothiourea or inhibition of PARS activity by 3-aminobenzamide or

 prevented the decrease in mitochondrial respiration and the depletion of 

[Effect of nicotinamide on the uptake and release of serotonin and GABA by cerebral cortex synaptosomes in rats with diabetes induced by streptozotocin].

The modulating effect of in vivo administered

 which binds specifically with synaptic membranes.

Large supplements of nicotinic acid and nicotinamide increase tissue NAD+ and poly(ADP-ribose) levels but do not affect diethylnitrosamine-induced altered hepatic foci in Fischer-344 rats.

 and nicotinamide, at 1000 mg/kg diet, caused elevations in 

Modulation by nicotinamide adenine dinucleotide of sympathetic and sensory‐motor neurotransmission via P1‐purinoceptors in the rat mesenteric arterial bed

Structure‐activity relationships of NAD, NADP, ADP and … showed that the P1‐purinoceptor activity of

, or ribose plus nicotinamide, to yield the structurally‐related ADP‐ribose and ADP respectively, … when there is phosphorylation of the 2′‐hydroxyl group of NAD to yield NADP.

Nicotinamide‐adenine dinucleotide regulates muscarinic receptor‐coupled K+ (M) channels in rodent NG108‐15 cells.

 levels and prevented depletion by streptozotocin.

Analysis of oxygen radical toxicity in pancreatic islets at the single cell level.

 depletion and in parallel resulted in islet cell survival.

Elevated expression of the Cyp1a2 gene in the presence of nicotinamide by adult mouse hepatocytes in primary culture.

 were considerably elevated by addition of 

Interrelationship of changes in islet nicotine adeninedinucleotide, insulin secretion, and cell viability induced by interleukin-1 beta.

 and thymidine prevented the IL-1 beta-induced loss of cell viability and suppression of 

, but had no effect on sustaining insulin secretion.

NADP+ biosynthesis by rats receiving a pellagragenic diet.

 content to 317 micrograms/g liver but had no statistical effect on NADP+ content (75 micrograms/g liver) or NADP+ synthesis (46.5 in the free niacin group vs 37.0 nmol h-1 g-1 in the niacin-supplemented group).

[Features of poly-ADP-ribosylation and chromatin structure under conditions of varying NAD content in the rat liver].

Under conditions of vitamin PP deficiency

 administered to animals has increased the 14C 

 incorporation into histones 2 times (as compared with the control).

Thiol redox and phosphate transport in renal brush-border membrane. Effect of nicotinamide.

 (10 mM) induced an oxidative effect on redox states of cytosolic 

, NADP systems as inferred from decreased cellular lactate/pyruvate, malate/pyruvate, respectively.

On the cytotoxicity of chrysotile asbestos fibers toward pulmonary alveolar macrophages. II. Effects of nicotinamide on the cell metabolism.

After an 18-hr incubation period with 20 mM

 pools of control PAM increased by approximately 300% comparatively to a approximately 40% increase for the NADP+ content.

Specific inhibition of rat renal Na+/phosphate cotransport by picolinamide.

 is both a precursor for NAD synthesis and an inhibitor of intracellular 

ADP‐Ribosylation of Highly Purified Rat Brain Mitochondria

 glycohydrolase was inhibited totally by 

, the transfer of ADP‐ribose from NAD to mitochondrial proteins still occurred.

Dynamics of NAD in cortical nephron segments: effect of nicotinamide and of dietary phosphate intake.

 content increased significantly in all nephron segments except CAL; the greatest (delta + 277%) increase was found in PCT, with less (delta + 82%) in PST.

In experiments conducted on TPTX rats stabilized on a low-phosphorus diet,

 injection in PCT (delta + 197%), but did not change significantly in PST.

5-Methylnicotinamide inhibits renal brush-border phosphate transport with no change in NAD.

 to rats produces a dose-dependent increase in 

 (NAD) content in the renal cortex and specific inhibition of sodium gradient-dependent phosphate transport across the renal brush-border membrane (BBM).

 acts both as a precursor for NAD synthesis and as an inhibitor of 

Kinetic properties and physiological regulation of NAD glycohydrolase.

Kinetic studies on horse spleen NAD-glycohydrolase demonstrate that the hydrolysis of

 is extensively inhibited by physiological concentrations of 

Actions of NAD+ on renal brush border transport of phosphate in vivo and in vitro.

, the apparent Vmax was decreased, but the apparent Km was not different, indicating apparent noncompetitive inhibition.

Nicotinamide Does Not Protect Islet B-Cell Metabolism Against Alloxan Toxicity

, which was observed after alloxan treatment, could be prevented by 

Nicotinamide methylation and its relation to NAD synthesis in rat liver tissue culture. Biochemical basis for the physiological activities of 1-methylnicotinamide.

 concentration to the levels that cause cytotoxicity (1-10 mM and higher), the rate of 

 synthesis dramatically increased and reached a level 6-fold higher than that of 1-methylnicotinamide.

ADP-ribosyltransferase in Plasmodium (malaria parasites).

, exhibits an apparent Km of 500 microM, and the activity of the enzyme is inhibited by four chemical classes of inhibitors: 

, methylxanthines, thymidine and aromatic amides.

Cardiac synthesis and degradation of pyridine nucleotides and the level of energy-rich phosphates influenced by various precursors.

 (50 μM) together with adenine and ribose significantly enhanced the total 

 level under aerobic conditions by 77%, ATP by 37%, and AN by 24% during a 24-hr period.

Simultaneously, the high concentration of

 could be protected, compared with controls, by this high 

Changes in cellular levels of ATP and its catabolites in ischemic rat liver.

 was also degraded gradually with concomitant accumulation of 

Teratogenic effects of cholinergic insecticides in chick embryos--II. Effects on the NAD content of early embryos.

 content of the embryos by 20–30 per cent.

Metabolism of NAD and N1-methylnicotinamide in growing and growth-arrested cells.

, but not from N1-methylnicotinamide, is increased about twofold by addition of excess 

Nicotinamide and liver xanthine oxidase.

When rats receive injection of high doses of

, there is a temporary 10 fold increase in the 

Relationship between the ability of nicotinamide to maintain nicotinamide-adenine dinucleotide in rat liver cell culture and its effect on cytochrome P-450.

 as well as the previously reported loss of cytochrome P-450, suggesting a possible causal relationship.

Catabolism of NAD+ in rabbit reticulocyte lysates.

, inhibitors of NADase, prevent the conversion of 

Chicken embryo NAD levels lowered by teratogenic organophosphorus and methylcarbamate insecticides.

 and other NAD precursors prevents the decrease in 

 levels and alleviates most of the teratogenic signs.

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Possible Interaction: NAD and Niacin

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Research Papers that Mention the Interaction