Inhibition of<i>N</i><sup>1</sup>-Methylnicotinamide Oxidase Activity by a Large Nicotinamide Injection into Rats

Shibata, Katsumi; Matsuo, Hiroko

doi:10.1080/00021369.1989.10869617

Cited by 3 publications

(2 citation statements)

References 3 publications

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“…Nam phosphoribosyltransferase (NamPRT, EC 2.4.2.12) plays a critical role in maintaining normal NAD 1 concentration (Fig. 4) (28)(29)(30). This enzyme is inhibited when a certain amount of NAD 1 exists the cell.…”

Section: Mechanism For Maintaining Nad 1 Concentrationmentioning

confidence: 99%

Organ Co-Relationship in Tryptophan Metabolism and Factors That Govern the Biosynthesis of Nicotinamide from Tryptophan

Shibata

2018

Journal of Nutritional Science and Vitaminology

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The pathway of tryptophan (Trp)-nicotinamide is very important nutritionally because a vitamin nicotinamide is biosynthesized from an amino acid Trp. Until we started studying the factors that affect the Trp-nicotinamide conversion rate, little data existed. Data obtained from TDO (Trp 2,3-dioxygenase)-KO (knock-out) mice have revealed that mice can biosynthesize a necessary amount of nicotinamide from Trp by indoleamine 2,3-dioxygenase (IDO) even when TDO is lacking. It has also been shown that 3-hydroxyanthranilic acid is a key intermediate. Urine upper metabolites such as kynurenic acid and xanthurenic acid originate from non-hepatic tissues but not from the liver. Data obtained from quinolinic acid phosphoribosyltransferase (QPRT)-KO mice indicated that the Trp→quinolinic acid conversion ratio was 6%. Urine quinolinic acid levels and the conversion ratio of Trp to nicotinamide were the same between hetero and wild mice. These findings indicate that QPRT is not the rate-limiting enzyme in the conversion. Thus, the limiting factors in the conversion of Trp to nicotinamide are the amounts of 3-hydroxyanthranilic acid and quinolinic acid in the liver and the activity of liver 3-hydroxyanthranilic acid 3,4-dioxygenase. Studies on factors have shown that conversion of Trp to nicotinamide is increased by adequate intake of good quality protein, and adequate intake of unsaturated fatty acids and starch. However, conversion was decreased by deficient niacin, vitamin B, or vitamin B, excessive intake of protein, saturated fatty acids, or glucose and fructose, or intake of protein with low Trp content, and insufficient mineral intake.

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Section: Mechanism For Maintaining Nad 1 Concentrationmentioning

confidence: 99%

Organ Co-Relationship in Tryptophan Metabolism and Factors That Govern the Biosynthesis of Nicotinamide from Tryptophan

Shibata

2018

Journal of Nutritional Science and Vitaminology

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“…In the "nicotinamide experiment," the 2-Py-forming MNA oxidase activity was 45% of normal and the 4-Py-forming MNA oxidase activity 7%. 7 ) In the "MNA experiment," the 2-Py-forming MNA oxidase activity was 59% of normal and the 4-Py-forming MNA oxidase activity 11 %. 8 l The 4-Py-forming MNA oxidase is more unstable than the 2-Py-forming MNA oxidase; that is, 4-Py-forming MNA oxidase is more inactivated during the course of catalysis than 2-Py-forming MNA oxidase.…”

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Effect of Pyridoxal on the Urinary Excretion of Nicotinamide Metabolites in Rats

Shibata¹

1990

Agricultural and Biological Chemistry

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Potential urinary and plasma biomarkers of peroxisome proliferation in the rat: identification ofN-methylnicotinamide andN-methyl-4-pyridone-3-carboxamide by¹H nuclear magnetic resonance and high performance liquid chromatography

et al. 2003

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This study identified two potential novel biomarkers of peroxisome proliferation in the rat. Three peroxisome proliferator-activated receptor (PPAR) ligands, chosen for their high selectivity towards the PPARalpha, -delta and -gamma subtypes, were given to rats twice daily for 7 days at doses known to cause a pharmacological effect or peroxisome proliferation. Fenofibrate was used as a positive control. Daily treatment with the PPARalpha and -delta agonists produced peroxisome proliferation and liver hypertrophy. 1H nuclear magnetic resonance spectroscopy and multivariate statistical data analysis of urinary spectra from animals given the PPARalpha and -delta agonists identified two new potential biomarkers of peroxisome proliferation--N-methylnicotinamide (NMN) and N-methyl-4-pyridone-3-carboxamide (4PY)--both endproducts of the tryptophan-nicotinamide adenine dinucleotide (NAD+) pathway. After 7 days, excretion of NMN and 4PY increased 24- and three-fold, respectively, following high doses of fenofibrate. The correlation between total NMN excretion over 7 days and the peroxisome count was r=0.87 (r2=0.76). Plasma NMN, measured using a sensitive high performance liquid chromatography method, was increased up to 61-fold after 7 days' treatment with high doses of fenofibrate. Hepatic gene expression of aminocarboxymuconate-semialdehyde decarboxylase (EC 4.1.1.45) was downregulated following treatment with the PPARalpha and -delta agonists. The decrease was up to 11-fold compared with controls in the groups treated with high doses of fenofibrate. This supports the link between increased NMN and 4PY excretion and regulation of the tryptophan-NAD+ pathway in the liver. In conclusion, NMN, and possibly other metabolites in the pathway, are potential non-invasive surrogate biomarkers of peroxisome proliferation in the rat.

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Inhibition ofN¹-Methylnicotinamide Oxidase Activity by a Large Nicotinamide Injection into Rats

Cited by 3 publications

References 3 publications

Organ Co-Relationship in Tryptophan Metabolism and Factors That Govern the Biosynthesis of Nicotinamide from Tryptophan

Organ Co-Relationship in Tryptophan Metabolism and Factors That Govern the Biosynthesis of Nicotinamide from Tryptophan

Effect of Pyridoxal on the Urinary Excretion of Nicotinamide Metabolites in Rats

Potential urinary and plasma biomarkers of peroxisome proliferation in the rat: identification ofN-methylnicotinamide andN-methyl-4-pyridone-3-carboxamide by¹H nuclear magnetic resonance and high performance liquid chromatography

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Inhibition ofN1-Methylnicotinamide Oxidase Activity by a Large Nicotinamide Injection into Rats

Cited by 3 publications

References 3 publications

Organ Co-Relationship in Tryptophan Metabolism and Factors That Govern the Biosynthesis of Nicotinamide from Tryptophan

Organ Co-Relationship in Tryptophan Metabolism and Factors That Govern the Biosynthesis of Nicotinamide from Tryptophan

Effect of Pyridoxal on the Urinary Excretion of Nicotinamide Metabolites in Rats

Potential urinary and plasma biomarkers of peroxisome proliferation in the rat: identification ofN-methylnicotinamide andN-methyl-4-pyridone-3-carboxamide by1H nuclear magnetic resonance and high performance liquid chromatography

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Inhibition ofN¹-Methylnicotinamide Oxidase Activity by a Large Nicotinamide Injection into Rats

Potential urinary and plasma biomarkers of peroxisome proliferation in the rat: identification ofN-methylnicotinamide andN-methyl-4-pyridone-3-carboxamide by¹H nuclear magnetic resonance and high performance liquid chromatography