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Fate of Nicotinamide Differs Due to an Intake of Nicotinamide
Author(s) -
Katsumi Shibata,
Shimada Hisako,
Hiroshi Taguchi
Publication year - 1996
Publication title -
bioscience biotechnology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.509
H-Index - 116
eISSN - 1347-6947
pISSN - 0916-8451
DOI - 10.1271/bbb.60.1204
Subject(s) - nicotinamide , metabolite , niacin , toxicity , catabolism , chemistry , catabolite repression , limiting , excretion , endocrinology , medicine , metabolism , biochemistry , biology , mechanical engineering , mutant , engineering , gene , enzyme , organic chemistry
We found that the catabolism of nicotinamide (Nam) differs due to an intake of Nam itself in rats. When rats were fed with a Nam-free, tryptophan-limiting diet, the major catabolite of niacin was N1-methyl-4-pyridone-3-carboxamide (4-Py). However, its percentage was changed with increasing the intake of Nam. The major metabolite was N1-methylnicotinamide (MNA) in the diet containing 0.006% Nam, or 0.1% Nam. The toxicity of excess Nam was observed when rats were fed with a 0.5% Nam-containing diet. In this diet, the major metabolite was Nam N-oxide and it was noted that the urinary excretion of nicotinic acid and its metabolite nicotinuric acid was observed. Therefore, these acids might be detected only when the toxicity of Nam appears.

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