Abstract
Summary
In rats fed synthetic amino-acid test diets containing tryptophan but deficient in nicotinic acid or nicotinamide, an excess of dietary methionine lowers the urinary level of N1-methylnicotinamide (MNA) and raises the urinary level of indoleacetic acid (IAA). The urinary creatinine (CR) level is only slightly increased. Excess methionine administered intraperitoneally to rats fed the same diet results in a similar urinary excretion pattern of MNA and IAA. As a working hypothesis, it is suggested that excess methionine may favor the channeling of tryptophan metabolism into indoleacetic acid production by inhibiting the nicotinic acid pathway or stimulating those pathways leading to formation of indoleacetic acid.
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