Nineteen healthy humans (2 men and 17 women) served as experimental subjects in 4 experiments using diets having different levels of leucine and also a valine-deficient diet. The effect of an excess intake of leucine, with and without addition of vitamin B-6, and the effect of a deficiency of valine on urinary excretions of N1-methylnicotinamide, N1-methyl-2-pyridone-5-carboxamide, nicotinic acid, quinolinic acid, and 5-hydroxyindole acetic acid, and on the level of plasma amino acids were investigated. There was no effect of leucine on the excretion of these metabolites, but a marked decrease in the plasma (or serum) valine level was observed. The same decrease was seen when a valine-deficient diet was fed.

SummaryThe effects of an excess intake of leucine, for a short period (3 to 4 weeks) and a long period (12 weeks), on growth and excretion of tryptophan and niacin metabolites in rats were studied. Excess intake of leucine (4 or 5%) for a short period did not affect increase in body weight or organ weight (liver, kidney and heart) compared with those of rats fed the control diet. Excess intake of leucine for a long period resulted in a decrease in body weight, and an increase in the relative weight of the liver and kidney. Urinary excretions of N1 methyl nicotinamide (N-MNA), N1-methyl-2-pyridone-5-carboxamide (2 Py), niacin, quinolinic acid and 5-hydroxyindole acetic acid did not differ in rats fed an excess-leucine diet and rats fed a control diet. In niacin deficiency, the excretions of N-MNA, 2-Py and NiA decreased. Excess leucine intake increased the plasma levels of leucine and alanine and decreased those of valine, isoleucine, tryptophan and cystine. Excess leucine intake decreased the levels of valine, isoleucine, methionine and leucine in the liver, but these changes were not observed in niacin deficient rats. Changes in the levels of nicotinamide mononucleotide (NMN), nicotinamide adenine dinucleotide (NAD), nicotinamide adenine dinucleotide phosphate (NADP) in erythrocytes, suggested to occur in pellagra, were not observed. These findings do not support the idea that an excess intake of leucine results in changes in metabolism similar to those observed in pellagra.

No abstract

The effect of tryptophan deficiency on the urinary excretion of tryptophan and niacin metabolites and riboflavin, and on nitrogen balance has been examined in rats. The excretion of xanthurenic acid decreases, and the excretion of N1 -methylnicotinamide (MNA) slightly increases when tryptophan is def icient. But the increase in MNA excretion was not statistically signi ficant, perhaps owing to the scatter of the data. Decrease in the excretion of N-methyl-2-pyridone-5-carboxamide (pyridone) is as low as 1/2 to 1/20 of the control level when tryptophan is deficient. The excretion of riboflavin increases when tryptophan is deficient.

The determination of nicotinamide adenine nucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) levels in the liver and urinary excretion of tryptophan niacin metabolites were made in rats fed a tryptophan-deficient diet. Under experimental conditions excretion of N1-methyl-2-pyridone-5 carboxiamide (pyridone) decreased by approximately one-third in the tryptophan-deficient group when compared with the control group. A rapid decrease in body weight was shown in the tryptophan-deficient group when compared with the control group. The level of NAD+ and NADP+ and total PN+ in the tryptophan and niacin-deficient group was decreased significantly when compared with other deficient group (niacin or nicotinamide-added group) and the control group except for NADP+. No statistical difference was seen on the addition of nicotinic acid or nicotinamide. But a slightly lower level of urinary nicotinic acid was observed in the group with nicotinamide added when compared with group with nicotinic acid added. Simultaneously, a,high level of NAD+ was observed in the group with nicotinamide added. Thus, a difference in availability between nicotinic acid and nicotinamide might be expected.It is well known that NAD and NADP are synthesized in the body not only from nicotinamide and nicotinic acid, but also from tryptophan. We wished to investigate the change of NAD and NADP level on the basis of whether or not the substrate is present and difference in substrate.We also wanted to study the effect of tryptophan deficiency on the urinary excretion of tryptophan niacin metabolites in rats.257