The Excretion of N1-Methylnicotinamide and Creatinine as Influenced by Vitamin B12 and Various Methyl Donors

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Abstract
Young vitamin B12-deficient rats were fed a labile-methylfree ration with the following supplements in the presence or absence of vitamin B12: none; methionine; choline; homocystine; homocystine plus choline, betaine, or formate. The urinary excretion of N1-methylnicotinamide or creatinine was determined following an intraperitoneal dose of nicotinamide or guanidoacetic acid. Only when the basal ration was supplemented with homocystine in the presence of choline, betaine, or vitamin B12 were the growth and the excretion of N1-methylnicotinamide similar to those observed with the methionine-supplemented ration. The administration of vitamin B12 effected a further improvement in growth and increase in N1-methylnicotinamide excretion when the diet contained homocystine plus choline or betaine. Formate in the absence of vitamin B12 was ineffective as a methyl donor to homocystine. When the basal ration contained homocystine, the administration of vitamin B12 or additional supplementation with choline caused an increase in growth and excretion of creatinine comparable to the increase obtained with the methionine-supplemented ration. Choline alone, although incapable of supporting growth, effected a similar increase in creatinine output. The implication of these results with respect to the role of vitamin B12 in the biosynthesis of methionine has been discussed.