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The Excretion of N¹-Methylnicotinamide and Creatinine as Influenced by Vitamin B₁₂ and Various Methyl Donors¹

Division of Agricultural Biochemistry, University of Minnesota, St. Paul

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.

Manuscript received 27 July 1951.

This article has been cited by other articles:

				W. G. UNGLAUB, G. A. GOLDSMITH, and J. GIBBENS RECENT ADVANCES IN NUTRITION AND METABOLISM: II. Review of the Literature on Vitamins, 1952 Arch Intern Med, October 1, 1954; 94(4): 618 - 647. [Abstract] [PDF]