A relationship between nicotinamide methylkinase and folic acid

Abstract

Reports have appeared on growth inhibition and production of fatty livers in rats, due to forced methylation of ingested compounds such as glycocyamine, cystine or homocystine, pyridine and nicotinamide. The fatty livers caused by nicotinamide administration in large doses are known to be susceptible to the action of choline, while the growth inhibition is alleviated by methionine. An involvement of folic acid in this nicotinamide metabolism would seem predictable on the basis of its well-known mediation in biological methylations. The present work was undertaken to ascertain this relationship. The studies included the effects of methanol and of formate as well, since in vivo and in vitro observations have now established that methyl synthesis could occur from glycine via formate and that the reverse, namely, the degradation of labile methyl to formate, could also take place. Folic acid is concerned directly in formate production from glycine and in its utilization for serine synthesis.