Response of Rats to Diets High in Methionine and Related Compounds

Abstract

The growth retardation and accelerated deposition of splenic iron noted upon adding excess methionine to a basal diet were not markedly altered by the further addition of glycocyamine to favor creatine and homocysteine production. Supplementation with glycine, with glycine and arginine, or with ethanolamine decreased the growth-retarding effect of the excess methione, but apparently not its stimulation of iron deposition. Replacement of the excess methionine by homocystine produced the same striking retardation of growth, but little or no increase in splenic iron. Methionine sulfoxide produced less growth retardation than homocystine, but was more effective in stimulating the deposition of splenic iron. Supplementation of the basal diet with cystine, α-amino-n-butyric acid, or homoserine produced little change in the rate of growth and no stimulation of iron deposition. Cystine and homocystine together suppressed the rate of growth more markedly than homocystine alone. Dimethylthetin was as effective as methionine in suppressing growth and stimulating the deposition of splenic iron. Choline and betaine alone produced moderate increments in splenic iron, but little or no growth retardation. When they were fed in diets which contained homocystine, they decreased the growth depression as effectively as glycine or serine, presumably because they may undergo conversion to glycine, but feeding them jointly with homocystine did not alter markedly their capacities to promote the deposition of splenic iron. The provision of extra vitamins did not alleviate the growth suppression or the iron deposition induced by excess methionine. Paired feeding showed that the limited intake of the high methionine diets was probably largely responsible for the growth retardation, but not for the characteristic decrease in the erythrocyte count. It is tentatively assumed that the accelerating effect of methionine upon the erythrocyte turnover is associated primarily with its participation in transmethylation reactions, its growth-depressing effect primarily with the metabolism of its homocysteine moiety.