2-Keto-4-methylthiobutyric Acid in Urine of Rats Fed an Excess Methionine Diet

volved in those two Met metabolic pathways that excess Met is metabolized by the transsulfuration pathway3A) and that the limited capacity of this pathway is primarily responsible for the adverse effects of Met, at least on growth and food intake, probably resulting from its high level in the plasma and tissues.5) A direct NMRstudy provided support for the importance of Gly methylation, not transamination, in the catabolism of excess Met in rat liver.6) On the other hand, the quantitative importance of the transamination pathway remains unsolved.7) We have attempted to compare the patterns of components in plasma, various tissues, and urine of rats fed a low casein diet and a low casein diet supplemented with excess Met and proposed the pathway that OPA accumulated in the liver during sulfur-containing amino acids deficiency was used for the synthesis of GSHafter excess Met feeding, resulting in the decrease of OPAand increase ofGSHand a-ABA.8>9) This paper deals with the presence ofKMTBand HMTB,a transamination product of Met and its derivative, in urine of rats fed an excess Met diet and the significant decrease ofKMTBby addition ofGly to the excess Met diet.