The Metabolism of Amino Acids

It was shown by Seth and Luck (1) that the intestinal absorption of glycine and alanine by rabbits was followed by pronounced aminoacidemia. Other amino acids when administered in similar amounts provoked smaller increases in the amino nitrogen content of the blood. Glutamic acid and aspartic acid were absorbed with but a slight aminoacidemia. The question then arose as to whether these striking differences in behavior were due to equally profound differences in the rates of absorption from the alimentary canal, in the rates of diffusion into liver, muscle, and other tissues, and in the rates of metabolism of the amino acids therein. It may be recalled that Bang (2) demonstrated marked inequalities in the absorption of various amino acids by isolated fragments of liver suspended in solutions of these substances. A not unlikely explanation of the results of Seth and Luck would seem to be that the glycine-alanine aminoacidemia was due to slow diffusion of the substances into liver and muscle, or a low rate of oxidation of the metabolites, or both. In contrast, the failure of glutamic and aspartic acids to provoke an appreciable increase in the amino acid content of the blood might be attributed to their rapid absorption therefrom. According to such a theory it might be expected that the ingestion of glycine and alanine would cause but a small increase in the amino acid content of liver and muscle, or a slow conversion of the amino nitrogen to urea. On ,the other hand glutamic acid might be expected to increase more markedly the amino acid content of liver and muscle or to lead to more rapid urea formation than is observed with glycine and alanine. Finally one may advance the view that the differences in the degree of aminoacidemia may be due in part to specific differences in the excretion of amino acids by the kidney.