A possible source of
glutamine, for inclusion in the parenteral solutions, is
glycylglutamine. The aim of this article is to review briefly the information on metabolism of
glycylglutamine when administered intravenously. The fact that there is efficient utilization of intravenously infused
glycylglutamine was evident with very little excretion in the urine. Although all the tissues examined, except brain, participated in the removal of
glycylglutamine from plasma, kidney predominated in this regard. This may be related to the presence of carrier-mediated systems for cellular uptake of
glycylglutamine in the kidney and the lack of them in other tissues.
Starvation did not alter the metabolic clearance of
glycylglutamine, although it reduced the removal by the kidney. Renal metabolism of
glycylglutamine resulted in the release of constituent
amino acids that were largely utilized by the liver in the postabsorptive state and by skeletal muscle in
starvation. This alteration was accompanied by a selective inhibition of muscle release of
amino acids that are substrates for enhanced hepatic gluconeogenesis and renal ammoniagenesis in
starvation. Because there was no change either in plasma
glucose level or
ammonia excretion during the infusion of
glycylglutamine in starved human subjects, apparently the
amino acid residues of
glycylglutamine fulfilled the substrate needs for these functions. These results provide a metabolic basis for further investigations of the possible nutritional benefit of including
glycylglutamine in
parenteral nutrition.