Metabolism of glutamine by the intact functioning kidney of the dog. Studies in metabolic acidosis and alkalosis

Abstract

The renal conversion of glutamine to glucose and its oxidation to CO(2) were compared in dogs in chronic metabolic acidosis and alkalosis. These studies were performed at normal endogenous levels of glutamine utilizing glutamine-(34)C (uniformly labeled) as a tracer. It was observed in five experiments in acidosis that mean renal extraction of glutamine by one kidney amounted to 27.7 mumoles/min. Of this quantity, 5.34 mumoles/min was converted to glucose, and 17.5 mumoles/min was oxidized to CO(2). Acidotic animals excreted an average of 41 mumoles/min of ammonia in the urine formed by one kidney. In contrast, in five experiments in alkalosis, mean renal extraction of glutamine amounted to 8.04 mumoles/min. Of this quantity, 0.92 mumole/min was converted to glucose, and 4.99 mumoles/min was oxidized to CO(2). Alkalotic animals excreted an average of 3.23 mumoles/min of ammonia in the urine. We conclude that renal gluconeogenesis is not rate limiting for the production and excretion of ammonia in either acidosis or alkalosis. Since 40% of total CO(2) production is derived from oxidation of glutamine by the acidotic kidney and 14% by the alkalotic kidney, it is apparent that renal energy sources change with acid-base state and that glutamine constitutes a major metabolic fuel in acidosis.