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Citation Information: J Clin Invest. 1972;51(3):557-565. https://doi.org/10.1172/JCI106844.
Abstract
The renal conversion of glutamine to glucose and its oxidation to CO2 were compared in dogs in chronic metabolic acidosis and alkalosis. These studies were performed at normal endogenous levels of glutamine utilizing glutamine-34C (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 μmoles/min. Of this quantity, 5.34 μmoles/min was converted to glucose, and 17.5 μmoles/min was oxidized to CO2. Acidotic animals excreted an average of 41 μmoles/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 μmoles/min. Of this quantity, 0.92 μmole/min was converted to glucose, and 4.99 μmoles/min was oxidized to CO2. Alkalotic animals excreted an average of 3.23 μmoles/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 CO2 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.
Authors
R. F. Pitts, L. A. Pilkington, M. B. MacLeod, E. Leal-Pinto
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