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Research Article Free access | 10.1172/JCI105554

Renal Metabolism of Alanine

Robert F. Pitts and William J. Stone

Department of Physiology, Cornell University Medical College, New York, N. Y.

†

Address requests for reprints to Dr. Robert F. Pitts, Dept. of Physiology, Cornell University Medical College, 1300 York Ave., New York, N. Y. 10021.

‡

Postdoctoral research fellow of the New York Heart Association.

*

Submitted for publication October 14, 1966; accepted December 15, 1966.

Aided by research grant 5R01 HE00814-15 (CV) and training grant 5T1 HE5264-08 of the National Heart Institute, National Institutes of Health, and by the Life Insurance Medical Research Fund.

Find articles by Pitts, R. in: JCI | PubMed | Google Scholar

Department of Physiology, Cornell University Medical College, New York, N. Y.

†

Address requests for reprints to Dr. Robert F. Pitts, Dept. of Physiology, Cornell University Medical College, 1300 York Ave., New York, N. Y. 10021.

‡

Postdoctoral research fellow of the New York Heart Association.

*

Submitted for publication October 14, 1966; accepted December 15, 1966.

Aided by research grant 5R01 HE00814-15 (CV) and training grant 5T1 HE5264-08 of the National Heart Institute, National Institutes of Health, and by the Life Insurance Medical Research Fund.

Find articles by Stone, W. in: JCI | PubMed | Google Scholar

Published April 1, 1967 - More info

Published in Volume 46, Issue 4 on April 1, 1967
J Clin Invest. 1967;46(4):530–538. https://doi.org/10.1172/JCI105554.
© 1967 The American Society for Clinical Investigation
Published April 1, 1967 - Version history
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Abstract

In the acidotic dog, alanine is extracted from plasma and utilized as a precursor of ammonia. Simultaneously, it is formed de novo within tubular cells and added to renal venous blood. When plasma concentration is within a normal range, production of alanine greatly exceeds utilization. Increasing the plasma concentration reduces production and increases utilization of plasma alanine. The infusion of glutamine increases the renal production of alanine without appreciable change in utilization of plasma alanine. These results are consonant with the view that alanine is metabolized by transamination with α-ketoglutarate to form glutamate, which is subsequently deaminated oxidatively to liberate ammonia. Conversely, alanine is formed by transamination of pyruvate with either glutamate or glutamine and is added to renal venous blood. The balance between production and utilization is dependent, at least in part, on the concentrations of the reactants.

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