Studies in the Ketosis of Fasting

Daniel W. Foster

doi:10.1172/JCI105621

Department of Internal Medicine, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas

†

Research Career Development Awardee (5-K3-AM 9968), U. S. Public Health Service.

Address requests for reprints to Dr. Daniel W. Foster, Dept. of Internal Medicine, University of Texas Southwestern Medical School at Dallas, 5323 Harry Hines Blvd., Dallas, Texas 75235.

Submitted for publication August 1, 1966; accepted May 8, 1967.

This study was supported by grant CA 08269, U. S. Public Health Service.

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Published August 1, 1967 - More info

Published in Volume 46, Issue 8 on August 1, 1967
J Clin Invest. 1967;46(8):1283–1296. https://doi.org/10.1172/JCI105621.
© 1967 The American Society for Clinical Investigation

Published August 1, 1967 - Version history

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Abstract

A series of experiments was performed during the induction of starvation ketosis and in the acute reversal of the ketotic state. In contrast to the predictions of two widely held theories of ketogenesis, control of acetoacetate production by the liver appeared to be unrelated to changes in fatty acid mobilization from the periphery, fatty acid oxidation, fatty acid synthesis, or the acetyl coenzyme A concentration in the liver.

Ketosis of fasting was shown to be reversible within 5 minutes by the injection of glucose or insulin. This effect was due to a prompt cessation of acetoacetate production by the liver. The possibility is raised that the ketosis of fasting is due to a direct activation of acetoacetate-synthesizing enzymes secondary to a starvation-induced depression of insulin secretion by the pancreas.

Studies in the Ketosis of Fasting

Daniel W. Foster

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Daniel W. Foster

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