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The adrenocorticosteroids, cortisol, cortisone and corticosterone, may be regarded as catabolic hormones in that the long-term injection of these substances into rodents prevents growth and brings about a drop in body weight (Bodansky & Money, 1954; Cannon, Frazier & Hughes, 1956). The steroids differ widely in their potency (Noble, 1955), but the common action involves the breakdown of skeletal muscle (Engel, 1951) with an associated increase in the size of the liver (Silber & Porter, 1953; Bodansky & Money, 1954; Morita & Kamei, 1962). The latter effect may be a secondary response induced by an increased flow of amino acids to the liver for deamination. In this respect it is known that several hepatic processes concerned with amino acid metabolism are activated in response to a single injection of cortisol. For example, glycogen is deposited in the liver of the starved animal by gluconeogenesis (Long, Katzin & Fry, 1940) and there are corresponding increases in the activity of glutamate-pyruvate transaminase (L-alanine-2-oxoglutarate aminotransferase, EC 2.6.1.2) (Morita & Kamei, 1962; Morita & Kawada, 1962) and the rate of urea synthesis (Long et al. 1940; Engel, 1951). To investigate the possibility that all these responses were linked together, and dependent on a primary effect of cortisol on the release of amino acids from peripheral tissues, the rate of change of all three processes, and their doseresponse relationships, were examined after single injections of cortisol into starved rats.

The effect of cortisol on the activity of glutamate-pyruvate transaminase and the formation of glycogen and urea in starved rats