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It is now well established that the adrenal cortex is involved in some fundamental manner in the metabolic response to injury and illness, but the precise mechanism by which this gland exerts its influence remains clouded. Originally, based on the observations that certain of the metabolic responses to injury do not occur in the absence of the adrenal cortex, and on the evidence of increased secretion of adrenal steroids during stress, it seemed reasonable to interpret the metabolic changes which occur after stress as direct manifestations of hypersecretion of adrenocorticotrophic hormone (ACTH) and adrenocortical steroids (1, 2, 3). The demonstration that overdosage with ACTHor cortisone produced metabolic changes comparable to those after stress made such an interpretation even more attractive. However, as investigation in this area has been pursued, it has become increasingly apparent that the concept described above is an oversimplification and needs modification. Ingle, in a brilliant series of studies, beginning in 1943, has been chiefly responsible for demonstrating, in animals at least, that the adrenal cortex is not directly responsible for the changes under consideration, although adrenocortical hormone must be present for certain of the changes to take place (4, 5, 6, 7, 8). Thus, the adrenalectomized animal exhibits a normal metabolic response to injury if maintained with an amount of adrenocortical hormone which itself does not produce overdosage effects. Under such circumstances, no increase in adrenal activity is possible, and hence adrenocortical hormone may be considered as necessary but not re-

STUDIES ON THE INTERDEPENDENT EFFECTS OF STRESS AND THE ADRENAL CORTEX ON CARBOHYDRATE METABOLISM IN MAN 1