Abstract
AN INCREASE in the excretion of nitrogen following the administration of corticotropin (ACTH) is reported in animals and in humans. The explanation offered by Albright1is that it represents loss of protoplasm and may be attributed to the secretion of the sugar hormone from the adrenal cortex. It is considered an antianabolic rather than a catabolic effect. Clark's2work with tagged glycine supports the concept of antianabolism. That diversion by way of gluconeogenesis is not adequate to explain quantitatively the phenomenon as brought out by Ingle,3who feels that inhibition of the oxidation of glucose may be an added factor to explain the loss. Much of the effect may be further conditioned by the state of the organism, the diversion of protein being diminished or prevented by previous administration of dextrose and accentuated by insulin (Engel).4In animals the effect is not sustained, an adaptation occurring
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