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Traditionally, the glucocorticoids have been viewed as catabolic hormones. However, with the present knowledge about how the glucocorticoid receptor protein functions in the stimulation of mRNA synthesis, a new view must be accepted: These steroids also have an anabolic function. They are anabolic because they stimulate the de novo synthesis of enzymes of anabolic pathways. In the liver, stimulation of lipogenic enzymes has been shown. These findings suggest that glucocorticoids can increase feed efficiency and thereby play a role in the etiology of obesity.

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Experiments designed to determine whether the role of glucocorticoid (GC) in the induction of the enzyme overshoot response to starvation-refeeding was direct or permissive through insulin were conducted. Intact, adrenalectomized (ADX), and streptozotocin (STREP) treated rats with or without insulin and/or GC replacements were starved for 48 hours and refed a 65% glucose diet for 48 hours. The typical enzyme overshoot response to starvation-refeeding was observed in the intact rats, ADX rats given GC, STREP rats given insulin and ADX-STREP rats given glucocorticoid plus insulin. No overshoot was observed if glucocorticoid was absent whereas a modest increase in enzyme activity could be observed in insulin deficient rats treated with GC.