Abstract
Abstract Glucokinase that appears in normal rat liver after the 16th postnatal day was evoked prematurely, a week earlier, by three injections of hydrocortisone (one per day for 3 days) followed by an injection of glucose. As a result of such treatment 9-day-old rats can exhibit as much glucokinase activity as seen in 21-day-old control rats. The prematurely induced rise of glucokinase in developing rats was prevented by actinomycin, by mannoheptulose, or by estradiol administered 6 hours before each hydrocortisone injection. The normal developmental accumulation of glucokinase was partially inhibited by adrenalectomy, by preventing access to solid food, and by treatment with estradiol. The results suggest that adrenocortical secretion (known to increase after the 10th postnatal day) and the intake of solid food (starting after the 13th day) are the physiological stimuli that trigger the formation of glucokinase in normal rats. Our inability to evoke glucokinase before the 5th day may be due to the presence of estrogen in the newborn organism. The prenatal and postnatal levels of liver hexokinase are also presented; there were no changes observed as a result of any of the treatments that altered the levels of glucokinase.
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