The antagonism of salicylate to diethylstilbestrol upon liver glycogen in the rat.

Abstract

Since salicylate has been reported to antagonize liver glycogenesis after cortisone, an experiment was designed to test the antagonism of salicylate to diethylstilbestrol upon liver glycogen in normal, fasted, female rats. Liver glycogen levels, elevated by estrogen treatment for two weeks, were found to be lowered by a subsequent injection of sodium salicylate, 5–8 hours before sacrifice. The action of the estrogen in producing liver and adrenal enlargement, moderate depletion of adrenal ascorbic acid,and maximal depletion of adrenal cholesterol was confirmed. Salicylate alone produced only a moderate depletion of adrenal ascorbic acid, while the combined effect of the drugs was seen in a marked depletion of this substance. Diethylstilbestrol and sodium salicylate were synergistic with regard to the stimulation of activity in the rat adrenal cortex under these conditions (probably by release of ACTH), but their actions on liver glycogen levels were in the opposite directions. The estrogen stimulated glycogen accumulation while salicylate was glycogenolytic; in combination, the substances were antagonistic in this respect. It is concluded that the mechanism is a salicylate-glucocorticosteroid antagonism.