Participation of calcium ion on depletion mechanism of liver glycogen by purified glucocorticoid antagonizing factor released in blood during endotoxemia.

The present study was conducted by the use of purified glucocorticoid antagonizing factor (GAF) released in blood of endotoxemic mice to determine whether or not the factor (GAF and Ca2+) may play a possible role of mediator in depletion mechanism of liver glycogen in endotoxemia. The liver glycogen level in 2 hr after injection with GAF plus cortisone-treated mice was markedly lower than that in cortisone alone-treated mice. However, the administration of trifluoperazine or verapamil markedly increased glycogen levels in liver of GAF plus cortisone-injected mice. On the other hand, when the mice fed a calcium-free diet were injected with GAF plus cortisone, there was merely a significant difference in liver glycogen level as compared to cortisone alone-treated mice. The level of Ca2+ in liver cytosol fraction in cortisone-treated mice was higher 2 hr after GAF injection than that in the cortisone alone-treated one. The phosphorylase a activity in liver 2 hr after injection of GAF plus cortisone did not show a significant difference as compared to that in mice treated with cortisone alone. However, the activity ratio of glycogen synthase enzyme (synthase I synthase I + D) was decreased in GAF plus cortisone-treated mice as compared to that in cortisone alone-treated mice. These findings suggest that there are participations of Ca2+ and mediator GAF released from reticuloendothelial system (RES macrophages in glucoregulation of endotoxemia. Thus, it may be speculated that intracellular Ca2+ may mediate glycogenesis rather than glycogenolysis in the depletion mechanism of liver glycogen during GAF-poisoning.