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 Ca
2+) may play a possible role of mediator in depletion mechanism of liver glycogen in endotoxemia. The liver glycogen level in 2hr 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 Ca
2+ in liver cytosol fraction in cortisone-treated mice was higher 2hr after GAF injection than that in the cortisone alone-treated one. The phosphorylase a activity in liver 2hr 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 Ca
2+ and mediator GAF released from reticuloendothelial system (RES) macrophages in glucoregulation of endotoxemia. Thus, it may be speculated that intracellular Ca
2+ may mediate glycogenesis rather than glycogenolysis in the depletion mechanism of liver glycogen during GAF-poisoning.
View full abstract