title: Participation of calcium ion on depletion mechanism of liver glycogen by purified glucocorticoid antagonizing factor released in blood during endotoxemia.
abstract: 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.
authors: First Department of Hygienic Chemistry, Tohoku College of Pharmacy, Miyagi.
authors: S
authors: S
authors: Sakaguchi
authors: H
authors: H
authors: Ibata
authors: K
authors: K
authors: Yokota
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003348:Cortisone / Q000031:analogs & derivatives / Q000494:pharmacology; D004767:Enterotoxemia / Q000150:complications / Q000378:metabolism*; D006008:Glycogen Storage Disease / Q000150:complications / Q000378:metabolism; D006006:Glycogen Synthase / Q000378:metabolism; D006023:Glycoproteins / Q000097:blood*; D008112:Liver Glycogen / Q000378:metabolism*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010762:Phosphorylase a / Q000378:metabolism; D014700:Verapamil / Q000494:pharmacology
chemical_list: D006023:Glycoproteins; D008112:Liver Glycogen; D014700:Verapamil; D010762:Phosphorylase a; D006006:Glycogen Synthase; D002118:Calcium; D003348:Cortisone