Response of mouse liver glycogen cycle enzymes to endotoxin treatment.
The present study was undertaken to characterize endotoxin-induced changes in carbohydrate metabolism and more specifically, to determine the contribution of glycogenolysis to the loss of liver glycogen. Female ICR mice, fasted overnight, were injected with a median lethal dose (LD50, 9 mg/kg) of endotoxin extracted from Salmonella typhimurium strain SR-11. Glycogen synthase and glycogen phosphorylase activities were measured at 0.5 and 6 h after treatment. Endotoxin treatment did not alter total glycogen synthase activity, but the amount of enzyme present in the active form was significantly lower in endotoxic mice. There was no significant increase in glycogen phosphorylase activity in endotoxin-treated mice. Glycogen phosphorylase was activated to the same extent in control and endotoxic mice by decapitation or intravenous epinephrine (25 or 1 mug/kg). The results of this study indicate no significant increase in glycogen phosphorylase activity in endotoxic mice, contraindicating enhanced glycogenolysis as a mechanism for depletion of carbohydrate following endotoxin injection. Altered activation of glycogen synthase, however, may contribute to the loss of glycogen during endotoxemia.
D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology*; D004789:Enzyme Activation; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006006:Glycogen Synthase / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000201:enzymology*; D008112:Liver Glycogen / Q000378:metabolism*; D051379:Mice; D006005:Phosphorylases / Q000378:metabolism*; D012486:Salmonella typhimurium
D004731:Endotoxins; D008112:Liver Glycogen; D000242:Cyclic AMP; D006005:Phosphorylases; D006006:Glycogen Synthase; D004837:Epinephrine