Giger O, McCallum R E
Am J Physiol. 1976 Oct;231(4):1285-9. doi: 10.1152/ajplegacy.1976.231.4.1285.
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.
本研究旨在描述内毒素诱导的碳水化合物代谢变化，更具体地说，是确定糖原分解对肝糖原损失的作用。将禁食过夜的雌性ICR小鼠注射从鼠伤寒沙门氏菌SR-11菌株中提取的半数致死剂量（LD50，9mg/kg）内毒素。在处理后0.5小时和6小时测量糖原合酶和糖原磷酸化酶活性。内毒素处理未改变总糖原合酶活性，但内毒素血症小鼠中以活性形式存在的酶量显著降低。内毒素处理的小鼠中糖原磷酸化酶活性没有显著增加。通过断头或静脉注射肾上腺素（25或1μg/kg），对照小鼠和内毒素血症小鼠中的糖原磷酸化酶被激活到相同程度。本研究结果表明，内毒素血症小鼠中糖原磷酸化酶活性没有显著增加，这与内毒素注射后碳水化合物消耗增加的机制为糖原分解增强相矛盾。然而，糖原合酶激活的改变可能导致内毒素血症期间糖原的损失。
