Wilder M S, Sword C P
J Bacteriol. 1967 Feb;93(2):538-43. doi: 10.1128/jb.93.2.538-543.1967.
Several enzymes and metabolites concerned with carbohydrate metabolism were examined in mice infected with Listeria monocytogenes. Liver glycogen and glucose decreased parallel to severity of infection. The concentration of glucose in the blood fell to abnormally low levels with a hypoglycemia being most evident at 72 hr. There was a significant decrease in the activity of hepatic uridine diphosphate glucose-glycogen transglucosylase. This decrease in enzymatic activity correlated with the rate of glycogen depletion. Phosphorylase activity declined in a similar fashion, contraindicating enhanced glycogenolysis as the mechanism responsible for glycogen depletion. Although glucose-6-phosphatase decreased throughout the infection period, it did not appear to be the major metabolic defect causing hypoglycemia in Listeria-infected mice. Further distortion of carbohydrate metabolism was indicated by findings of increased levels of pyruvate and lactate in the blood of infected animals.
对感染单核细胞增生李斯特菌的小鼠体内几种与碳水化合物代谢相关的酶和代谢产物进行了检测。肝糖原和葡萄糖水平随感染严重程度平行下降。血液中葡萄糖浓度降至异常低水平，低血糖在72小时时最为明显。肝尿苷二磷酸葡萄糖-糖原转葡萄糖基酶的活性显著降低。这种酶活性的降低与糖原消耗速率相关。磷酸化酶活性以类似方式下降，这与糖原分解增强是糖原消耗的机制相矛盾。尽管葡萄糖-6-磷酸酶在整个感染期间都有所下降，但它似乎不是导致李斯特菌感染小鼠低血糖的主要代谢缺陷。感染动物血液中丙酮酸和乳酸水平升高的结果表明碳水化合物代谢进一步紊乱。
