Sreenath T L, Polasa H
Biochem Int. 1985 Dec;11(6):885-91.
Enfenamic acid, a new non-steroidal anti-inflammatory drug was studied for its effect on hepatic gluconeogenesis and some of the enzymes involved in this process in mice. Incubation of liver cells in the presence of 1.0 mM enfenamic acid inhibited the output of glucose. And also the in vitro addition of various concentrations of enfenamic acid (0.25 to 3.0 mM) to the tissue extracts of liver inhibited the activities of important gluconeogenic enzymes such as pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase (PEPCK) and fructose 1,6-diphosphatase (FDPase). The oral and intraperitoneal administrations of the drug for 15 and 3 days respectively, exhibited significant decrease in the hepatic PC, PEPCK and FDPase. These findings indicated that the impairment of gluconeogenesis might be due to the inactivation of the enzymes by the drug.
对一种新型非甾体抗炎药甲灭酸进行了研究,观察其对小鼠肝糖异生及该过程中一些相关酶的影响。在1.0 mM甲灭酸存在的情况下培养肝细胞,可抑制葡萄糖的输出。此外,向肝组织提取物中体外添加不同浓度的甲灭酸(0.25至3.0 mM),可抑制重要糖异生酶如丙酮酸羧化酶(PC)、磷酸烯醇式丙酮酸羧激酶(PEPCK)和果糖1,6 -二磷酸酶(FDPase)的活性。分别口服和腹腔注射该药物15天和3天,可使肝脏中的PC、PEPCK和FDPase显著降低。这些发现表明,糖异生受损可能是由于该药物使这些酶失活所致。