Imesch E, Rous S
Prostaglandins. 1975 Jun;9(6):945-57. doi: 10.1016/0090-6980(75)90081-7.
Using perfused livers of rats fasted for 48 hours, glucose production and incoroporation of 2-14C pyruvate (trace dose) into perfusate glucose were studied. Both were found to be inhibited by PGE1 (infuced at a concentration of 0.5 mu/min) by about 60%. The incorporation of 1-14C glycerol into perfusate glucose and into glycerol-glyceride part of the liver glycerides were also studied, using the same test conditions. The former incorporation was significantly inhibited (56%) and the latter strongly stimulated (360 %) by PGE1. PGE1 had no effect on glucose production in a perfusate overloaded with sodium pyruvate, nor on pyruvate carboxylase and phospho-enolpyruvate carboxykinase activity. this was in contrast with the results obtained in perfusions with a trace dose of 2-14C pyruvate. The results showed that PGE1, at the physiological concentration used, stimulated the incorporation of 1-14C glycerol into glycerol-glyceride part of liver glycerides and, when there was no overload of pyruvate present in the perfusion medium, inhibited gluconeogensis at some point, possibly, but perhaps not exclusively, between the glycerol and glucose steps.
利用禁食48小时的大鼠的灌注肝脏,研究了葡萄糖生成以及2-¹⁴C丙酮酸(微量剂量)掺入灌注液葡萄糖中的情况。发现二者均受到PGE1(以0.5微克/分钟的浓度注入)的抑制,抑制率约为60%。在相同的试验条件下,还研究了¹⁴C甘油掺入灌注液葡萄糖以及肝脏甘油酯中甘油-甘油酯部分的情况。PGE1使前者的掺入显著受到抑制(56%),而使后者受到强烈刺激(360%)。PGE1对丙酮酸过载的灌注液中的葡萄糖生成没有影响,对丙酮酸羧化酶和磷酸烯醇式丙酮酸羧激酶的活性也没有影响。这与用微量剂量的2-¹⁴C丙酮酸进行灌注所获得的结果形成对比。结果表明,在所使用的生理浓度下,PGE1刺激¹⁴C甘油掺入肝脏甘油酯的甘油-甘油酯部分,并且当灌注介质中不存在丙酮酸过载时,在某个点抑制糖异生,可能但不一定仅仅是在甘油和葡萄糖步骤之间。