Casado M, Boscá L, Martín-Sanz P
Instituto de Bioquímica, Facultad de Farmacia, Madrid, Spain.
Endocrinology. 1993 Sep;133(3):1044-50. doi: 10.1210/endo.133.3.8396007.
Fructose 2,6-bisphosphate concentration, 6-phosphofructo 2-kinase/fructose 2,6-bisphosphatase (PFK-2/FBPase2) activity, and messenger RNA decreased in maternal rat liver during the last days of gestation, and the recovery started after delivery. Phospho(enol)pyruvate carboxykinase activity and messenger RNA increased in contrast to PFK-2 changes. Measurement of the glycolytic capacity in isolated hepatocytes prepared from rats 1 h after parturition showed a low glucose consumption and an impaired capacity to metabolize glucose. These results stress the relevance of the PFK-2/fructose 2,6-bisphosphate system in the control of the glycolytic flux in liver, and these changes are intended to prevent glucose consumption by maternal liver and contribute to allow gluconeogenesis to proceed at the end of gestation. The physiological basis of this adaptation may lay on the diversion of glucose from maternal to fetal metabolism.
在妊娠最后几天，母鼠肝脏中的果糖2,6 -二磷酸浓度、6 -磷酸果糖-2 -激酶/果糖2,6 -二磷酸酶（PFK - 2/FBPase2）活性及信使核糖核酸减少，分娩后开始恢复。与PFK - 2的变化相反，磷酸烯醇式丙酮酸羧激酶活性及信使核糖核酸增加。对产后1小时大鼠分离肝细胞糖酵解能力的测定显示，葡萄糖消耗较低且代谢葡萄糖的能力受损。这些结果强调了PFK - 2/果糖2,6 -二磷酸系统在控制肝脏糖酵解通量中的相关性，这些变化旨在防止母鼠肝脏消耗葡萄糖，并有助于在妊娠末期进行糖异生。这种适应性的生理基础可能在于葡萄糖从母体代谢向胎儿代谢的转移。
