Rognstad R
Biochim Biophys Acta. 1981 Sep 4;676(3):373-8. doi: 10.1016/0304-4165(81)90173-2.
We have examined the effects of glucose and lactate, the products of the gluconeogenic-glycolytic pathways, on phosphofructokinase flux during gluconeogenesis in hepatocytes from fasted rats. With dihydroxyacetone as substrate, phosphofructokinase flux is rather active. Addition of lactate, at concentrations of 5-10 mM, causes a lowering of this flux to the levels found when lactate alone is the substrate. Inhibitor studies suggest that a mitochondrially formed metabolite of lactate is the likely effector involved. Addition of glucose (10mM or greater) to dihydroxyacetone causes an increase in phosphofructokinase flux. Only small effects are seen unless the cells are preincubated with glucose, in which case an estimated 2-3-fold increase in phosphofructokinase flux occurs.
我们研究了糖异生-糖酵解途径的产物葡萄糖和乳酸对禁食大鼠肝细胞糖异生过程中磷酸果糖激酶通量的影响。以二羟基丙酮为底物时，磷酸果糖激酶通量相当活跃。添加浓度为5-10 mM的乳酸会使该通量降低至仅以乳酸为底物时的水平。抑制剂研究表明，乳酸的线粒体形成代谢产物可能是相关效应物。向二羟基丙酮中添加葡萄糖（10 mM或更高）会导致磷酸果糖激酶通量增加。除非细胞预先用葡萄糖孵育，否则只会观察到微小的影响，在这种情况下，磷酸果糖激酶通量估计会增加2-3倍。
