Belyaeva N F, Golubev M A, Grigorovich J A, Dubinsky Z V, Semenova N A, Pitkänen E, Korovkin B F
Institute of Biological and Medical Chemistry RAMS, Moscow, Russia.
Experientia. 1994 Aug 15;50(8):780-4. doi: 10.1007/BF01919382.
The role of fructose 2,6-bisphosphate in the interconversion of sedoheptulose 7-phosphate and sedoheptulose 1,7-bisphosphate in rat liver cytosol fractions was studied by means of phosphorus magnetic resonance spectroscopy. When the activity of 6-phosphofructo-1-kinase was inhibited by a high concentration of ATP, the addition of fructose 2,6-bisphosphate led to a marked decrease in sedoheptulose 7-phosphate levels, accompanied by an increased concentration of ADP. Fructose 2,6-bisphosphate essentially inhibited both the decrease in sedoheptulose 1,7-bisphosphate concentration and the accumulation of Pi in the incubation mixture. The data provided evidence that fructose 2,6-bisphosphate can regulate the substrate cycle: sedoheptulose 7-phosphate<-->sedoheptulose 1,7-bisphosphate in the liver, and thus control the flux through the nonoxidative stage of the pentose phosphate pathway.
通过磷磁共振波谱法研究了果糖-2,6-二磷酸在大鼠肝细胞溶胶组分中景天庚酮糖-7-磷酸和景天庚酮糖-1,7-二磷酸相互转化中的作用。当高浓度ATP抑制6-磷酸果糖-1-激酶的活性时,添加果糖-2,6-二磷酸会导致景天庚酮糖-7-磷酸水平显著降低,同时伴随着ADP浓度升高。果糖-2,6-二磷酸基本上抑制了景天庚酮糖-1,7-二磷酸浓度的降低以及孵育混合物中无机磷酸(Pi)的积累。这些数据证明果糖-2,6-二磷酸可以调节肝脏中的底物循环:景天庚酮糖-7-磷酸⇄景天庚酮糖-1,7-二磷酸,从而控制通过磷酸戊糖途径非氧化阶段的通量。