English: When energy need increases, organs, especially muscles, make more glycolysis. Thus glucose level of blood decreases. Therefore glucagon released from pancreas Langerhans Islets. In liver, glucagon activates cAMP dependent protein kinase. This activated enzyme activates the action of FBPase-2 while inhibits activity of PFK-2. So F6P is produced from F26BP. Therefore, F26BP is absent means that there is no factor to inhibit FBPase-1 and in order to support PFK-1. Thus mostly F16BP is converted to F6P instead of the reverse reaction. Now there is high amount of F6P which compete with glucose to decide where Hexokinase-regulatory protein complex will be located at cytoplasm (to provide phosphorylation of glucose to G6P) or nucleus (to leave glucose its non-phosphorylated form), at liver. Because in this condition F6P "wins" the race, F6P triggers the movement of complex towards nucleus. Thus now new glucose molecules cannot enter glycolytic pathway. By this mechanism, liver lowers its glucose consumption to preserve glucose reservoir. After stop of glycolysis at liver, liver utilizes fatty acids to gain energy. When blood glucose level rising, insulin is released. This hormone causes formation of F26BP from F6P. F26BP limits FBPase-1 while supports PFK-1. So reaction goes to F16BP direction. Now, there is not much F6P to win the race for regulating place of hexokinase at liver, by the help of its regulatory protein. Thus Hexokinase come into play at cytoplasm and new glucose molecules continue to be degraded.