Regulation of PFK and fructose 1, 6-bisphosphatase:

When the level of AMP is high, this indicates the requirement for more ATP synthesis. AMP stimulates PFK raises the rate of glycolysis and inhibits fructose 1 and 6- bisphosphatase turning off gluconeogenesis. Equally, when ATP and citrate stages are high, this signals which no more ATP required to be made.  ATP and citrate inhibit PFK, decreasing the rate of citrate and glycolysis stimulates fructose 1, 6- bisphosphatase, raise the rate of gluconeogenesis.

Glycolysis and gluconeogenesis are made responsive to starvation by the level of the regulatory molecule fructose 2, 6-bisphosphate (F-2, 6-BP).  F-2 and 6-BP is synthesized from fructose 6-phosphate and hydrolyzed back to fructose 6-phosphate by a single polypeptide with two enzymatic activities (PFK2 and FBPase2). The level of F-2, 6-BP is under hormonal control.

Figure:  Reciprocal regulation of glycolysis and gluconeogenesis.

During starvation, when the stage of blood glucose is low and the hormone glucagon is released into the bloodstream and triggers a cAMP cascade, eventually causing phosphorylation of the PFK2 or FBPase2 polypeptide. This activates inhibits PFK2 and FBPase2 and lowering the level of F-2 and 6-BP. In the fed state when blood glucose is at a high level the hormone insulin is released and has the differing effect causing an elevation in the level of F-2, 6-BP. Because F-2 and 6-BP inhibits fructose 1 and strongly stimulates PFK, 6-bisphosphatase, glycolysis is stimulated and gluconeogenesis is inhibited in the fed animal. Conversely in during of starvation the low level of F-2, 6-BP permits gluconeogenesis to predominate.