Control of the synthesis and degradation of fructose 2,6-bisphosphate. A low blood-glucose level as signaled by glucagon leads to the phosphorylation of the bifunctional enzyme and hence to a lower level of fructose 2,6-bisphosphate, slowing glycolysis. Insulin accelerates the formation of fructose 2,6-bisphosphate by facilitating the dephosphorylation of the bifunctional enzyme.