PFKFB3 and diabetes mellitus: The present evidence that glucagon antagonises the action of elevated glucose on translocation of glucokinase from the nucleus and binding to PFK2/FBPase2 in the cytoplasm adds a new perspective to the acute control of glucokinase activity and shows that absolute or relative glucagon excess as occurs in diabetes [3] is most likely a contributing factor to the defective glucokinase translocation in animal models of diabetes [25,37,38,49,50].