Glucose taken orally is more effective at stimulating insulin release because it stimulates the release of incretin hormone in the gut than if administered IV.
Glucose-dependent insulinotropic polypeptide (GIP) achieves its insulinotropic effects by binding to its specific receptor (GIPR), which is positively coupled to increases in intracellular cAMP and Ca2+ levels in β cells.
Glucagon binds to the receptors on its target cells, activating the adenyl cyclase, stimulating the production of cAMP, which is the eventual trigger for the reactions.