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TZP binds its receptor, leading to the activation of adenylyl cyclase-cAMP-protein kinase A (PKA) pathway and thus stimulating glucose metabolism (glycolysis and Krebs Cycle)

Brief Bioinform

This results in a lower ability to promote receptor internalization compared with endogenous GLP-1, so it allows to have an increased GLP-1R expression on the cell surface, which translates in more robust insulinotropic properties, possibly explaining the enhanced insulin secretion (in both diabetic and not diabetic human islets), induced by TZP (48) ( Figure 1 )