GLP1R and pancreatitis: The suggested possible underlying mechanism was as follows: the glucagon-like peptide 1 receptor, which is abundantly expressed in the pancreatic duct and islets, is stimulated by DPP-4i via inhibition of DPP-4 and increased glucagon-like peptide 1 [21], resulting in overgrowth of pancreatic acinar and ductal cells into the small pancreatic ducts; this could lead to ductal occlusion, thereby triggering pancreatitis [22].