This theoretically enhances the release of glucagon-like peptide-1, which stimulates insulin secretion.[23] Another possible explanation is that the early relief of tumor-induced pancreatic duct obstruction and fibrosis of the adjacent parenchyma by PD can preserve a relatively large amount of functional pancreatic tissue in new-onset diabetes, regardless of the origin of the periampullary cancer. Here, INS is linked to periampullary adenocarcinoma.