Published: 12 June 2024
Author(s): Gea Ciccarelli, Gianfranco Di Giuseppe, Laura Soldovieri, Giuseppe Quero, Enrico Celestino Nista, Michela Brunetti, Francesca Cinti, Simona Moffa, Umberto Capece, Vincenzo Tondolo, Andrea Mari, Antonio Gasbarrini, Alfredo Pontecorvi, Sergio Alfieri, Andrea Giaccari, Teresa Mezza
Section: Original Article

Diabetes of the exocrine pancreas (DEP), - also defined as pancreatic, pancreatogenic, or type 3c diabetes - arises from the structural or functional loss of insulin secretion secondary to exocrine pancreatic diseases [1,2]. The most common etiologies of DEP are acute and chronic pancreatitis (CP) followed by pancreatic ductal adenocarcinoma [2]. The widely accepted pathophysiology for DEP is insulin deficiency, with two potential mechanisms responsible for relative or absolute insulin deficit: the inflammatory environment and extensive fibrosis of the exocrine pancreas [2].

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