PANCREAS: Edited by Timothy B. GardnerPanorama of mediators in postpancreatitis diabetes mellitusPetrov, Maxim S.Author Information School of Medicine, University of Auckland, Auckland, New Zealand Correspondence to Maxim S. Petrov, MD, MPH, PhD, Auckland City Hospital, Room 12.085A, Level 12, Auckland 1023, New Zealand. Tel: +64 9 923 2776; fax: +64 9 377 9656; e-mail: email@example.com Current Opinion in Gastroenterology: September 2020 - Volume 36 - Issue 5 - p 443-451 doi: 10.1097/MOG.0000000000000654 Buy Metrics Abstract Purpose of review To provide an overview of mediators involved in the pathogenesis of postacute pancreatitis diabetes mellitus. Recent findings The ‘holistic prevention of pancreatitis’ framework has brought to the fore the sequelae of not only end-stage chronic pancreatitis and extensive pancreatic necrosis but also mild acute pancreatitis. Insights from the DORADO project have provided a wealth of information on the signalling molecules that do and do not affect glucose metabolism in individuals after mild acute pancreatitis and have challenged conventional views of the pathogenesis of postpancreatitis diabetes mellitus. Summary Growing evidence compels a reconsideration of the dogma that mechanical β-cell destruction (and the resulting insulin deficiency) is the only underlying mechanism of postpancreatitis diabetes mellitus. Chronic low-grade inflammation, β-cell compensation, lipolysis, altered secretion of gut hormones, and changes in iron metabolism characterize postacute pancreatitis diabetes mellitus. Some of these are druggable targets that offer novel opportunities to reduce the burden of pancreatitis through tertiary prevention. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.