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.