Nesidioblastosis as a mechanism to prevent fibrosis-induced diabetes after pancreatic duct obstruction.

Does obstruction of the main pancreatic duct that results in exocrine atrophy also result in diabetes? We followed 11 mongrel dogs for 3 years after approximately three-fourths of the pancreas had been removed and the main pancreatic duct obstructed in the pancreatic tail remnant. At 3 years after surgery, all dogs showed total exocrine atrophy (remnants weighed 0.2-1.2 g). None of the animals became diabetic despite only 6% of the original pancreatic tail remaining. During the 3-year period, fasting blood insulin increased during the last half of the study, and this was associated with islets that were 1,300% larger than in control animals (nesidioblastosis). An in situ pancreatic remnant with an obstructed duct and total exocrine atrophy can maintain a nondiabetic state for > 3 years. Perhaps the mechanism is associated with the observed nesidioblastosis.