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 yea rs 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 (re mnants 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 st udy, and this was associated with islets that were 1,300% larger than in control animals (nesidioblastosis). An in situ pancreatic remnant w ith an obstructed duct and total exocrine atrophy can maintain a nondi abetic state for >3 years. Perhaps the mechanism is associated with th e observed nesidioblastosis.