title: Nesidioblastosis as a mechanism to prevent fibrosis-induced diabetes after pancreatic duct obstruction.
abstract: 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.
authors: Department of Surgery, Virginia Mason Medical Center, Seattle, Washington.
authors: L W
authors: LW
authors: Traverso
authors: D E
authors: DE
authors: Bockman
authors: S K
authors: SK
authors: Pleis
authors: D H
authors: DH
authors: Dail
mesh_terms: D000818:Animals; D001284:Atrophy; D003921:Diabetes Mellitus, Experimental / Q000209:etiology / Q000517:prevention & control*; D004285:Dogs; D005260:Female; D005355:Fibrosis; D007515:Islets of Langerhans / Q000473:pathology*; D008297:Male; D010179:Pancreas / Q000473:pathology*; D010180:Pancreatectomy; D010182:Pancreatic Diseases / Q000150:complications* / Q000473:pathology; D010183:Pancreatic Ducts / Q000473:pathology*