Exocrine pancreatic insufficiency syndrome in CBA/J mice. III. Pathological and genetic analysis.
A clinical and histopathological description of exocrine pancreatic insufficiency syndrome in CBA/J mice is presented. Amelioration of clinical symptoms by pancreatic enzyme replacement therapy is described, as are breeding experiments designed to test the hypothesis that the etiology of this syndrome is a recessive mutation. Our failure to propagate the expected numbers of animals with the syndrome by genetic means leads us to the conclusion that it is not transmitted as an autosomal recessive mutation. Our finding of focal histological lesions of the exocrine pancreas in large numbers of clinically normal CBA/J mice suggests that the CBA/J genetic background is some way predisposes this strain to the spontaneous necrosis and atrophy of exocrine cells that is pathognomonic of this disease.
D000818:Animals; D001284:Atrophy; D005260:Female; D005951:Glucose Tolerance Test; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D009336:Necrosis; D010179:Pancreas / Q000473:pathology*; D010182:Pancreatic Diseases / Q000235:genetics / Q000473:pathology / Q000635:transmission; D010189:Pancreatic Juice / Q000378:metabolism*; D014357:Trypsin / Q000378:metabolism
D007328:Insulin; D014357:Trypsin