Exocrine pancreatic insufficiency syndrome in CBA/J mice. Ultrastructural study.
The pathogenesis of a spontaneously occurring exocrine pancreatic insufficiency (EPI) syndrome in CBA/J mice was studied at the ultrastructural level. Initial cytologic manifestations of this syndrome are seen as a progressive digestion of the zymogen granules, beginning at the periphery and proceeding toward the granule interior. Granule membrane breakdown, fusion of neighboring granules, and a release of zymogen contents into the cytoplasm are frequently observed in later stages; in some cases the entire granule contents appear digested before membrane breakdown is observed. In either case, pathologic changes are subsequently observed in mitochondria and rough endoplasmic reticulum. Remnants of lysed cells are then engulfed by invading macrophages, and infiltration by fat cells is observed. Secretory ducts and islets of Langerhans show no pathologic changes even after total autolysis of the exocrine pancreas. Morphologic evidence showing zymogen granule destabilization, coupled with biochemical evidence presented in an accompanying paper, indicate that intracellular autodigestion is the mechanism of exocrine cell death.
D000818:Animals; D003594:Cytoplasmic Granules / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D004792:Enzyme Precursors / Q000378:metabolism; D051379:Mice; D008808:Mice, Inbred CBA; D010179:Pancreas / Q000648:ultrastructure; D010182:Pancreatic Diseases / Q000473:pathology / Q000662:veterinary*; D012376:Rodent Diseases / Q000382:microbiology / Q000473:pathology*; D014357:Trypsin / Q000502:physiology; D014777:Virus Diseases / Q000150:complications
D004792:Enzyme Precursors; D014357:Trypsin