Exocrine pancreatic insufficiency syndrome in CBA/J mice. II. Biochemical studies.

Authors

E H. LeiterFollow
E C. Dempsey
J J. EppigFollow

Document Type

Article

Publication Date

1977

Keywords

Chymotrypsin: me, Chymotrypsinogen: me, Cytoplasmic-Granules: ul, Electrophoresis-Polyacrylamide-Gel, Enzyme-Precursors, Female, Fractionation, Male, Mice, Mice-Inbred-CBA, Pancreatic-Diseases: en, pa, ve, Rodent-Diseases: en, pa, Stains-and-Staining, Trypsin: me, Trypsinogen: me

First Page

31

Last Page

46

JAX Source

Am-J-Pathol. 1977 Jan; 86(1):31-46.

Abstract

Premature activation of proteolytic zymogens (trypsinogen, chymotrypsinogen) as an early step in the pathogenesis of exocrine pancreatic insufficency (EPI) syndrome in CBA/J mice was investigated in electrophoresed pancreatic homogenates. Polyacrylamide gels containing extracts from control pancreas required prior activation of trypsinogen and chymotrypsinogen (with exogenously added enterokinase and trypsin, respectively) to produce activity staining with specific synthetic substrates. On the contrary, bands of activity staining in gels containing homogenates from mice with EPI syndrome could be readily detected without trypsin or enterokinase preincubation. Subcellular fractionation of control and diseased pancreas revealed that the premature intracellular proteolysis was confined to the zymogren granule fraction, which, even in very moderately affected pancreases (10 to 30% acinar cell autolysis), was very labile in vitro. These proteolytic events reflect the biochemical consequences of zymogen granule destabilization that were observed at the ultrastructural level.

Recommended Citation

Leiter EH, Dempsey EC, Eppig JJ. Exocrine pancreatic insufficiency syndrome in CBA/J mice. II. Biochemical studies. Am-J-Pathol. 1977 Jan; 86(1):31-46.