Pancreatic Hypertrophy in Ki- ras -Induced Actin-Interacting Protein Gene Knockout Mice

Objectives: Pancreatic functions were determined in a Ki- ras -induced actin-interacting protein (KRAP) Ydeficient ( j/j) mouse mutant. Methods: Pancreatic enzyme, protein, and DNA contents were measured, and histological examinations were conducted. The mixture of bile-pancreatic juice was collected, and amylase and bile acid outputs were determined. Oral glucose tolerance test was determined. Moreover, the gene expression of KRAP was determined in cholecystokinin (CCK)-A(1) receptor ( j/j) mice. Results: The body weight was smaller, and the ratio of pancreatic wet weight/body weight was higher in KRAP( j/j) mice compared with wild-type mice. The enzyme contents, but not DNA content, in the pancreas of KRAP( j/j) mice were higher than those of wild-type mice. Histological examination revealed the increase in the number of zymogen granules in the pancreatic acinar cells of KRAP( j/j) mice. Amylase secretions in response to CCK-octapeptide sulfate were significantly higher in KRAP( j/j) than wild-type mice, whereas the basal secretion did not differ between the 2 genotypes. A normal glucose tolerance was observed in KRAP( j/j) mice. The gene expression of KRAP in CCKA(1) receptor ( j/j) mice was significantly lower than in wild-type mice. Conclusions: The lack and/or decrease in KRAP level in the pancreas may promote the pancreatic growth and hypertrophy.