Details

Autor(en) / Beteiligte

• Miyasaka, Kyoko
• Fujimoto, Takahiro
• Kawanami, Takako
• Takiguchi, Soichi
• Jimi, Atsuo
• Funakoshi, Akihiro
• Shirasawa, Senji

Titel

Pancreatic hypertrophy in Ki-ras-induced actin-interacting protein gene knockout mice

Ist Teil von

• Pancreas, 2011-01, Vol.40 (1), p.79-83

Ort / Verlag

United States

Erscheinungsjahr

2011

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• Pancreatic functions were determined in a Ki-ras-induced actin-interacting protein (KRAP)-deficient (-/-) mouse mutant. 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 (-/-) mice. The body weight was smaller, and the ratio of pancreatic wet weight/body weight was higher in KRAP(-/-) mice compared with wild-type mice. The enzyme contents, but not DNA content, in the pancreas of KRAP(-/-) 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(-/-) mice. Amylase secretions in response to CCK-octapeptide sulfate were significantly higher in KRAP(-/-) than wild-type mice, whereas the basal secretion did not differ between the 2 genotypes. A normal glucose tolerance was observed in KRAP(-/-) mice. The gene expression of KRAP in CCK-A(1) receptor (-/-) mice was significantly lower than in wild-type mice. The lack and/or decrease in KRAP level in the pancreas may promote the pancreatic growth and hypertrophy.