Funakoshi A, Miyasaka K, Jimi A, Kawanai T, Takata Y, Kono A
Department of Gastroenterology, National Kyushu Cancer Center, Fukuoka, Japan.
Biochem Biophys Res Commun. 1994 Mar 15;199(2):482-8. doi: 10.1006/bbrc.1994.1254.
Expression of the CCK-A receptor gene in the pancreas and pancreatic exocrine function was examined in diabetic model rats (OLETF) at 5 wks of age. Little or no CCK-A receptor was detected in the pancreas of OLETF rats. Pancreatic exocrine function in response to exogenous CCK and to bile-pancreatic juice diversion (endogenous CCK) was impaired in conscious OLETF rats. The pancreatic insulin and protein contents of OLETF (Otsuka Long-Evans Tokushima Fatty) and control LETO (Long-Evans Tokushima Otsuka) rats were not significantly different. No histological abnormalities or expression of pancreatitis associated protein (PAP) mRNA was detected in the pancreas in either group. These results suggest that OLETF rats are a new experimental model for congenital deficiency of CCK-A receptor in the pancreas.
在5周龄的糖尿病模型大鼠(OLETF)中检测了胆囊收缩素A(CCK-A)受体基因在胰腺中的表达以及胰腺外分泌功能。在OLETF大鼠的胰腺中几乎检测不到或未检测到CCK-A受体。清醒的OLETF大鼠对外源性CCK和胆胰液分流(内源性CCK)的胰腺外分泌功能受损。OLETF(大冢长-埃文斯-德岛肥胖)大鼠和对照LETO(长-埃文斯-德岛大冢)大鼠的胰腺胰岛素和蛋白质含量无显著差异。两组大鼠的胰腺均未检测到组织学异常或胰腺炎相关蛋白(PAP)mRNA的表达。这些结果表明,OLETF大鼠是胰腺先天性CCK-A受体缺乏的新实验模型。