Modification of pancreatic carcinogenesis in the hamster model. VIII. Inhibitory effect of exogenous insulin.

The effect of exogenous insulin, which has been known to suppress beta-cell function of islets, was investigated on pancreatic carcinogenesis induced by N-nitrosobis(2-oxopropyl) amine [(BOP) CAS: 60599-38-4; 2,2'-dioxo-N-nitrosodipropylamine]. Three groups of Syrian golden hamsters were treated sc once with BOP (20 mg/kg body wt) simultaneously with (group 1), 120 minutes before (group 2), or 120 minutes after (group 3) a single sc injection of porcine insulin (5 U/kg body wt). Group 4 was a BOP-treated control. Survivors were killed 46 weeks after BOP administration, and the pancreas, common duct, and gallbladder were examined histologically. When given 120 minutes before or after BOP, insulin inhibited the induction of benign and malignant pancreatic lesions in a statistically significant fashion. However, the simultaneous administration of BOP also led to similar (although not statistically significant) results as did the administration of insulin 120 minutes after BOP. Insulin also seemed to inhibit tumor induction in the common duct and gallbladder, regardless of when it was administered; however, the differing incidence was statistically significant only in hamsters from group 3 killed at the experiment's end. The overall data suggest that the inhibitory effect of exogenous insulin on pancreatic carcinogenicity is not merely through islet cells, but rather through other (or additional) mechanisms.