© 1990 Oxford University Press
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Role of cholecystokinin in the development of BOP-induced pancreatic lesions in hamsters
Department of Biological Toxicology, TNO-CIVO Toxicology and Nutrition Institute Zeist
1Department of Gastroenterology and Hepatology, University Hospital Leiden, The Netherlands Monza, Milan, Italy
2Department of Gastroenterology and Hepatology, University Hospital Leiden, The Rotta Research Laboratorium Monza, Milan, Italy
3To whom reprint requests should be sent
Cholecystokinin (CCK) has been shown to promote pancreatic growth and azaserine-induced pancreatic carcinogenesis in rats. The present study was carried out to determine effects of CCK on pancreatic growth and carcinogenesis in the N-nitrosobis(2-oxopropyl)amine (BOP) hamster model. One hundred male Syrian golden hamsters were injected s.c. once weekly with 20 mg BOP/kg body wt at 6, 7 and 8 weeks of age, and divided into four groups of 25 animals each, which received one of the following treatments (once daily, 3 days/week for 16 weeks): gelatin; CR-1409, a potent CCK-receptor antagonist; CCK-8, 2.5 µg/kg body wt; or CCK-8 in combination with CR-1409 (30 mm before CCK treatment). The animals were killed after 19 weeks. The growth of the pancreas but not the incidence of pancreatic (pre)neoplastic lesions was enhanced by CCK-8. CR-1409 did not influence the effect of CCK on pancreatic growth.