EFFECTS OF DIETARY GALACTOOLIGOSACCHARIDE ON AZASERINE-INDUCED ACINARPANCREATIC CARCINOGENESIS IN MALE WISTAR RATS

In the present study the effects of dietary galacto-oligosaccharide (G OS) an dietary fat-promoted pancreatic carcinogenesis in azaserine-tre ated rats were investigated. The aims of this study were to determine 1) whether GOS acts as art inhibitor of pancreatic carcinogenesis and 2) whether GOS interacts with dietary fat-promoted pancreatic tumor de velopment. Four groups of 39 azaserine-treated rats were maintained on different experimental diets that were formulated as follows: 4.3 wt% fat-8.3 wt% GOS (low fat-low GOS), 3.5 wt% fat-27.4 wt% GOS (low fat- high GOS), 15.5 wt% fat-9.5 wt% GOS (high fat-low GOS), and 14.3 wt% f at-28.6 wt% GOS (high fat-high GOS). Autopsies were performed after 6 months (9 animals/group) and 12 months (30 animals/group). Five rats p er group were treated with bromodeoxyuridine before autopsy. Parallel sections of the pancreas were stained with hematoxylin and eosin or wi th hematoxylin and a monoclonal antibody against bromodeoxyuridine and examined by light microscopy. A high-fat diet caused a significant de crease, whereas a diet high in GOS caused a significant increase, in a bsolute and relative weight of the cecum content. A high level of diet ary fat caused a highly significant increase in multiplicity and incid ence of pancreatic (pre)neoplastic lesions after 6 and 12 months of fe eding. A high level of GOS in the diet did not influence the number of atypical acinar cell nodules or the tumor incidence in comparison wit h controls. Dietary fat and dietary GOS caused a significant increase in cell proliferation in atypical acinar cell nodules after six months . It was concluded that dietary GOS has no modulating effect on pancre atic carcinogenesis in azaserine-treated rats or on the tumor-promotin g effect of a high-fat diet.