In the present study the effects of dietary galactooligosaccharide (GOS) on
dietary fat-promoted pancreatic
carcinogenesis in
azaserine-treated rats were investigated. The aims of this study were to determine 1) whether GOS acts as an inhibitor of pancreatic
carcinogenesis and 2) whether GOS interacts with
dietary fat-promoted pancreatic
tumor development. 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% fat-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 per group were treated with
bromodeoxyuridine before autopsy. Parallel sections of the pancreas were stained with
hematoxylin and
eosin or with
hematoxylin and a
monoclonal antibody against
bromodeoxyuridine and examined by light microscopy. A high-fat diet caused a significant decrease, whereas a diet high in GOS caused a significant increase, in absolute and relative weight of the cecum content. A high level of
dietary fat caused a highly significant increase in multiplicity and incidence of pancreatic (pre)neoplastic lesions after 6 and 12 months of feeding. A high level of GOS in the diet did not influence the number of atypical acinar cell nodules or the
tumor incidence in comparison with 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 pancreatic
carcinogenesis in
azaserine-treated rats or on the
tumor-promoting effect of a high-fat diet.