DOSE-RESPONSE EFFECTS OF DIETARY FIBER ON NMU-INDUCED MAMMARY TUMORIGENESIS, ESTROGEN-LEVELS AND ESTROGEN EXCRETION IN FEMALE RATS

The dose-related effects of the fiber-rich isolate, soft white wheat b ran (SWWB), and the pure fiber, cellulose, on N-nitrosomethylurea (NMU )-induced mammary tumorigenesis was assessed in F344 female rats, SWWB (45% total dietary fiber, TDF) was added to the ALN-76A high-fat diet at 9, 12, 15 and 18%; cellulose (98% TDF) was added to the same diet at 4.5, 6, 7.5 and 9%, to give equivalent amounts of TDF, The experime ntal diets were fed 3 days post-NMU and continued for a period of 25 w eeks, at which time the experiment was terminated and tumors enumerate d, It was found that significant inhibition of mammary carcinoma occur red only at 9% SWWB, nonsignificant inhibition occurred at 12% SWWB, a nd no inhibition was seen at higher doses. Cellulose-fed animals exhib ited consistently higher tumor yields regardless of dose, The differen ce in tumor yields between the 9% SWWB group and the remaining seven g roups was attributable to an increased incidence in tumors characteriz ed histologically as intraductal proliferation and ductal carcinoma in situ in the latter. Analysis of blood, urine and fecal estrogens was conducted to test whether dietary fiber exerted its tumor-inhibiting e ffect by altering the enterohepatic recycling of estrogens, Although S WWB, in general, lowered urinary estrogen excretion, increased fecal e strogen excretion and lowered blood estrogens, there was no consistent correlation between the amount of SWWB consumed, estrogen status and tumor yields, These results suggest that (i) wheat bran fiber at 9%, o r minor constituents associated with it, contain anti-promoting proper ties that cellulose lacks; (ii) SWWB appears to exert its effects by s uppressing the clonal expansion phase of mammary carcinogenesis; (iii) there is an upper limit (12-15% w/w) to the protective effects of SWW B; and (iv) the effects of SWWB on mammary tumorigenesis may not be at tributed to alterations in the enterohepatic recycling of estrogens.