No effect of adult dietary fat on tumors induced prenatally by diethylstilbestrol

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Abstract
Strain CD‐1 female mice exposed prenatally to diethylstilbestrol (DES) or vehicle were placed on semipurified diets containing 2.6%, 10%, 20%, or 29% fat by weight at four weeks of age. These mice were used as a breeding colony for a few weeks and then maintained to terminal illness on the semipurified diets. Females exposed prenatally to DES developed mammary tumors, pituitary tumors, and glandular tumors of the reproductive tract. There was no significant difference in tumor frequency between low‐ and high‐fat dietary groups. Fewer tumors appeared in the vehicle‐exposed mice, as expected, and their frequency did not differ between the dietary groups. Pregnancy reduced tumor frequency in DES‐exposed mice, but the incidence of pregnancy was not significantly different between low‐ and high‐fat dietary groups. In the adult the failure of a high‐fat diet to increase the frequency of reproductive system tumors induced prenatally is in marked contrast to the effectiveness of high‐fat diets in promoting mammary tumors induced by carcinogens given to rats postna‐tally. This difference is critical in the interpretation of epidemiological studies. The relationship of dietary fat to reproductive system cancer in human populations was reviewed in comparison with these two animal models. The epidemiological literature was found to be more consistent with the animal model, showing high sensitivity to dietary fat prenatally but no significant sensitivity at the adult stage of life.