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[Cancer Research 44, 1321-1326, April 1, 1984]
© 1984 American Association for Cancer Research

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Similarity between trans Fat and Saturated Fat in the Modification of Rat Mammary Carcinogenesis1

Sandra L. Selenskas, Margot M. Ip2 and Clement Ip2

Department of Breast Surgery [S. L. S., C. I.] and Grace Cancer Drug Center [M. M. I.], Roswell Park Memorial Institute, Buffalo, New York 14263

Commercial hydrogenation of vegetable oils results in the introduction of trans fatty acids. In the present study, we have investigated the effect of feeding a fat which contained approximately 38% trans isomers (designated trans fat) on the induction of mammary tumors by dimethylbenz(a)anthracene in rats. The corresponding control fat (designated cis fat), which had a similar fatty acid composition, consisted of only cis isomers. Since both the trans and cis fats were rather saturated, a comparison was also made between these 2 types of fat and corn oil, which contains about 60% linoleic acid (C18:2). Each fat was present in the diet at 2 levels, 5 and 20% by weight. Although rats fed the 20% trans fat or cis fat diets had a slightly higher tumor incidence and yield than did those on the corresponding 5% fat control diets, the difference was not statistically significant. In contrast, rats fed the 20% corn oil diet developed a much greater number of tumors than did rats fed a diet containing only 5% corn oil. Further analysis of the data showed that diets containing either trans fat or cis fat were much less effective than were the corn oil diets in promoting the development of mammary neoplasia at either the 5 or 20% level. Our results thus suggest that trans fat behaves very much like a saturated fat in the modification of mammary tumorigenesis. A determination of the fatty acid content of the mammary fat pad indicated that its composition generally reflected the dietary fatty acid intake, with the incorporation of trans isomers into the mammary tissue found to be dependent on the quantity of trans fat in the diet.

1 This work was supported by Grants CA 33240 and CA 24538 from the National Cancer Institute, NIH.

2 To whom requests for reprints should be addressed.

Received 8/10/83. Accepted 12/13/83.







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Copyright © 1984 by the American Association for Cancer Research.