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A Role of Estrogens and Insulin Binding in the Dietary Lipid Alteration of R3230AC Mammary Carcinoma Growth in Rats¹

Department of Biochemistry [J. M. F., R. H.] and University of Rochester Cancer Center [R. H.], University of Rochester, School of Medicine and Dentistry, Rochester, New York 14642

The importance of estrogens in the dietary lipid alteration of R3230AC mammary carcinoma growth and insulin binding was studied. Animals were divided into three groups [intact, ovariectomized, and ovariectomized treated with estradiol valerate (EV)] and were fed diets containing either 0% fat (fat free), 0.5% corn oil (low fat), or 20% corn oil (high fat). An alteration of tumor burden between animals fed high-fat versus either low-fat or fatfree diets was observed and appeared to be influenced by the estrogen status of the animal. The difference in tumor burden attributed to dietary lipid seen in intact rats was less in ovariectomized rats and greater in ovariectomized rats treated with EV, despite the fact that absolute tumor burden was reduced by this treatment. A similar relationship was observed for dietary lipidinduced differences in insulin binding to plasma membranes from these tumors. Reduction of tumor growth resulting from estrogen treatment was greater in low-fat- and fat-free-fed animals than in high-fat-fed rats. Again, tumor growth behavior appeared to be related to the reduction of insulin binding induced by estrogen treatment; insulin binding to plasma membranes from animals fed a low unsaturated lipid diet was decreased to a greater extent by EV treatment than in membranes from high-fat-fed rats. Altered tumor growth and membrane insulin binding, resulting from dietary perturbations and/or EV treatment, were not invariably related to serum insulin levels, nor to differences in membrane preparation, as reflected by 5'-nucleotidase activity, nor to membrane fatty acid composition or uptake of proline. Taken together, these results suggest a potential role of estrogens and insulin receptors as mediators of the dietary lipid alterations of growth of the R3230AC mammary carcinoma.

¹ Supported by USPHS Grant CA16660, NIH. Presented in part at the 75th Annual Meeting of the American Association for Cancer Research (19).

² Portions of this material come from the dissertation to be submitted in partial fulfillment of the Ph.D. degree.

³ To whom requests for reprints should be addressed, at Department of Biochemistry, Box 607, University of Rochester Medical Center, 601 Elmwood Ave., Rochester, NY 14642.

Received 7/ 9/84. Revised 1/14/85. Accepted 1/18/85.