Enhancement of mammary tumorigenesis in rats by high-fat diets has been postulated to be due to altered hormonal status. Elevated serum prolactin and, in some cases, estrogen have been reported in rats fed diets high in corn oil or lard that increase 7,12-dimethylbenz(a)anthracene (DMBA) tumorigenesis. However, we have found no difference in plasma prolactin during the proestrus surge or at the other stages of the estrous cycle in rats fed a diet high (24%) in corn oil that augments DMBA-induced tumorigenesis or a control diet containing 5% corn oil. There was no effect of the same dietary treatment on plasma progesterone or serum estradiol in the same experiments. In addition, we found that DMBA administration did not change the blood concentration of any of the three hormones.

Female Sprague-Dawley rats, bearing atrial cannulae and given a carcinogenic dose of DMBA at 8 weeks of age, were studied 2 to 5 weeks or 10 to 13 weeks after DMBA administration. Rats given only the oil vehicle for DMBA were studied at the same ages. Blood samples were taken from rats with 4-day estrous cycles at 3-hr intervals on the day of proestrus and at 6- to 12-hr intervals on the other days of the cycle. No effect of dietary corn oil content or of DMBA administration on plasma prolactin and progesterone was detected in either age group. On the afternoon of proestrus, rats were sampled more frequently to examine the hormonal patterns in detail; again, no dietary effect was detected. Serum estradiol was measured in rats that were fed the control or high-corn-oil diets, treated with DMBA or vehicle, and decapitated on one of the 4 days of the estrous cycle. There was no detectable effect of dietary corn oil content or DMBA treatment during any stage of the cycle. All three hormones showed qualitative and quantitative patterns identical to normal cycling rats at both ages studied.

Our results indicate that earlier reports of an effect of dietary fat on blood prolactin and estrogen content may have been due either to diets low in essential fatty acids or to anesthesia-induced hormonal responses.

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This investigation was supported in part by USPHS Grant CA 25538 awarded by the National Cancer Institute, Department of Health and Human Services, and by the Massachusetts Institute of Technology Undergraduate Research Opportunities Program.

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