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(Journal of Nutrition. 1999;129:587-590.)
© 1999 The American Society for Nutritional Sciences


Supplement

Modulation of Estrogen Action in the Rat Pituitary and Mammary Glands by Dietary Energy Consumption

Thomas J. Spady3 , Djuana M. E. Harvell3 , Athena Lemus-Wilson, Tracy E. Strecker, Karen L. Pennington, Eric A. Vander Woude, Diane F. Birt4 , Rodney D. McComb and James D. Shull 1

Eppley Institute for Research in Cancer and Allied Diseases, Department of Biochemistry and Molecular Biology, and Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE

We are investigating the mechanisms through which estrogens induce development of prolactin (PRL)-producing pituitary tumors and mammary carcinomas in rats and how these mechanisms are affected by dietary energy consumption. The hypothesis under examination is that dietary energy restriction inhibits tumorigenesis in estrogen-responsive tissues by altering cellular responsiveness to estrogenic hormones. In the Fischer 344 (F344) rat strain, a 40% restriction of energy consumption virtually abolishes development of estrogen-induced pituitary tumors. Inhibition of pituitary tumorigenesis in the F344 strain by energy restriction results from modulation of estrogen regulation of cell survival, not cell proliferation. In contrast, energy restriction has no inhibitory effect on estrogen-induced pituitary tumor development in the ACI rat strain. However, energy restriction markedly inhibits induction of mammary carcinomas in female ACI rats treated with 17ß-estradiol. Data presented herein indicate that dietary energy restriction modulates the responsiveness of specific cell populations to estrogenic hormones and thereby inhibits estrogen-induced tumorigenesis in a manner specific to both rat strain and tissue.


KEY WORDS: • estrogen • rats • pituitary tumor • mammary cancer • dietary energy restriction • prolactin







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