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PNAS 102 (28): 9960-9965

Copyright © 2005 by the National Academy of Sciences.


Variation in commercial rodent diets induces disparate molecular and physiological changes in the mouse uterus

Haibin Wang * {dagger}, Susanne Tranguch * {dagger}, {ddagger}, Huirong Xie *, Gregory Hanley §, Sanjoy K. Das *, ¶, and Sudhansu K. Dey *, {ddagger}, ||, **

Departments of *Pediatrics, §Pathology, Cancer Biology, {ddagger}Cell and Developmental Biology, and ||Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232

Edited by George E. Seidel, Jr., Colorado State University, Fort Collins, CO, and approved May 13, 2005

Received for publication March 1, 2005.

Abstract: Although ovarian estrogen, estradiol-17{beta}, is a key modulator of normal reproductive functions, natural and synthetic compounds with estrogen-like activities can further influence reproductive functions. Plant-derived phytoestrogens specifically have received much attention because of associated health benefits. However, a comprehensive understanding of the beneficial and/or detrimental impacts of phytoestrogen consumption through commercial rodent diets on uterine biology and early pregnancy at the molecular level remains largely unexplored. Using multiple approaches, we demonstrate here that exposure of adult female mice to a commercial rodent diet with higher phytoestrogen levels facilitates uterine growth in the presence or absence of ovarian estrogen, alters uterine expression of estrogen-responsive genes, and advances the timing of implantation compared with a diet with lower phytoestrogen levels. The finding that variability in phytoestrogen content in commercial rodent diets, both within and between brands, influences experimental results stresses the importance of this investigation and raises caution for investigators using rodents as animal models.

Key Words: dietary phytoestrogen • embryo implantation • uterine gene expression

Author contributions: H.W., G.H., S. K. Das, and S. K. Dey designed research; H.W., S.T., H.X., and S. K. Das performed research; H.W., S.T., and S. K. Dey analyzed data; and H.W., S.T., G.H., and S. K. Dey wrote the paper.

This paper was submitted directly (Track II) to the PNAS office.

Abbreviations: E2, estradiol-17{beta}; P4, progesterone.

{dagger} H.W. and S.T. contributed equally to this work.

** To whom correspondence should be addressed at: Department of Pediatrics, Division of Reproductive and Developmental Biology, Vanderbilt University Medical Center, MCN-D4100, Nashville, TN 37232-2678. E-mail: sk.dey{at}

© 2005 by The National Academy of Sciences of the USA

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