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Muddled studies? Blame the chow

Soon after reproductive and developmental biologist Sudhansu Dey's group at the University of Kansas moved to new quarters at Vanderbilt University in Nashville, Tenn., they began noticing that once well-established results on uterine gene expression and reproductive function in female mice procured from the same supplier, and of the same genetic strain, had become a lot less predictable.

By | August 1, 2005

Soon after reproductive and developmental biologist Sudhansu Dey's group at the University of Kansas moved to new quarters at Vanderbilt University in Nashville, Tenn., they began noticing that once well-established results on uterine gene expression and reproductive function in female mice procured from the same supplier, and of the same genetic strain, had become a lot less predictable. Three years later, they seem to have discovered the ghost in the cage: rodent chow.

In a study published last month in the Proceedings of the National Academy of Science (102:9960–5, 2005), Dey and his colleagues describe feeding female mice two types of Purina Mills LabDiet, a leading brand of rodent chow, containing markedly different amounts of isoflavones. This family of molecules is common in food plants such as soy and alfalfa and can simulate estrogen. Mice at Vanderbilt typically eat the high-isoflavone Purina mix, while those at Kansas were fed another variety.

Mice on the high-isoflavone diet had strikingly heavier wombs (more than 40% heavier by "wet weight" on a scale) than the animals that ate the other food. Their uterine cells also showed different patterns of gene expression, particularly among those involved in the response to estrogen. And, their blastocysts implanted faster. How that might affect offspring is unclear, Dey says, though it's not necessarily serious. On the other hand, he adds, "you don't want to play with this normal window."

Each of the effects Dey's group uncovered could influence studies designed to measure the impact of plant estrogens (phytoestrogens) on rodents, and by implication, on people. Some evidence suggests that phytoestrogens and synthetic estrogens, both of which can bind to estrogen receptors and thus mimic the human sex hormone, can cause reproductive complications in people, especially young children (see story pg. 24).

Christopher Gardner, a plant chemicals expert at Stanford University's Prevention Research Center, says phytoestrogens are typically weaker than human estrogens. Moreover, phytoestrogens can in some cases block the human hormone by preventing it from meeting its proper receptors. "So it is perfectly understandable that the presence or absence of these phytoestrogens could have an effect in rodent studies that are examining outcomes that are responsive to estrogens," he says.

While the health effects for mice of eating plant estrogens are not clear, the amount of the chemicals in lab chow "should probably be standardized" for the sake of consistent research, Gardner says. Indeed, the National Institute of Environmental Health Sciences is sponsoring a "brainstorming session" in September to examine the effects of diet on animals used in toxicology and endocrine experiments, says Jerrold Heindel, a scientific program administrator at the agency, based in Research Triangle Park, NC.

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