Developmental Exposure to Endocrine Disruptors and the Obesity Epidemic

Environmental chemicals are contributing to overweight and obesity

image of Control-and-DES-treated-Mice
Image captured with PIXImus™ mouse densitometry at 6 months of age. Images are representative of control (left) and DES (right) treated mice. Note that DES mice are significantly larger. Image by NCBI, 2007.

2007 Study Abstract

Xenobiotic and dietary compounds with hormone-like activity can disrupt endocrine signaling pathways that play important roles during perinatal differentiation and result in alterations that are not apparent until later in life. Evidence implicates developmental exposure to environmental hormone-mimics with a growing list of health problems. Obesity is currently receiving needed attention since it has potential to overwhelm health systems worldwide with associated illnesses such as diabetes and cardiovascular disease. Here, we review the literature that proposes an association of exposure to environmental endocrine disrupting chemicals with the development of obesity. We describe an animal model of developmental exposure to diethylstilbestrol (DES), a potent perinatal endocrine disruptor with estrogenic activity, to study mechanisms involved in programming an organism for obesity. This experimental animal model provides an example of the growing scientific field termed “the developmental origins of adult disease” and suggests new targets of abnormal programming by endocrine disrupting chemicals.

Summary and Conclusions

Taken together, our data supports the idea that brief exposure early in life to environmental endocrine disrupting chemicals, especially those with estrogenic activity like DES, increases body weight as the mice age. These data also suggest that these chemicals may contribute to overweight and obesity and other obesity-associated diseases such as type 2 diabetes and cardiovascular disease. Whether our results can be extrapolated to humans as the reproductive abnormalities from the DES mouse model did, remain to be determined but it provides a fruitful area of further research. In addition, the use of this animal model to study “obesogens” and mechanisms involved in altered weight homeostasis (direct and/or endocrine feedback loops, i.e., ghrelin, leptin, etc.) by environmental endocrine disrupting chemicals is an important basic research area that may be addressed by using this model. No longer can we assume than overweight and obesity are simply personal choices, but we have to consider that complex events including environmental chemicals are contributing to this mounting human health problem.

  • Developmental Exposure to Endocrine Disruptors and the Obesity Epidemic, Retha R. Newbold, Elizabeth Padilla-Banks, Ryan J. Snyder,1 Terry M. Phillips and Wendy N. Jefferson, Reprod Toxicol doi: 10.1016/j.reprotox.2006.12.010, NCBI PMCID: PMC1931509, 2007 Jan 17.
  • All images, PMC 17321108, 2007.
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