Journal
REPRODUCTIVE TOXICOLOGY
Volume 23, Issue 3, Pages 290-296Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.reprotox.2006.12.010
Keywords
fetal exposure; neonatal exposure; overweight; obese; adipocytes; obesogens; diabetes; cardiovascular disease; epigenetic; DOHaD
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Funding
- Intramural NIH HHS [Z01 ES070060-32] Funding Source: Medline
- NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING [Z01EB000018] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [Z01ES070060] Funding Source: NIH RePORTER
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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. Published by Elsevier Inc.
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