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Updated: Jul 16, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
07:08

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants

Published on: March 6, 2018

Developmental exposure to endocrine disruptors and the obesity epidemic

Retha R Newbold1, Elizabeth Padilla-Banks, Ryan J Snyder

  • 1Developmental Endocrinology and Endocrine Disruptor Section, Laboratory of Molecular Toxicology, Mail-Drop E4-02, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC 27709, United States. newbold1@niehs.nih.gov

Reproductive Toxicology (Elmsford, N.Y.)
|February 27, 2007
PubMed

Insights

Developmental exposure to endocrine-disrupting chemicals can program individuals for obesity later in life. This review highlights the link between environmental hormone mimics and obesity, using a diethylstilbestrol (DES) animal model.

Area of Science:

  • Endocrinology
  • Environmental Health
  • Developmental Biology

Background:

  • Xenobiotics and dietary compounds can mimic hormones, disrupting endocrine signaling during critical developmental periods.
  • Developmental exposure to endocrine-disrupting chemicals (EDCs) is linked to various health issues, including obesity.
  • Obesity poses a significant global health challenge due to associated diseases like diabetes and cardiovascular disease.

Purpose of the Study:

  • To review the scientific literature associating environmental EDC exposure with obesity development.
  • To describe an animal model for studying the mechanisms of EDC-induced obesity programming.
  • To explore the concept of the developmental origins of adult disease in relation to EDCs.

Main Methods:

  • Literature review on environmental endocrine disruptors and obesity.
  • Description of an animal model using developmental exposure to diethylstilbestrol (DES).
  • Investigation of mechanisms underlying EDC-induced metabolic programming.

Main Results:

  • Evidence suggests a link between developmental exposure to EDCs and increased risk of obesity.
  • The diethylstilbestrol (DES) animal model demonstrates how perinatal exposure can program for obesity.
  • EDCs can induce abnormal programming, contributing to the developmental origins of adult disease.

Conclusions:

  • Developmental exposure to endocrine-disrupting chemicals is implicated in the etiology of obesity.
  • Animal models like the DES model are crucial for understanding EDC-induced metabolic programming.
  • EDCs represent potential targets for intervention in preventing obesity and related diseases.

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