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, 23 (3), 290-6

Developmental Exposure to Endocrine Disruptors and the Obesity Epidemic


Developmental Exposure to Endocrine Disruptors and the Obesity Epidemic

Retha R Newbold et al. Reprod Toxicol.


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.


Figure 1
Figure 1. Representative Photograph of Control and DES-treated Mice
Photograph of 4 month old mice showing the difference in body weight of a control mouse (left panel) and a neonatally DES-treated mouse (right panel).
Figure 2
Figure 2. Body Weights of Mice Following Neonatal DES Exposure
Body weights were measured at various ages. Mice treated with DES had significantly lower body weights during the time of treatment as compared to controls. By 1 month of age the DES treated mice caught up to the controls and by 2 months of age, DES treated mice had surpassed the controls with a significantly higher body weight (n= 16 mice per group); numbers plotted are the mean ± s.e.m.; * denotes significance using ANOVA fallowed by Dunnett’s test (p<0.05).
Figure 3
Figure 3. Images of Control and DES-treated Mice as Generated by Piximus Densitometry
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.
Figure 4
Figure 4. Ambulatory Activity of Adult Mice Following Neonatal DES Exposure
Graph represents total ambulatory activity including movement across the same plane and rearing movement in control and DES treated mice at 2 months of age (n= 8 mice per group). Data is plotted in 5 min intervals over a 20 minute session. The DES mice had less movement as compared to controls at the start of the session although this difference is not significant. DES treated mice exhibited similar activity as controls by the end of the session.
Figure 5
Figure 5. Feed Consumption of Adult Mice Following Neonatal DES Exposure
Bars represent the mean total amount of feed consumed in a week for controls and DES treated mice (n=8 per group). Although DES treated mice consumed an average of ~ 3 g more than controls, this increase was not significant.
Figure 6
Figure 6. Glucose Test of Adult Mice Following Neonatal DES Exposure
Glucose tolerance was determined at 2 and 6 months of age by measuring morning glucose (mg/dL) after 18 hour fasting period (n=8 per group). Mice were challenged with a glucose solution (2 g/kg) and then glucose levels were measured at 20 min intervals for 180 min. Glucose measurements were plotted individually. Panel A: 2 month control; Panel B: 2 month DES treated; Panel C: 6 month control; Panel D: 6 month DES treated.

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