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Developmental exposure to bisphenol A leads to cardiometabolic dysfunction in adult mouse offspring

Published online by Cambridge University Press:  23 March 2012

F. R. Cagampang*
Affiliation:
Human Development and Health, Institute of Developmental Sciences, University of Southampton Faculty of Medicine, Southampton General Hospital, Southampton, UK
C. Torrens
Affiliation:
Human Development and Health, Institute of Developmental Sciences, University of Southampton Faculty of Medicine, Southampton General Hospital, Southampton, UK
F. W. Anthony
Affiliation:
Human Development and Health, Institute of Developmental Sciences, University of Southampton Faculty of Medicine, Southampton General Hospital, Southampton, UK
M. A. Hanson
Affiliation:
Human Development and Health, Institute of Developmental Sciences, University of Southampton Faculty of Medicine, Southampton General Hospital, Southampton, UK
*
*Address for correspondence: F. R. Cagampang, Human Development and Health, Institute of Developmental Sciences, University of Southampton Faculty of Medicine, Southampton General Hospital, Mailpoint 887, Southampton SO16 6YD, UK. (Email [email protected])

Abstract

Bisphenol A (BPA) is a chemical compound that has adverse health outcomes in adults when exposed during the perinatal period. However, its effect on cardiovascular function remains to be elucidated. In this study, we examined the effects of daily administration of BPA to pregnant mice from gestational days 11 to 19 on cardiometabolic outcomes in the adult offspring. Prenatal BPA exposure resulted in altered growth trajectory and organ size, increase adiposity and impaired glucose homeostasis in male and female offspring. In addition, these BPA offspring exhibited raised systolic blood pressure, and in the males this was accompanied by impaired vascular tone. The aortas in females, but not in males, from the BPA group also showed reduced estrogen receptor gene expression. These results indicate that prenatal exposure to BPA increased susceptibility of the offspring to developing cardiovascular and metabolic dysfunction later in life.

Type
Brief Report
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2012

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