Organizational Effects of Early-Life Exposure to Low-Dose Bisphenol-A (BPA) and Diethylstilbestrol (DES) on Hypothalamic Circuits Regulating Energy Balance

H. MacKay, Z. Patterson, R. Khazall, A. Abizaid

Location: Hall F-J
Presentation Time: Sunday, Oct 14, 2012, 2:00 PM – 3:00 PM
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Bisphenol-A (BPA) is a ubiquitous chemical plasticizer that is used in the production of polycarbonate plastics and epoxy resins. Because in shares structural similarity with endogenous estrogens such as 17β-estradiol, as well as potent xenoestrogens such as diethylstilbesterol (DES), it has been suggested that BPA acts as an endocrine disrupter. Since BPA is readily released from plastic food and drink containers, the effect of low-dose oral exposure to human populations is of great concern. The EPA reference dose for BPA is 50μg/kg/day. BPA is capable of passing through the placental barrier, and is found in the milk of dams exposed to oral BPA. A growing body of evidence suggests that perinatal exposure to ecologically relevant levels of BPA predisposes offspring to increased body weight, food intake, and adiposity later in life.

Here we use a model of perinatal exposure to the xenoestrogens BPA and DES at ecologically relevant 60 doses to examine the possibility that they alter susceptibility to diet induced obesity and metabolic pathologies in adulthood. To better understand the possible neurobiological underpinnings of BPA induced 50 obesity, we examine the population of anorexigenic POMC expressing cells within the arcuate nucleus of 40 the hypothalamus (ARC) as well as the extent to which they innervate key downstream regions. Further, 30 we examine how BPA and DES exposure alter the transcriptional response to high-fat diet exposure in the 20 ARC. Together, the changes observed here may contribute to the phenomenon of BPA’s obesogenic effects.