In an article published on February 7, 2017 in the peer-reviewed journal Endocrinology, Harry MacKay and colleagues from the Department of Neurosciences, Carleton University, Ottawa, Canada, show that exposure of pregnant mice to low levels of bisphenol A (BPA, CAS 80-05-7) can disrupt the regulation of feeding behavior in their offspring.
Scientists exposed pregnant mice to 20 µg/kg BPA in the diet, and at different time points studied the neurogenesis in fetuses and regulation of feeding behavior in young pups. BPA was found to permanently alter the neurobiology in the exposed mice, making them prone to obesity as adults. In particular, young pups were found to be less responsive to leptin, which is a hormone responsible for controlling appetite. Normally, leptin’s communication with the hypothalamus results in the suppression of appetite at times when the body does not need energy. In BPA-exposed mice, this feedback circuitry was less efficient. These mice also exhibited reduced brain activity in hypothalamus regions involved in regulating energy expenditure.
Thus, this study sheds light on the molecular mechanisms involved in the metabolic disruption caused by BPA and potentially other similarly acting endocrine disrupting chemicals (EDCs). It further adds to the growing body of evidence demonstrating that exposure to EDCs, like BPA, during pregnancy can raise newborns’ obesity risk in later life.
Endocrine Society (February 7, 2017). “Prenatal bisphenol A exposure weakens body’s fullness cues.”
Mary Kekatos (February 7, 2017). “Why pregnant women should never drink from plastic bottles: They contain hormone-disrupting toxins that could make your baby obese.” Daily Mail
Will Chu (February 8, 2017). “Prenatal BPA exposure may lead to weight issues later in life: Mice study.” Beverage Daily
Cici Zhang (February 16, 2017). “Our mothers’ exposure to BPA might lead us to binge as adults.” Popular Science
MacKay, H., et al. (2017). “Perinatal exposure to low-dose bisphenol-A (BPA) disrupts the structural and functional development of the hypothalamic feeding circuitry.” Endocrinology (published February 7, 2017).