WEDNESDAY, Feb. 8, 2017 (HealthDay News) — Prenatal exposure to bisphenol A (BPA) may raise a child’s risk of obesity by altering hypothalamic circuits that regulate feeding behavior and energy balance, according to an experimental study published online Feb. 7 in Endocrinology.
Harry MacKay, Ph.D., from the Baylor College of Medicine in Houston, and colleagues examined leptin sensitivity and hypothalamic structure in young BPA-exposed animals before onset of a body weight or metabolic phenotype. They exposed pregnant and lactating CD-1 mice to BPA or diethylstilbestrol (DES) at low, environmentally relevant doses.
The researchers found that young adult offspring were resistant to leptin-induced suppression of food intake, body weight loss, and hypothalamic pro-opiomelanocortin (POMC) upregulation. Reduced density of POMC projections into the paraventricular hypothalamus (PVN) was seen for male and female BPA-exposed mice. BPA- and DES-exposed pups had delayed and blunted postnatal leptin surges, respectively; in female BPA-exposed animals given daily injections of supplemental leptin, POMC projections into the PVN were rescued.
“Our findings suggest that BPA, a putative obesogen, may exert its effects through developmental programming of the hypothalamic melanocortin circuitry, permanently altering the neurobiology of metabolic homeostasis,” the authors write.
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