Perinatal bisphenol A exposure promotes hyperactivity, lean body composition, and hormonal responses across the murine life course

*Department of Environmental Health Sciences, †Center for Human Growth and Development, and ‡Department of Biostatistics, University of Michigan, Ann Arbor, Michigan, USA.
The FASEB Journal (Impact Factor: 5.48). 01/2013; 27(January):1-9. DOI: 10.1096/fj.12-223545

ABSTRACT The development of adult-onset diseases is influenced by perinatal exposure to altered environ-mental conditions. One such exposure, bisphenol A (BPA), has been associated with obesity and diabetes, and consequently labeled an obesogen. Using an iso-genic murine model, we examined the effects of peri-natal exposure through maternal diet to 50 ng (n20), 50 g (n21), or 50 mg (n18) BPA/kg diet, as well as controls (n20) on offspring energy expenditure, spontaneous activity, and body composition at 3, 6, and 9 mo of age, and hormone levels at 9 and 10 mo of age. Overall, exposed females and males exhibited in-creased energy expenditure (P<0.001 and 0.001, re-spectively) throughout the life course. In females, horizontal and vertical activity increased (P0.07 and 0.06, respectively) throughout the life course. Gener-ally, body composition measures were not different throughout the life course in exposed females or males (all P>0.44), although body fat and weight decreased in exposed females at particular ages (all P<0.08). Milli-gram-exposed females had improved glucose, insulin, adiponectin, and leptin profiles (all P<0.10). Thus, life-course analysis illustrates that BPA is associated with hyperactive and lean phenotypes. Variability across studies may be attributable to differential exposure duration and timing, dietary fat and phytoestrogen content, or lack of sophisticated phenotyping across the life course.—Anderson, O. bisphenol A exposure promotes hyperactivity, lean body composition, and hormonal responses across the murine life course. FASEB J. 27, 000 – 000 (2013). Key Words: developmental origins of health and disease energy expenditure glucose insulin metabolic homeostasis

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