| Title: | Paternal bisphenol A exposure in mice impairs glucose tolerance in female offspring |
| Author(s): | Rashid CS; Bansal A; Mesaros C; Bartolomei MS; Simmons RA; |
| Address: | "Center for Research in Reproduction and Women's Health, University of Pennsylvania, Philadelphia, PA, 19104, USA; Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, PA, 19104, USA. Center for Research in Reproduction and Women's Health, University of Pennsylvania, Philadelphia, PA, 19104, USA; Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, PA, 19104, USA; ANU Medical School, John Curtin School of Medical Research, College of Health and Medicine, Australian National University, Canberra, ACT, 2601, Australia. Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, PA, 19104, USA; Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, Philadelphia, PA, 19104, USA. Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, PA, 19104, USA; Epigenetics Institute, Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA, 19104, USA. Center for Research in Reproduction and Women's Health, University of Pennsylvania, Philadelphia, PA, 19104, USA; Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, PA, 19104, USA; Division of Neonatology, Children's Hospital of Philadelphia, Philadelphia, PA, 19104, USA. Electronic address: rsimmons@pennmedicine.upenn.edu" |
| DOI: | 10.1016/j.fct.2020.111716 |
| ISSN/ISBN: | 1873-6351 (Electronic) 0278-6915 (Print) 0278-6915 (Linking) |
| Abstract: | "Humans are ubiquitously exposed bisphenol A (BPA), and epidemiological studies show a positive association between BPA exposure and diabetes risk, but the impact of parental exposure on offspring diabetes risk in humans is unknown. Our previous studies in mice show disruption of metabolic health upon maternal BPA exposure. The current study was undertaken to determine whether exposure in fathers causes adverse metabolic consequences in offspring. Male C57BL/6 J mice were exposed to BPA in the diet beginning at 5 weeks of age resulting in the following dietary exposure groups: Control (0 mug/kg/day), Lower BPA (10 mug/kg/day) and Upper BPA (10 mg/kg/day). After 12 weeks of dietary exposure, males were mated to control females. Mothers and offspring were maintained on the control diet. Post-pubertal paternal BPA exposure did not affect offspring body weight, body composition or glucose tolerance. However, when fathers were exposed to BPA during gestation and lactation, their female offspring displayed impaired glucose tolerance in the absence of compromised in vivo insulin sensitivity or reduced ex vivo glucose-stimulated insulin secretion. Male offspring exhibited normal glucose tolerance. Taken together, these studies show there is an early window of susceptibility in which paternal BPA exposure can cause sex-specific impairments in glucose homeostasis" |
| Keywords: | "Animals Benzhydryl Compounds/*adverse effects Endocrine Disruptors/*adverse effects Female Glucose/metabolism Glucose Intolerance/*metabolism Humans Insulin/metabolism Insulin Secretion/drug effects Male Mice Mice, Inbred C57BL Paternal Exposure/*adverse;" |
| Notes: | "MedlineRashid, Cetewayo S Bansal, Amita Mesaros, Clementina Bartolomei, Marisa S Simmons, Rebecca A eng T32 HD060556/HD/NICHD NIH HHS/ R01 ES028206/ES/NIEHS NIH HHS/ P30 ES013508/ES/NIEHS NIH HHS/ R01 ES023284/ES/NIEHS NIH HHS/ P30 DK019525/DK/NIDDK NIH HHS/ England 2020/09/06 Food Chem Toxicol. 2020 Nov; 145:111716. doi: 10.1016/j.fct.2020.111716. Epub 2020 Sep 3" |
