title: Prenatal exposure to bisphenol A alters mouse fetal pancreatic morphology and islet composition.
abstract: BACKGROUND
  Exposure to bisphenol A (BPA), an endocrine disrupting chemical, during gestation is associated with a variety of metabolic dysfunctions in adulthood, including hyperinsulinemia, glucose intolerance and insulin resistance. These modifications in glucose homeostasis largely stem from alterations in pancreatic function. However, the effects of BPA on the fetal pancreas have never been explored. The present study addressed this important question by examining the effects of prenatal BPA exposure on the mouse fetal pancreatic development.
  
  
  METHODS
  Pregnant mice were fed a BPA diet (25 mg BPA/kg diet) from embryonic day 7.5 (E7.5) to E18.5. At E18.5, fetal pancreata were collected and analyzed for morphological changes in the endocrine pancreas such as islet size, number and β and α cell distribution.
  
  
  RESULTS
  We showed that BPA exposed fetal pancreata had a greater number of islet-cell clusters (ICCs; <300 μm(2); p<0.05) compared with controls. Furthermore, immunohistochemical analysis revealed that prenatal BPA exposure increased both glucagon expression in islets and the numbers of glucagon-expressing islet-cell clusters (p<0.05).
  
  
  CONCLUSIONS
  Considering that ICCs represent the initial stages of islet development in the fetal pancreas, our findings suggest that BPA promotes islet differentiation or delays the conversion of ICCs into mature islets. Moreover, the increase in glucagon expression suggests a potential alteration in the α:β-cell ratio in islets, which may have significant implications for the fetal pancreas both structurally and functionally. This study provides novel insight into the effects of BPA exposure on the fetal pancreata, indicating alterations in glucagon expression in islets and ICCs.
authors.forename: Rebecca
authors.initials: R
authors.lastname: Whitehead
authors.forename: Haiyan
authors.initials: H
authors.lastname: Guan
authors.forename: Edith
authors.initials: E
authors.lastname: Arany
authors.forename: Maria
authors.initials: M
authors.lastname: Cernea
authors.forename: Kaiping
authors.initials: K
authors.lastname: Yang
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds / Q000009:adverse effects*; D052244:Endocrine Disruptors / Q000009:adverse effects*; D005260:Female; D050416:Glucagon-Secreting Cells / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D050417:Insulin-Secreting Cells / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D007515:Islets of Langerhans / Q000187:drug effects* / Q000196:embryology* / Q000473:pathology / Q000648:ultrastructure; D051379:Mice; D008810:Mice, Inbred C57BL; D010636:Phenols / Q000009:adverse effects*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced* / Q000473:pathology; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D052244:Endocrine Disruptors; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds