{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T19:45:15Z","timestamp":1790711115531,"version":"4.1.0"},"reference-count":57,"publisher":"Walter de Gruyter GmbH","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    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.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Materials and methods:<\/jats:bold>\n                    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 \u03b2 and \u03b1 cell distribution.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    We showed that BPA exposed fetal pancreata had a greater number of islet-cell clusters (ICCs; &lt;300 \u03bcm\n                    <jats:sup>2<\/jats:sup>\n                    ; p&lt;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&lt;0.05).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    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 \u03b1:\u03b2-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.\n                  <\/jats:p>","DOI":"10.1515\/hmbci-2015-0052","type":"journal-article","created":{"date-parts":[[2016,1,20]],"date-time":"2016-01-20T14:49:17Z","timestamp":1453301357000},"page":"171-179","source":"Crossref","is-referenced-by-count":33,"title":["Prenatal exposure to bisphenol A alters mouse fetal pancreatic morphology and islet composition"],"prefix":"10.1515","volume":"25","author":[{"given":"Rebecca","family":"Whitehead","sequence":"first","affiliation":[{"name":"Children\u2019s Health Research Institute and Lawson Health Research Institute, Departments of Obstetrics and Gynaecology, and Physiology and Pharmacology, Western University, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haiyan","family":"Guan","sequence":"additional","affiliation":[{"name":"Children\u2019s Health Research Institute and Lawson Health Research Institute, Departments of Obstetrics and Gynaecology, and Physiology and Pharmacology, Western University, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edith","family":"Arany","sequence":"additional","affiliation":[{"name":"Lawson Health Research Institute; and Pathology and Laboratory Medicine, Western University, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Cernea","sequence":"additional","affiliation":[{"name":"Children\u2019s Health Research Institute and Lawson Health Research Institute, Departments of Obstetrics and Gynaecology, and Physiology and Pharmacology, Western University, London, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaiping","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"374","published-online":{"date-parts":[[2016,1,20]]},"reference":[{"key":"2025121207292648328_j_hmbci-2015-0052_ref_001_w2aab3b8c23b1b7b1ab2b1b1Aa","doi-asserted-by":"crossref","unstructured":"Rubin BS. Bisphenol A: an endocrine disruptor with widespread exposure and multiple effects. J Steroid Biochem Mol Biol 2011;127:27\u201334.10.1016\/j.jsbmb.2011.05.00221605673","DOI":"10.1016\/j.jsbmb.2011.05.002"},{"key":"2025121207292648328_j_hmbci-2015-0052_ref_002_w2aab3b8c23b1b7b1ab2b1b2Aa","doi-asserted-by":"crossref","unstructured":"Vandenberg LN, Chahoud I, Heindel JJ, Padmanabhan V, Paumgartten FJ, Schoenfelder G. Urinary, circulating, and tissue biomonitoring studies indicate widespread exposure to bisphenol A. Environ Health Perspect 2010;118:1055\u201370.10.1289\/ehp.0901716292008020338858","DOI":"10.1289\/ehp.0901716"},{"key":"2025121207292648328_j_hmbci-2015-0052_ref_003_w2aab3b8c23b1b7b1ab2b1b3Aa","unstructured":"CDC. Centers for Disease Control and Prevention: Fourth national report on human exposure to environmental chemicals. 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