2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and early human pancreatic development
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Environmental factors such as pollutants are associated with diabetes incidence. Of particular interest is exposure to persistent organic pollutants (POPs) during critical stages of fetal development. TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) is a potent ligand of the aryl hydrocarbon receptor, which leads to induction of cytochrome P450 (CYP) 1A1 enzymes. We hypothesize that POPs such as TCDD accumulate in the pancreas, thereby eliciting stress on developing beta cells through induction of CYP1A1. Here, I exposed rodent alpha and beta cell lines to TCDD in vitro, but did not observe induction of Cyp1a1 gene expression or enzyme activity, meaning that this pathway is not activated in immortalized pancreatic endocrine cell lines. I also differentiated human embryonic stem cells toward pancreatic cell fate in vitro to study how TCDD exposure impacts human beta cell development. I concluded that TCDD might impede normal development of beta cells, potentially through induction of CYP1A1 and other embryonic lineages.
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Copyright © 2019 the author(s). Theses may be used for non-commercial research, educational, or related academic purposes only. Such uses include personal study, research, scholarship, and teaching. Theses may only be shared by linking to Carleton University Institutional Repository and no part may be used without proper attribution to the author. No part may be used for commercial purposes directly or indirectly via a for-profit platform; no adaptation or derivative works are permitted without consent from the copyright owner.
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- 2019
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macfarlane-2378tetrachlorodibenzopdioxintcddandearly.pdf | 2023-05-05 | Public | Download |