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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/11150

Title: Uncoupling Protein-2 Modulation of Reactive Oxygen Species and Cell Viability in the Pancreatic Beta Cell
Authors: Lee, Simon
Advisor: Wheeler, Michael
Department: Physiology
Keywords: uncoupling protein-2
beta cell
reactive oxygen species
oxidative stress
cell viability
Issue Date: 30-Jul-2008
Abstract: Uncoupling protein-2 (UCP2) may be linked to the attenuation of reactive oxygen species (ROS), but it is unclear whether this phenomenon pertains to the pancreatic beta cell. In this study, a UCP2-deficient mouse model was used to assess the importance of UCP2 to beta cell viability. We investigated the effect of UCP2 absence in response to a beta cell cytotoxic model of diabetes induction. In vivo treatment by the cytotoxic agent streptozotocin led to overall beta cell loss, but severity was not exacerbated by UCP2 deficiency. We also examined ROS production and cell viability in islet cells exposed to various stressors associated with oxidative stress. In vitro measurements of ROS and cell death in islet cells demonstrated that the response was not influenced by UCP2 expression. In contrast with UCP2 overexpression studies showing cytoprotection, this study reveals that beta cell survival is not compromised by the absence of UCP2.
URI: http://hdl.handle.net/1807/11150
Appears in Collections:Master
Department of Physiology - Master theses

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