Document Detail
Uncoupling Protein-2 Modulation of Reactive Oxygen Species and Cell Viability in the Pancreatic Beta Cell
Abstract/OtherAbstract :
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., MAST
Authors :
Lee, Simon
Contributors :
Wheeler, Michael, Physiology
Publication Detail :
Publisher :  -     Type :  Thesis     Format :  849095 bytes, application/pdf    
Date Detail :
2008-06, 2008-07-30, NO_RESTRICTION, 2008-07-30, 2008-07-30
Subject :
uncoupling protein-2, diabetes, beta cell, reactive oxygen species, oxidative stress, cell viability, 0719
Coverage :
-
Relation :
-
Source :
-
Copyright Information :
-
Other Details :
Languages :  en_ca    
Export Citation :
APA/MLA Format     Download EndNote     Download BibTex

Previous Document:  The Mechanisms Underlying Free Fatty Acid-induced Hepatic Insulin Resistance
Next Document:  Characterization of APLF in the Nonhomologous End-joining Pathway