title: Pancreatic islet beta-cell and oxidative stress: the importance of glutathione peroxidase.
abstract: Pancreatic beta-cell function continuously deteriorates in type 2 diabetes despite optimal treatment regimens, which has been attributed to hyperglycemia itself via formation of excess levels of reactive oxygen species (ROS). Glutathione peroxidase GPx), by virtue of its ability to catabolize both H(2)O(2) and lipid peroxides, is uniquely positioned to protect tissues from ROS. The level of this antioxidant in beta cells is extremely low and overexpression of GPx in islets provides enhanced protection against oxidative stress. This suggests that GPx mimetics may represent a valuable ancillary treatment that could add a novel layer of protection for the beta-cell.
authors: Pacific Northwest Research Institute, University of Washington, 720 Broadway, Seattle, WA 98122, United States. rpr@pnri.org
authors: R Paul
authors: RP
authors: Robertson
authors: Jamie S
authors: JS
authors: Harmon
mesh_terms: D000818:Animals; D019610:Cytoprotection; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology / Q000517:prevention & control*; D005947:Glucose / Q000378:metabolism / Q000633:toxicity; D005979:Glutathione Peroxidase / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000201:enzymology*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D005979:Glutathione Peroxidase; D005947:Glucose