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- W2162228308 abstract "It is widely proposed that reactive oxygen species (ROS) contribute to beta-cell death in type 1 diabetes. We tested this in nonobese diabetic (NOD) mice using beta-cell-specific overexpression of three antioxidant proteins: metallothionein (MT), catalase (Cat), or manganese superoxide dismutase (MnSOD). Unexpectedly, the cytoplasmic antioxidants, MT and catalase, greatly accelerated diabetes after cyclophosphamide and accelerated spontaneous diabetes in male NOD mice. This occurred despite the fact that they reduced cytokine-induced ROS production and MT reduced streptozotocin diabetes in NOD mice. Accelerated diabetes onset coincided with increased beta-cell death but not with increased immune attack. Islets from MTNOD mice were more sensitive to cytokine injury. In vivo and in vitro studies indicated reduced activation of the Akt/pancreatic duodenal homeobox-1 survival pathway in MTNOD and CatNOD islets. Our study indicates that cytoplasmic ROS may have an important role for protecting the beta-cell from autoimmune destruction." @default.
- W2162228308 created "2016-06-24" @default.
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- W2162228308 date "2006-06-01" @default.
- W2162228308 modified "2023-10-01" @default.
- W2162228308 title "Metallothionein and Catalase Sensitize to Diabetes in Nonobese Diabetic Mice" @default.
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- W2162228308 doi "https://doi.org/10.2337/db05-1357" @default.
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