Deletion of Thioredoxin Reductase Disrupts Redox Homeostasis and Impairs β-Cell Function.

ABSTRACT: Reactive oxygen species (ROS) have been implicated as mediators of pancreatic β-cell damage. While β-cells are thought to be vulnerable to oxidative damage, we have shown, using inhibitors and acute depletion, that thioredoxin reductase, thioredoxin, and peroxiredoxins are the primary mediators of antioxidant defense in β-cells. However, the role of this antioxidant cycle in maintaining redox homeostasis and β-cell survival in vivo remains unclear. Here, we generated mice with a β-cell specific knockout of thioredoxin reductase 1 (Txnrd1^fl/fl; Ins1^Cre/+ , βKO). Despite blunted glucose-stimulated insulin secretion, knockout mice maintain normal whole-body glucose homeostasis. Unlike pancreatic islets with acute Txnrd1 inhibition, βKO islets do not

SUBMITTER: Stancill JS 

PROVIDER: S-EPMC9301323 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature