Pancreatic β-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 H2O2 and lipid peroxides, is uniquely positioned to protect tissues from ROS. The level of this antioxidant in β 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 β-cell.
Bibliographical noteFunding Information:
The authors are supported by NIH Grant R01-38325.
- Gluathione peroxidase
- Pancreatic β-cell
- Type 2 diabetes