Pancreatic islet β-cell and oxidative stress: The importance of glutathione peroxidase

R. Paul Robertson, Jamie S. Harmon

Research output: Contribution to journalShort surveypeer-review

128 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)3743-3748
Number of pages6
JournalFEBS Letters
Volume581
Issue number19
DOIs
StatePublished - Jul 31 2007

Bibliographical note

Funding Information:
The authors are supported by NIH Grant R01-38325.

Keywords

  • Gluathione peroxidase
  • Pancreatic β-cell
  • Type 2 diabetes

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