| First Author | Wang X | Year | 2018 |
| Journal | Biochem Biophys Res Commun | Volume | 498 |
| Issue | 4 | Pages | 975-980 |
| PubMed ID | 29550486 | Mgi Jnum | J:271658 |
| Mgi Id | MGI:6280043 | Doi | 10.1016/j.bbrc.2018.03.092 |
| Citation | Wang X, et al. (2018) Deficiency of voltage-gated proton channel Hv1 attenuates streptozotocin-induced beta-cell damage. Biochem Biophys Res Commun 498(4):975-980 |
| abstractText | Reactive oxygen species (ROS) impairs pancreatic beta-cells and plays an important role in development of diabetes. Streptozotocin (STZ) can lead to beta-cell dysfunction via inducing ROS production. The voltage-gated proton channel Hv1 contributes a majority of the charge compensation required for ROS production. Here, we investigated the effects of Hv1 on STZ-induced beta-cell damage. We found that deficiency of Hv1 obviously inhibits STZ-induced glucose intolerance in mice, and prevents the decrease in beta-cell mass and pancreatic insulin content from STZ-treatment. Further studies showed that loss of Hv1 significantly attenuates STZ-induced beta-cell damage and ROS production in pancreatic beta-cells. Our results suggest that Hv1 might contribute to development of diabetes through producing ROS. |
