Deficiency of voltage-gated proton channel Hv1 attenuates streptozotocin-induced β-cell damage.

Reactive oxygen species impairs pancreatic β-cells and plays an important role in development of diabetes. Streptozotocin (STZ) can lead to β-cell dysfunction via inducing production. The voltage-gated proton channel Hv1 contributes a majority of the charge compensation required for duanyu1670 production. Here, we investigated the effects of Hv1 on STZ-induced β-cell damage. We found that deficiency of Hv1 obviously inhibits STZ-induced glucose intolerance in mice, and prevents the decrease in β-cell mass and pancreatic insulin content from STZ-treatment. Further studies showed that loss of Hv1 significantly attenuates STZ-induced β-cell damage and duanyu1670 production in pancreatic β-cells. Our results suggest that Hv1 might contribute to development of diabetes through producing

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