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

Biochem Biophys Res Commun. 2018 Apr 15;498(4):975-980. doi: 10.1016/j.bbrc.2018.03.092. Epub 2018 Mar 17.

Abstract

Reactive oxygen species (ROS) impairs pancreatic β-cells and plays an important role in development of diabetes. Streptozotocin (STZ) can lead to β-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 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 ROS production in pancreatic β-cells. Our results suggest that Hv1 might contribute to development of diabetes through producing ROS.

Keywords: Damage; Diabetes; Hv1; Pancreatic β-cells; ROS; Voltage-gated proton channel.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Diabetes Mellitus / etiology*
  • Glucose Intolerance / chemically induced
  • Glucose Intolerance / etiology
  • Insulin / metabolism
  • Insulin-Secreting Cells / pathology*
  • Ion Channels / deficiency*
  • Ion Channels / physiology
  • Mice
  • Reactive Oxygen Species / metabolism*
  • Streptozocin

Substances

  • Hv1 proton channel, mouse
  • Insulin
  • Ion Channels
  • Reactive Oxygen Species
  • Streptozocin