Reactive oxygen species mediate insulin signal transduction in mouse hypothalamus

Neurosci Lett. 2016 Apr 21:619:1-7. doi: 10.1016/j.neulet.2016.03.011. Epub 2016 Mar 9.

Abstract

In the hypothalamus, several reports have implied that ROS mediate physiological effects of insulin. In this study, we investigated the mechanisms of insulin-induced ROS production and the effect of ROS on insulin signal transduction in mouse hypothalamic organotypic cultures. Insulin increased intracellular ROS, which were suppressed by NADPH oxidase inhibitor. H2O2 increased phospho-insulin receptor β (p-IRβ) and phospho-Akt (p-Akt) levels. Insulin-induced increases in p-IRβ and p-Akt levels were attenuated by ROS scavenger or NADPH oxidase inhibitor. Our data suggest that insulin-induced phosphorylation of IRβ and Akt is mediated via ROS which are predominantly produced by NADPH oxidase in mouse hypothalamus.

Keywords: Hypothalamus; Insulin signal; NADPH oxidase; Reactive oxygen species.

MeSH terms

  • Animals
  • Cells, Cultured
  • Electron Transport Complex II / antagonists & inhibitors
  • Hydrogen Peroxide / pharmacology
  • Hypothalamus / metabolism*
  • Insulin / pharmacology
  • Insulin / physiology*
  • Intracellular Space / metabolism
  • Mice, Inbred C57BL
  • NADP / antagonists & inhibitors
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt / metabolism
  • Reactive Oxygen Species / metabolism*
  • Receptor, Insulin / metabolism
  • Signal Transduction
  • Tissue Culture Techniques

Substances

  • Insulin
  • Reactive Oxygen Species
  • NADP
  • Hydrogen Peroxide
  • Electron Transport Complex II
  • Receptor, Insulin
  • Proto-Oncogene Proteins c-akt