title: Reactive oxygen species mediate insulin signal transduction in mouse hypothalamus.
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.
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Onoue
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan. Electronic address: goto@med.nagoya-u.ac.jp.
authors.forename: Motomitsu
authors.initials: M
authors.lastname: Goto
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Tominaga
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Mariko
authors.initials: M
authors.lastname: Sugiyama
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Taku
authors.initials: T
authors.lastname: Tsunekawa
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Hagiwara
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Ryoichi
authors.initials: R
authors.lastname: Banno
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Suga
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Sugimura
authors.affiliation: Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Arima
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D042963:Electron Transport Complex II / Q000037:antagonists & inhibitors; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007031:Hypothalamus / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology / Q000502:physiology*; D042541:Intracellular Space / Q000378:metabolism; D008810:Mice, Inbred C57BL; D009249:NADP / Q000037:antagonists & inhibitors; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D011972:Receptor, Insulin / Q000378:metabolism; D015398:Signal Transduction; D046509:Tissue Culture Techniques
chemical_list: D007328:Insulin; D017382:Reactive Oxygen Species; D009249:NADP; D006861:Hydrogen Peroxide; D042963:Electron Transport Complex II; D011972:Receptor, Insulin; D051057:Proto-Oncogene Proteins c-akt
keywords: Hypothalamus; Insulin signal; NADPH oxidase; Reactive oxygen species