Reactive oxygen species mediate insulin signal transduction in mouse hypothalamus

被引:10
|
作者
Onoue, Takeshi [1 ]
Goto, Motomitsu [1 ]
Tominaga, Takashi [1 ]
Sugiyama, Mariko [1 ]
Tsunekawa, Taku [1 ]
Hagiwara, Daisuke [1 ]
Banno, Ryoichi [1 ]
Suga, Hidetaka [1 ]
Sugimura, Yoshihisa [1 ]
Arima, Hiroshi [1 ]
机构
[1] Nagoya Univ, Dept Endocrinol & Diabet, Grad Sch Med, Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668550, Japan
关键词
Reactive oxygen species; Hypothalamus; Insulin signal; NADPH oxidase; PROTEIN-TYROSINE PHOSPHATASES; VASCULAR SMOOTH-MUSCLE; II DIABETIC-PATIENTS; OXIDATIVE STRESS; FOOD-INTAKE; ORGANOTYPIC CULTURES; REVERSIBLE OXIDATION; PLASMA-MEMBRANE; BODY-WEIGHT; OXIDASE;
D O I
10.1016/j.neulet.2016.03.011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 beta (p-IR beta) and phospho-Akt (p-Akt) levels. Insulin-induced increases in p-IR beta and p-Akt levels were attenuated by ROS scavenger or NADPH oxidase inhibitor. Our data suggest that insulin-induced phosphorylation of IR beta and Akt is mediated via ROS which are predominantly produced by NADPH oxidase in mouse hypothalamus. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:1 / 7
页数:7
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