The molecular mechanism of insul in resistance induced by overnutrition

胰岛素抗营养过剩的分子机制

• 批准号: 20890279
• 负责人: TSUTSUMI Rie
• 金额: $ 2.11万
• 依托单位: Mukogawa Women's University Junior College Division
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (Start-up)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20890279/
• 关键词: mTOR; 栄養; Rheb; 肝臓; インスリン抵抗性; たんぱく質合成; トランスロケーション; Vps34; アミノ酸

Liver has the critical role in amino acids uptake and protein synthesis from amino acid as well as some insulin actions. p70 rebosomal protein kinase 1 (S6K1) is the key regulator of translation and its over activation induces insulin resistance by negative feedback to IRS1. However, its regulation of S6K1 has not be clear yet. In this study, we hypothesized that Vps34 and Rheb play a role of mTOR-S6K1 signaling as a nutrient sensor and GTP-bound Rheb induces endosome trafficking to activate mTOR. There results indicate Vps34 and Rheb, which is activated by nutritional uptake, regulate S6K1 and translocation of Rheb is critical for activation of mTOR-S6K1 signaling.

肝脏在氨基酸摄取和氨基酸蛋白质合成以及一些胰岛素作用中起着关键作用。 p70 核糖体蛋白激酶 1 (S6K1) 是翻译的关键调节因子，其过度激活通过对 IRS1 的负反馈诱导胰岛素抵抗。但其对S6K1的监管尚未明确。在这项研究中，我们假设 Vps34 和 Rheb 作为营养传感器在 mTOR-S6K1 信号传导中发挥作用，并且 GTP 结合的 Rheb 诱导内体运输以激活 mTOR。结果表明，Vps34 和 Rheb（通过营养摄取激活）调节 S6K1，并且 Rheb 的易位对于 mTOR-S6K1 信号传导的激活至关重要。

项目成果

pulsality, the pituitary response and reproductive dysfunction.

脉动、垂体反应和生殖功能障碍。

• 发表时间: 2009
• 作者: RIE TSUTSUMI; NICHOLAS J.C.; WEBSTER; GnRH
• 通讯作者: GnRH

GnRH Pulsatility, the pituitary response and reproductive dysfunction

GnRH 搏动、垂体反应和生殖功能障碍

• 发表时间: 2009
• 作者: RIE TSUTSUMI