The molecular mechanism of insul in resistance induced by overnutrition
| Project/Area Number |
20890279
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| Research Category |
Grant-in-Aid for Young Scientists (Start-up)
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | Mukogawa Women's University Junior College Division |
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Principal Investigator |
TSUTSUMI Rie Mukogawa Women's University Junior College Division, 大学院・ヘルスバイオサイエンス研究部, 学術研究員 (80510172)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥3,302,000 (Direct Cost: ¥2,540,000、Indirect Cost: ¥762,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,742,000 (Direct Cost: ¥1,340,000、Indirect Cost: ¥402,000)
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| Keywords | 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 |
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| Research Abstract |
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.
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Report
(3 results)
Research Products
(2 results)
