| Project/Area Number |
26870257
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General internal medicine(including psychosomatic medicine)
Applied health science
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| Research Institution | Nagoya City University (2015-2016)
Nagoya University (2014) |
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Principal Investigator |
NISHIO Naomi 名古屋市立大学, 大学院医学研究科, 研究員 (80513457)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | GADD34 / 老化 / 脂肪肝 / インスリンシグナル伝達系 / 炎症 / Insulin/IGF1レセプターシグナル伝達系 / 細胞膜タンパク質 / 免疫 / 代謝 / 脂肪肝形成 / 高脂肪食摂取 |
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| Outline of Final Research Achievements |
In this report, we analyzed the role of GADD34 gene on fatty liver and typeⅡ diabetes using GADD34 -deficient mice. We found that GADD34-deficient mice developed the fatty liver and liver inflammation with aging. Then displayed liver damage, which could proceed to NAFLD/NASH with age, some mice extended for a cancer or typeⅡ diabetes. Furthermore GADD34 deficiency developed obesity by enhancement the adipocyte proliferation and differentiation. TNF-α produced by adipocytes inhibited IGF-1/Insulin signaling, then induced insulin resistance.
This report concluded that Mechanism of fatty liver and typeⅡ diabetes in GADD34 KO mice may be mainly comes from the effect of GADD34 on insulin signaling which related to cell proliferation and aging. GADD34 suppress adipocyte differentiation by decreasing IGF-1/Insulin signaling and inhibited the fat accumulation.
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