| Project/Area Number |
15H02904
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Eating habits
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| Research Institution | National Institute of Advanced Industrial Science and Technology |
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Principal Investigator |
MORITA Naoki 国立研究開発法人産業技術総合研究所, 生命工学領域, 総括研究主幹 (60371085)
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| Co-Investigator(Kenkyū-buntansha) |
芳賀 早苗 北海道大学, 保健科学研究院, 特任講師 (60706505)
酒井 佳夫 金沢大学, 医学系, 准教授 (80401925)
野田 なつみ 北海道大学, 保健科学研究院, 助教 (30624358)
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| Co-Investigator(Renkei-kenkyūsha) |
OZAWA Takeaki 東京大学, 大学院理学系研究科, 教授 (40302806)
SAKASHITA Mami 国立研究開発法人産業技術総合研究所, 生命工学領域生物プロセス研究部門, 主任研究員 (20357099)
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| Research Collaborator |
OZAKI Michitaka
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
Fiscal Year 2017: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2016: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2015: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
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| Keywords | 非アルコール性脂肪性肝炎（NASH） / 脂肪肝 / マーカー分子 / メタボリック症候群 / 機能性食品 |
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| Outline of Final Research Achievements |
We tried to measure p62/SQSTM1 in blood using ELISA method, however, the ELISA method for p62/SQSTM1 using conventional antibodies remains problems to be overcome in terms of sensitivity. It seemed that it is optimal at this time to perform measurement using liver tissue for the measurement of p62/SQSTM1 with molecular biological method. In the clinical study, we confirmed the usefulness of evaluating p62/SQSTM1 expression together with antioxidant capacity by using Keap-1 molecule. This combination method would improve the specificity of diagnosis. In addition, we identified new molecular marker(s) associated with lipidification. This molecule(s) is expressed on the lipid bilayer membrane that covers the lipid droplet. It is considered that the new molecule(s) enhanced further lipidification, and promoteed liver cell injury by fatty liver, which is related to the progression of NASH pathology.
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