| Project/Area Number |
16K19325
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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 |
Gastroenterology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
Hasebe Takumu 旭川医科大学, 大学病院, 医員 (10596282)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 非アルコール性脂肪性肝疾患 / 鉄過剰症 / ヘプシジン / BMP / BMPER / 類洞内皮細胞 / 脂肪肝 / 鉄過剰 / 内科 |
|---|
| Outline of Final Research Achievements |
Iron overload is often seen in non-alcoholic fatty liver disease condition, however, the mechanism is not clear. Our study demonstrated that the fatty liver model mice had decreased expression of iron regulating molecule hepcidin. To further elucidate the mechanism of iron overload, we performed RNA-seq. The result showed that the decreased hepcidin was due to decreased level of BMP-SMAD signal pathway. BMPER which is a inhibitor of BMP signaling was increased in the liver. Also we demonstrated that the BMPER is expressed by liver sinusoid epithelial cells. Thus, we described that increased BMPER in the fatty liver is one of the mechanism for iron overload.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、肥満による脂肪肝モデルマウスを用いて、その病態形成に鉄過剰症が関与することについて検討した。その結果、鉄制御蛋白であるヘプシジンの発現低下が関与することを指摘し、この制御にBMPシグナルの破綻があることを見いだした。非アルコール性脂肪性肝疾患の病態は依然不明な点が多く、本研究成果が非アルコール性脂肪性肝疾患の病態解明につながるとともに、今後の治療介入に関して治療標的となる分子を検討する助けとなる。
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