| Project/Area Number |
17K19938
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Health science and related fields
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| Research Institution | Tezukayama Gakuin University |
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Principal Investigator |
MUKAI TAKAKO 帝塚山学院大学, 人間科学部, 助手 (60701464)
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| Co-Investigator(Kenkyū-buntansha) |
楠堂 達也 帝塚山学院大学, 人間科学部, 准教授 (00460535)
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| Project Period (FY) |
2017-06-30 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | FABP1 / 脂肪酸結合たんぱく質 / NASH / 非アルコール性脂肪肝 / 脂肪酸結合タンパク質 / NAFLD / 脂肪肝 / 脂肪肝改善 / 非アルコール性脂肪肝炎 |
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| Outline of Final Research Achievements |
In this study, we investigated the effects of FABP1 repression on NASH pathology and pathogenesis. The expression of FABP1 in the liver of NASH model mice fed a high-fat and high-cholesterol was suppressed by adeno-associated virus vector-mediated FABP1 knockdown. The silencing of FABP1 did not improve inflammation and fibrosis of these mice. However, FABP1 knockdown mice exhibited an improvement in glucose tolerance, which is an important factor in the development of lifestyle-related diseases, including NASH.
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| Academic Significance and Societal Importance of the Research Achievements |
近年、NASHの罹患者数は増加しており、予防法・治療法の開発が求められている。本研究で得られた高脂肪・高コレステロール食によるNASH進行過程のデータは、今後のNASH研究進展の足場となり得る。また、本研究ではFABP1抑制が耐糖能を改善することを明らかにした。耐糖能異常は、NASHを含めた生活習慣病の重要ファクターであることから、新たな治療シーズの発見という点で学術的・社会的意義は大きい。
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