| Project/Area Number |
22590354
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Gunma University |
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Principal Investigator |
INOUE Yusuke 群馬大学, 大学院・工学研究科, 准教授 (90304302)
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| Co-Investigator(Kenkyū-buntansha) |
KUWAHARA Masayasu 群馬大学, 大学院・工学研究科, 准教授 (40334130)
NAMEKI Nobukazu 群馬大学, 大学院・工学研究科, 准教授 (80302959)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 脂肪肝 / 核内受容体 / HNF4α / PPARα / モデルマウス / PPAR / 肝臓 |
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| Research Abstract |
Deletion of haptic PPARα in liver-specific HNF4α-null mice (KO mice) improved fatty livers. To investigate the pathogenic mechanism of fatty livers, DNA binding activity of haptic PPARα was analysed. As a result, DNA binding activity of hepatic PPARα was decreased in KO mice. Expression of hepatic PPARγ1 and PGC1α was also increased and transactivation of hepatic PPARα target genes was observed in KO mice. These results indicate that hepatic PPARγ1, PGC1α, and unidentified ligands for PPARα /γ1 could transactivate the PPARαtarget genes and induce fatty lives in KO mice.
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