Analysis of the pathological mechanism of NASH by the nuclear receptors and establishment of the therapeutic application

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460490
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Gunma University
• Principal Investigator: Inoue Yusuke 群馬大学, 大学院理工学府, 准教授 (90304302)
• Co-Investigator(Kenkyū-buntansha): NAMEKI Nobukazu 群馬大学, 大学院理工学府, 准教授 (80302959) ; SAKAGUCHI Mayakiyo 岡山大学, 大学院医歯薬総合研究科, 准教授 (70379840)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: NASH / 核内受容体 / HNF4α / PPARα

Outline of Final Research Achievements

Deletion of PPARα in liver-specific HNF4α-null mice (KO mice) improved NASH. Expression of FATP1, CD36, and CideA was increased in KO mice, but the expression of these genes were decreased in double KO mice. Also, DNA binding activity of PPARα and the amount of hepatic fatty acid was increased in KO mice. These results indicate that ligand-activated PPARα/PGC1α could transactivate the PPARα target genes and might induce NASH in KO mice.

Free Research Field

分子細胞生物学