Analyses of involvement mechanism of NRF2 and mitochondrial abnormality in pathophysiology of NASH

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460983
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Niigata University
• Principal Investigator: KAWAI Hirokazu 新潟大学, 医歯学総合病院, 講師 (80419291)
• Co-Investigator(Kenkyū-buntansha): SUDA Takeshi 新潟大学, 医歯学総合病院, 教授 (10361916)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 非アルコール性脂肪肝炎 / 脂肪肝 / ミトコンドリアDNA / 酸化ストレス / ダイエット

Outline of Final Research Achievements

An increasing tendency of mitochondrial DNA (mtDNA) copy number was found in the liver of a rodent model of fatty liver, however the number was normalized with diet intervention. In contrast, mtDNA copy number was decreased in the liver of a rodent model of nonalcoholic steatohepatitis (NASH). MtDNA copy number in these models appeared to be regulated by altering a balance between expression levels of genes related to biogenesis and degradation of mitochondria. It has been revealed that pathophysiological progression in NASH is closely related to oxidative stress along with alteration of mtDNA copy number.

Free Research Field

肝臓病学