Mechanism of formation of hepatic steatosis in Non-alcoholic fatty liver disease (NAFLD)

• Project/Area Number: 25461007
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Osaka City University
• Principal Investigator: Hideki Fujii 大阪市立大学, 大学院医学研究科, 特任講師 (20382070)
• Co-Investigator(Kenkyū-buntansha): 村上 善基 大阪市立大学, 大学院医学研究科, 准教授 (00397556) ; 河田 則文 大阪市立大学, 大学院医学研究科, 教授 (30271191)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Project Status: Completed (Fiscal Year 2016)
• Budget Amount: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000); Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000); Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
• Keywords: マクロファージ / 肝脂肪化 / MSR-A / MSr-A / 脂肪肝炎

Outline of Final Research Achievements

Mechanism of formation of hepatic steatosis in Non-alcoholic fatty liver disease (NAFLD). Macrophages actively uptake modified LDL (acetyl- and oxidized LDL) via macrophage scavenger receptors (MSR). In 1990, Kodama et al. isolated cDNAs encoding two versions of the bovine macrophage scavenger receptor, MSR-AI and MSR-AII. Functional MSR-As are trimers of 2 C-terminally different subunits generated by alternative splicing. A number of studies have reported the importance of MSR-A in the process of atherosclerosis.We have examined the mechanism of formation of hepatic fibrosis and carcinogenesis in Non-alcoholic steatohepatitis (NASH) using mouse model. In this research, we examined the role of macrophage in formation of hepatic steatosis using both in vivo and in vitro model.