Project/Area Number |
15K12715
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Applied health science
|
Research Institution | Kobe Gakuin University |
Principal Investigator |
OBATA TOKIO 神戸学院大学, 薬学部, 講師 (80625244)
|
Co-Investigator(Kenkyū-buntansha) |
徳山 尚吾 神戸学院大学, 薬学部, 教授 (70225358)
中本 賀寿夫 神戸学院大学, 薬学部, 講師 (30432636)
|
Co-Investigator(Renkei-kenkyūsha) |
HIRASAWA Akira 京都大学, 大学院・薬学研究科, 准教授 (70242633)
|
Project Period (FY) |
2015-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | 非アルコール性脂肪性肝炎(NASH) / GPR120/FFAR4 / DHA / fatty acid / NASH / NAFLD / 肝臓 / 白色脂肪組織 |
Outline of Final Research Achievements |
We investigated the involvement of long chain fatty acid receptor GPR120/FFAR4 in the progression of nonalcoholic steatohepatitis (NASH). We used choline-deficient and 0.1% methionine added high-fat diet (CDAHFD) in order to produce NASH pathology. In CDAHFD-induced NASH model mice, the liver cell injury, hepatic fat deposit, hepatic inflammation and fibrosis markers significantly increased, but these were suppressed by administration of DHA, an agonist of GPR120/FFAR4. On the other hand, GPR120/FFAR4 knockout mice further exacerbated hepatocyte damage and inflammation by CDAHFD-induced. These findings suggested that GPR 120/FFAR 4 is involved the development of NASH and DHA suppresses in progression.
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