2017 Fiscal Year Final Research Report
Analysis for the pathogenesis of development of NASH via ER stress by PNPLA3 gene mutant mice
Project/Area Number |
15K09009
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Gastroenterology
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Research Institution | Kochi University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
小野 正文 高知大学, 教育研究部医療学系臨床医学部門, 准教授 (70304681)
西原 利治 高知大学, 教育研究部医療学系臨床医学部門, 教授 (60145125)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | NASH / PNPLA3 / 遺伝子多型 |
Outline of Final Research Achievements |
Because XBP-1 was regulated by ATF6 and hyperglycemia, and expression of ATF6 was not different between wild type and Knockout mice, it was considered that regulation of XBP-1 gene was involved by PMPLA3 gene. In gene expression of lipid synthesis, expression of SREBP1c, ACC2, FASN, CPT1α, DGAT1, 2 were not different in between wild type and knockout mice, and saturated fatty acids/unsaturated fatty acids ratios were high both before and after ER stress. Therefore, we concluded that PNPLA3 may have roles for the changes of fatty acids composition. In addition, we have created PNPLA3 mutant transgenic mice (Tg: PNPLA3 KO mice with mutant PNPLA3 gene(I148M) which is liver specific regulated by albumin promoter.
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Free Research Field |
NASH
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