| Project/Area Number |
16K09786
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
村尾 孝児 香川大学, 医学部, 教授 (20291982)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 非アルコール性脂肪肝炎 / 生活習慣病 / PREB / ABCA1 / 脂肪肝 / アディポネクチン / 脂肪細胞 / トランスジェニックマウス / 内分泌代謝学 / 非アルコール性脂肪性肝炎 / メタボリックシンドローム / 転写因子 |
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| Outline of Final Research Achievements |
Previously, we reported that the transcriptional factor, prolactin regulatory element binding (PREB) relates with lifestyle disease, such as diabetes mellitus and atherosclerosis. That is, we showed that PREB acts as anti-diabetic in pancreatic β cells and regulates adiponectin expression in adipocytes. In this study, we tried to clear the role of PREB on lifestyle disease. Results are; (1) ABCA1 is a pivotal regulator of lipid efflux from cells, and PREB increases ABCA1 expression in hepatocyte by binding to ABCA1 promoter. As a result, PREB improve fatty liver. (2) PREB regulates adiponectin expression in vivo. (3)PREB may effect protects pancreatic β cells improving lipotoxicity via ABCA expression.
Thus ABCA1 should be the target molecule of PREB, and we need to elucidate the mechanism of ABCA1 expression by PREB for lifestyle disease treatment.
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| Academic Significance and Societal Importance of the Research Achievements |
転写因子PREBがABCA1分子発現調節を通じて細胞内脂肪蓄積やそれによる細胞機能障害により生活習慣病に関連していることが判明した。今後さらにPREBによるABCA1遺伝子の発現調節が新たな生活習慣病の治療方法に繋がると考えられる。
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