| Project/Area Number |
17H07056
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | Jichi Medical University |
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Principal Investigator |
YAMADA Hodaka 自治医科大学, 医学部, 助教 (70807247)
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | GPR120 / 脂肪細胞 / 膵β細胞 / インスリン抵抗性 / インスリン分泌 / 慢性炎症 / β細胞 / 脂肪酸 / G蛋白共役型受容体 |
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| Outline of Final Research Achievements |
The anti-inflammatory effects of unsaturated fatty acids in adipocytes have yet to be elucidated. Hence, the aims of the present study were to evaluate the anti-inflammatory effects of eicosapentaenoic acid (EPA) via GPR120 in adipocytes.EPA attenuated palmitate-induced increases in inflammatory gene expression and NF-κB phosphorylation in 3T3-L1 adipocytes. Silencing of GPR120 abolished the anti-inflammatory effects of EPA. In GPR120 downstream signal analysis, EPA was found to decrease palmitate-induced increases in TAK1/TAB1 complex expression. EPA supplementation suppressed HFHS-induced crown-like structure formation in epididymal adipose tissue and altered macrophage phenotypes from M1 to M2 in the stromal vascular fraction. Moreover, the EPA-containing diet attenuated increases in adipose p-JNK and phospho-p65 NF-κB levels.The present study demonstrate that EPA suppresses palmitate-induced inflammation via GPR120 by inhibiting the TAK1/TAB1 interaction in adipocytes.
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| Academic Significance and Societal Importance of the Research Achievements |
GPR120は脂肪細胞及び膵β細胞に発現している。今回これらの細胞におけるGPR120の機能解析を行った。脂肪細胞の不飽和脂肪酸EPAによるGPR120刺激は飽和脂肪酸が引き起こす炎症を抑制していることを見出した。膵島を用いた実験では血糖依存性のインスリン分泌のメカニズムの一端を明らかにした。脂肪酸の質が生体、細胞に与える影響をGPR120の視点から明らかに出来た。
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