| Project/Area Number |
17K09867
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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 | Kyorin University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山本 隆史 杏林大学, 医学部, 助教 (00572033)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | メタボリックシンドローム / 内臓脂肪蓄積 / トランスポーター / SLC / ビリルビン / メタボローム / クロロキン / 脂肪蓄積 / 遺伝子 |
|---|
| Outline of Final Research Achievements |
We have previously identified SLC22A18 as a key molecule related to visceral fat accumulation, a major underlying cause of the Metabolic Syndrome. In the current study, we searched for physiological intrinsic substrates for SLC22A18 as a possible transporter by integration of the results of both uptake experiments with overexpressing cells and metabolome analyses. According to the results obtained with both genetically engineered animals and cultured cells, bilirubin was thought to be the strongest candidate substrate, but the overall results with overexpression of SLC22A18 alone did not support this hypothesis, indicating other possibilities such as possible involvement of another molecule required for normal function of SLC22A18 in vivo.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の目的は、メタボリックシンドロームの成因的基盤である内臓脂肪蓄積に関連する分子であるSLC22A18の機能を調節する分子の同定にある。今回の結果は、ビリルビンの関与を強く示唆するものであったが、研究をさらに発展させることにより内臓脂肪が蓄積するメカニズムの解明が進み、SLC22A18を標的分子としたメタボリックシンドロームの有効な治療法の開発につながることが期待される。
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