Physiological analysis of SLC22A18 gene associated with visceral fat accumulation
Project/Area Number |
24790909
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Metabolomics
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Research Institution | The University of Tokyo |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Project Status |
Completed (Fiscal Year 2013)
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Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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Keywords | メタボリックシンドローム / 連鎖解析 / 内臓脂肪 / トランスポーター |
Research Abstract |
In this study, to investigate the physiological functions of SLC22A18, an orphan transporter, in visceral fat accumulation and hepatic lipid accumulation, we analyzed SLC22A18-genetically modified mice and screened the endogenous substrate of SLC22A18. Animal experiments revealed that SLC22A18 positively regulates fat accumulation and triglyceride accumulation in liver. We found bilirubin as a candidate of SLC22A18 substrates. These results indicate the novel function of SLC22A18 and suggest the possibility of SLC22A18 as a therapeutic target of metabolic disorder.
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Report
(3 results)
Research Products
(4 results)
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[Journal Article] A novel link between Slc22a18 and fat accumulation revealed by a mutation in the spontaneously hypertensive rat.2013
Author(s)
Yamamoto, T., Izumi-Yamamoto, K., Iizuka, Y., Shirota, M., Nagase, M., Fujita, T., and Gotoda, T.
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Journal Title
Biochem Biophys Res Commun
Volume: 440
Issue: 4
Pages: 521-526
DOI
Related Report
Peer Reviewed
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