2016 Fiscal Year Final Research Report
Investigation of the physiological function of Slc22a18, a candidate identified by a genetic analysis on animal models for visceral fat accumulation
| Project/Area Number |
26461357
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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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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | メタボリックシンドローム / 脂肪蓄積 / トランスポーター |
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| Outline of Final Research Achievements |
Genetic factors underlying visceral fat accumulation, a principal component of the metabolic syndrome (MS), remain largely unknown. In this study, visceral fat accumulation was accelerated in transgenic mice overexpressing SLC22A18, a candidate gene revealed by our previous genetic studies on animal models. Oppositely, fat volume was decreased in SLC22A18 knockout mice as compared with normal mice. These results indicated that SLC22A18 plays a crucial role in regulating visceral fat accumulation. A series of our experiments have revealed a promising candidate for endogenous substrates transported by SLC22A18. Thus, SLC22A18 could be a novel therapeutic target for metabolic syndrome via its regulatory function upon visceral fat accumulation.
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| Free Research Field |
代謝内科学
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