| Project/Area Number |
25860739
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Metabolomics
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| Research Institution | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 肥満 / 糖尿病 / 脂肪蓄積 / 脂肪細胞 / TGFβ / TGFb |
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| Outline of Final Research Achievements |
We previously showed that ALK7, one of the TGFβ receptors, suppresses lipolysis to accumulate fat in obese mice. However, it remains unknown how the ALK7-signaling is activated during fat accumulation in obesity. In this study, we explored a novel endogenous ligand for ALK7 in TGFβ family. Under high-fat diet (or obesity) condition, several TGFβ family ligands were highly expressed in adipose tissue of mice compared with normal diet condition. These ligands have transactivation activity depend on ALK7 and its coreceptor, Cripto in 293T cells. Furthermore, these ligands were expressed in mature adipocytes or CD11b-positive macrophages in adipose tissue of obese mice. Further analysis should be done to validate that whether these ligands activate the ALK7-signaling in vivo.
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