| Project/Area Number |
16F16418
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| Research Category |
Grant-in-Aid for JSPS Fellows
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| Allocation Type | Single-year Grants |
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| Section | 外国 |
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| Research Field |
Metabolomics
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| Research Institution | Kobe University |
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Principal Investigator |
清野 進 神戸大学, 医学研究科, 特命教授 (80236067)
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| Co-Investigator(Kenkyū-buntansha) |
CARMEAN CHRISTOPHER 神戸大学, 医学研究科, 外国人特別研究員
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| Project Period (FY) |
2016-10-07 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2018: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2017: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2016: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | arcenic / diabetes / insulin secretion / serotonin / glucuronidation / toxicology / Insulin Secretion / Diabetes / Endocrin Disruptors / Arsenic / Serotonin / Metabolomics / Gene Expression / Detoxification / ヒ素 / 糖尿病 / 毒物学 / インスリン / グルコース |
|---|
| Outline of Annual Research Achievements |
Previously our RNA sequencing and metabolomics data identified the serotonin disposal pathway as a possible mediator of arsenic’s effects. We followed up on these results by measuring the gene expression of other serotonin metabolism-associated genes, and we measured the enzymatic rate of serotonin conjugation to glucuronic acid to form serotonin-glucuronide. Additionally, we developed a series of gene candidate knockouts. We evaluated their functional characteristics, including glucose-induced insulin secretion, serotonin levels, and serotonin glucuronidation enzymatic activity. We also confirmed that the same gene expression patterns observed in MIN6-K8 cells were also replicated in primary human islets. Both mouse and human islets up-regulated Ugt1a6a (mouse) or UGT1A6 (human) in response to arsenic exposure. A paper on these findings was published in a peer-reviewed journal.
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| Research Progress Status |
平成30年度が最終年度であるため、記入しない。
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| Strategy for Future Research Activity |
平成30年度が最終年度であるため、記入しない。
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