| Project/Area Number |
26870562
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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 |
General physiology
Biological pharmacy
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ビリルビン / 新生児黄疸 / 薬物代謝酵素 / UGT1A1 / グルクロン酸抱合 / 甲状腺ホルモン / 脳発達 / T4 / 抗酸化作用 / 核黄疸 |
|---|
| Outline of Final Research Achievements |
Human neonates develop mild hyperbilirubinemia. Bilirubin is solely metabolized by UDP-glucuronosyltransferase (UGT). As UGT also metabolizes thyroxine, which is an important bioactive hormone in brain development, it was hypothesized that bilirubin can inhibit the thyroxine metabolism and promote brain development. In humanized UGT1 mice, UGT1A1 was highly expressed in the brain. We observed that the thyroxine level was actually higher in hUGT1 mice compared to wild-type mice. It was further demonstrated that reduced thyroxine levels were tightly associated with the neurodevelopmental disorder.
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