| Project/Area Number |
15K09710
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
藤原 亮一 北里大学, 薬学部, 講師 (40631643)
松井 克之 滋賀医科大学, 医学部, 講師 (60595924)
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| Research Collaborator |
Tukey Robert H
Yanagi Takahide
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 母乳性黄疸 / 遺伝性非抱合型高ビリルビン血症 / ビリルビンUDP-グルクロン酸転移酵素 / UGT1A1 / Gilbert症候群 / 新生児 / 核黄疸 / 新生児高ビリルビン血症 / 新生児黄疸 / 体質性黄疸 |
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| Outline of Final Research Achievements |
For the safety management of brest milk jaundice (BMJ), I performed analysis UGT1A1 gene in infants with BMJ. I revealed UGT1A1*6 (p.G71R) variant which is a genetic cause of BMJ is also important cause for Gilbert syndrome (Maruo Y. J Pediatr 2016). UGT1A1*28 which is other important variant was also the cause of Gilbert syndrome but not a cause of BMJ. UGT1A1*6 is also the genetic cause of BMJ in low birth weight infants (Yanagi T. J Pediatr 2017) and a risk factor kernicteric in extreme preterm indants (Yanagi T. submitted).
I made p.G71R-humanized UGT1A mice in collaboration with Prof. Tukey in University of California San Diego. The mice will be brought to our laboratory and I continue further study.
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| Academic Significance and Societal Importance of the Research Achievements |
母乳性黄疸は後期新生児期にみられる母乳栄養に関連する遷延性高ビリルビン血症である。多くの赤ちゃんにみられ、核黄疸の危険性がある場合もある。そのため母乳性黄疸の背景を明らかにして、管理法を確立することは子育てをする家族や赤ちゃん自身の健康に寄与する。また、超早産児の核黄疸発生を予防するための研究にもつながり、社会に広く貢献するものと考える。
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