| Project/Area Number |
23591205
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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 |
Kidney internal medicine
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
JUTABHA Promsuk 獨協医科大学, 医学部, 助教 (90541748)
KIMURA Toru 杏林大学, 医学部, 講師 (30433725)
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| Co-Investigator(Renkei-kenkyūsha) |
HOSOYAMADA Makoto 帝京大学, 薬学部, 教授 (00291659)
MATSUO Hirotaka 防衛医科大学校, 医学部, 講師 (00528292)
NAKAMURA Makiko 東京薬科大学, 薬学部, 助教 (80447557)
NAKAMURA Yoshihiro 防衛医科大学校, 医学部, 准教授 (60415255)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 高尿酸血症 / 痛風 / 尿酸トランスポーター / ABCG2 / 腎外排泄低下型高尿酸血症 / 排泄低下型高尿酸血症 / 産生過剰型高尿酸血症 / 発症年齢 / 腎負荷型高尿酸血症 / 低尿酸血症 / URAT1 / GLUT9 / URATv1 |
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| Research Abstract |
A function of ABCG2, urate excretive transporter, is evaluated by the combination of the no-functional SNP, Q126X and the half functional SNP, Q141K. The estimated ABCG2 dysfunction leads to the urinary urate excretion increase and this mechanism was elucidated using Abcg2 knock-out mice. As a new mechanism for hyperuricemia, we demonstrated that hyperuricemia results from the intestinal urate excretion decrease via ABCG2, leading to urinary urate excretion increase (extra-renal urate underexcretion type hyperuricemia). We also indicated that ABCG2 dysfunction is related with early-onset gout and that the slight and mild dysfunctions mainly cause underexcretion type hyperuricemia, while severe dysfunction causes extra-renal urate underexcretion type hyperuricemia.
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