| Project/Area Number |
15K15227
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Epidemiology and preventive medicine
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| Research Institution | National Defense Medical College |
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Principal Investigator |
Matsuo Hirotaka 防衛医科大学校(医学教育部医学科進学課程及び専門課程、動物実験施設、共同利用研究, 分子生体制御学, 講師 (00528292)
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| Co-Investigator(Kenkyū-buntansha) |
山本 健 久留米大学, 医学部, 教授 (60274528)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 分子遺伝疫学 / 痛風遺伝子 / 腸炎 / マーカー / 尿酸 / 炎症性腸疾患 / 遺伝疫学 / 個別化医療 |
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| Outline of Final Research Achievements |
We investigated urate excretion mechanism at human intestine and kidney in the present research. We therefore collected many cases including acute gastroenteritis and inflammatory bowel disease, as well as hemodialysis (end-stage renal disease) patient to compare healthy controls. As results, dysfunction of transporter ABCG2 significantly elevated serum uric acid (SUA) level in acute gastroenteritis patients regardless of the degree of dehydration, which was not detected in their recovery period. Furthermore, ABCG2 dysfunction also significantly increased SUA levels in hemodialysis patients. Thus, urate, which is excreted from both intestine and kidney, is elevated in both acute gastroenteritis and hemodialysis by dysfunctional ABCG2 variants. Also, it was implied that increased SUA could be a useful marker not only for dehydration but also epithelial impairment of intestine.
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