| Budget Amount *help |
¥27,040,000 (Direct Cost: ¥20,800,000、Indirect Cost: ¥6,240,000)
Fiscal Year 2014: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
Fiscal Year 2012: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
Fiscal Year 2011: ¥8,320,000 (Direct Cost: ¥6,400,000、Indirect Cost: ¥1,920,000)
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| Outline of Final Research Achievements |
ABCG2, which is a physiological urate transporter and a major causative gene of gout, was revealed to mediate the intestinal secretion of urate by a series of in vivo experiments. In addition, ABCG2 dysfunction was revealed to increase the risk of classical overproduction type of hyperuricemia. From these pieces of information, it was suggested that classical overproduction type of hyperuricemia includes genuine overproduction type and extra-renal underexcretion type, which is caused by the dysfunction of ABCG2-mediated intestinal secretion of urate. Thus, we proposed a new classification of hyperuricemia, including extra-renal underexcretion hyperuricemia.
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