Construction of pharmacokinetic model of urate in the whole body to search for novel pharmacological target(s) of hyperuricemia

2014 Fiscal Year Final Research Report

• Project/Area Number: 23689008
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Single-year Grants
• Research Field: Medical pharmacy
• Research Institution: The University of Tokyo
• Principal Investigator: TAKADA Tappei 東京大学, 医学部附属病院, 講師 (90376468)
• Project Period (FY): 2011-04-01 – 2015-03-31
• Keywords: 薬理学 / 生理学 / ゲノム / トランスレーショナルリサーチ / トランスポーター

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.

Free Research Field

医療系薬学