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Nucleosides, Nucleotides & Nucleic Acids Volume 29, 2010 - Issue 4-6
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Original Articles

Establishment and Analysis of SLC22A12 (URAT1) Knockout Mouse

M. Hosoyamada Pharmacotherapeutics, Faculty of Pharmacy, Keio University, Tokyo, Japan
,
Y. Takiue Pharmacotherapeutics, Faculty of Pharmacy, Keio University, Tokyo, Japan
,
H. Morisaki Bioscience, National Cardiovascular Center Research Institute, Osaka, Japan
,
J. Cheng Bioscience, National Cardiovascular Center Research Institute, Osaka, Japan
,
M. Ikawa Genome Information Research Center, Osaka University, Osaka, Japan
,
M. Okabe Genome Information Research Center, Osaka University, Osaka, Japan
,
T. Morisaki Bioscience, National Cardiovascular Center Research Institute, Osaka, Japan
,
K. Ichida Pathophysiology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan
,
T. Hosoya Internal Medicine (Kidney and Hypertension), Jikei University School of Medicine, Tokyo, Japan
&
T. Shibasaki Pharmacotherapeutics, Faculty of Pharmacy, Keio University, Tokyo, Japan
 show all
Pages 314-320 | Published online: 11 Jun 2010
 
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Abstract

In order to elucidate the mechanisms of post-exercise acute renal failure, one of the complications of hereditary renal hypouricemia, we have targeted the mouse Slc22a12 gene by the exchange of exons 1–4 with pMC1neo-polyA. The knockout mice revealed no gross anomalies. The concentration ratio of urinary urate/creatinine of the knockout mice was significantly higher than that of wildtype mice, indicating an attenuated renal reabsorption of urate. The plasma levels of urate were around 11 μM and were similar among the genotypes. Although the fractional excretion of urate of knockout mice was tend to higher than that of wildtype mice, the urate reabsorption ability remained in the kidney of knockout mice, indicating a urate reabsorptive transporter other than Urat1.

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