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Sodium-dependent phosphate cotransporter type 1 (NPT1) sequence polymorphisms in male patients with gout
  1. Wako Urano (wako{at}ior.twmu.ac.jp)
  1. Institute of Rheumatology, Tokyo Women's Medical University, Japan
    1. Atsuo Taniguchi (amtanigu{at}ior.twmu.ac.jp)
    1. Institute of Rheumatology, Tokyo Women's Medical University, Japan
      1. Naohiko Anzai (anzai{at}ks.kyorin-u.ac.jp)
      1. Pharmacology and Toxicology, Kyorin University School of Medicine, Japan
        1. Eisuke Inoue (einoue{at}kde.biglobe.ne.jp)
        1. Institute of Rheumatology, Tokyo Women's Medical University, Japan
          1. Yoshikatsu Kanai
          1. Pharmacology and Toxicology, Kyorin University School of Medicine, Japan
            1. Mariko Yamanaka
            1. Institute of Rheumatology, Tokyo Women's Medical University, Japan
              1. Naoyuki Kamatani (kamatani{at}msb.biglobe.ne.jp)
              1. Institute of Rheumatology, Tokyo Women's Medical University, Japan
                1. Hitoshi Endou (endou{at}j-pharma.com)
                1. Pharmacology and Toxicology, Kyorin University School of Medicine, Japan
                  1. Hisashi Yamanaka (hisashi{at}pc4.so-net.ne.jp)
                  1. Institute of Rheumatology, Tokyo Women's Medical University, Japan

                    Abstract

                    Objectives: Molecular biological approaches recently have identified urate transporters in renal proximal tubular cells. Human sodium-dependent phosphate cotransporter type 1 (NPT1) encoded by SLC17A1 is a urate transporter localized to the renal proximal tubular cells and candidate molecule to secret urate from renal tubular cells to urine. Here, we investigated the roles of SLC17A1 in the development of gout.

                    Patients and Methods: SNPs in the human SLC17A1 gene (rs1165176, rs1165151, rs1165153, rs1165196, rs1165209, rs1165215, rs1179086, rs3799344, and rs3757131) were selected, and an association study was conducted using male patients with gout (n=175) and male controls (n=595).

                    Results: There were significant differences between gout and control groups in the distribution of genotypes at rs1165196 (T806C; Ile269Thr, OR = 0.55, p = 0.0035), rs1179086 (OR = 0.57, p = 0.0018), and rs3757131 (OR = 0.54, p = 0.0026). In controls, T806C alone had no effect on serum uric acid (sUA) levels. However, T806C showed significant interaction with reduction of sUA in obese individuals (body mass index ≥25) using multiple regression analysis.

                    Conclusions: Our data suggest that SLC17A1 polymorphisms are associated with the development of gout.

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