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Basic and translational research
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Sodium-dependent phosphate cotransporter type 1 sequence polymorphisms in male patients with gout
  1. Wako Urano1,
  2. Atsuo Taniguchi1,
  3. Naohiko Anzai2,
  4. Eisuke Inoue1,
  5. Yoshikatsu Kanai2,
  6. Mariko Yamanaka1,
  7. Hitoshi Endou2,3,
  8. Naoyuki Kamatani1,
  9. Hisashi Yamanaka1
  1. 1Institute of Rheumatology, Tokyo Women's Medical University, Tokyo, Japan
  2. 2Department of Pharmacology and Toxicology, Kyorin University School of Medicine, Tokyo, Japan
  3. 3J-Pharma Co, Ltd, Tokyo, Japan
  1. Correspondence to Dr Wako Urano, Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Sinjuku-ku, Tokyo 162-0054, Japan; wako{at}ior.twmu.ac.jp

Abstract

Objectives Molecular biological approaches have recently identified urate transporters in renal proximal tubular cells. Human sodium-dependent phosphate cotransporter type 1 encoded by SLC17A1 is a urate transporter localised to the renal proximal tubular cells and candidate molecule to secret urate from renal tubular cells to urine. This study investigated the roles of SLC17A1 in the development of gout.

Patients and Methods Single nucleotide polymorphisms 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, odds ratio (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 a 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.

https://doi.org/10.1136/ard.2008.106856

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    Footnotes

    • Funding This work was supported by Health and Labour Sciences Research grants for Research on Human Genome Tailor Made and a grant for the Research for the Future programme from the Japan Society for the Promotion of Science.

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval This study was conducted with the approval of the Hospital Ethics Committee for Human Genome Researches of Tokyo Women's Medical University.

    • Provenance and peer review Not commissioned; externally peer reviewed.