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Population-specific effects of SLC17A1 genotype on serum urate concentrations and renal excretion of uric acid during a fructose load
  1. Nicola Dalbeth1,
  2. Meaghan E House1,
  3. Gregory D Gamble1,
  4. Anne Horne1,
  5. Lauren Purvis1,
  6. Angela Stewart1,
  7. Marilyn Merriman2,
  8. Murray Cadzow2,
  9. Amanda Phipps-Green2,
  10. Tony R Merriman2
  1. 1Department of Medicine, University of Auckland, Auckland, New Zealand
  2. 2Department of Biochemistry, University of Otago, Dunedin, New Zealand
  1. Correspondence to Dr Nicola Dalbeth, Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, 85 Park Road, Grafton, Auckland 1023, New Zealand; n.dalbeth{at}

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Solute carrier family 17 member 1 (SLC17A1) is an anion exchanger that secretes uric acid into the urine.1 ,2 Genetic variation in SLC17A1 has been associated with hyperuricaemia and gout.3–5 The minor allele (A) of single nucleotide polymorphism (SNP) rs1183201 is associated with a reduced risk of gout in European and western Polynesian people, with a weaker (non-significant) effect in eastern Polynesian people.4 rs1183201 is a tag SNP in strong linkage disequilibrium for the possible aetiological variant (rs1165196) in SLC17A1.4

Variation in another renal uric acid transporter SLC2A9 influences serum urate (SU) and fractional excretion of uric acid (FEUA) responses to a fructose load in European, but not Polynesian participants.6 It is unknown whether other genetic factors also contribute to fructose-induced SU responses. The aim of this study was to determine the influence of SLC17A1 variation on SU and FEUA responses during a fructose load.

Healthy volunteers provided serum and urine samples immediately before and 30, 60, 120 and 180 min after ingesting a 64 g fructose solution, as previously described.6 Data were analysed based …

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  • Clinical Trials Registration The study was registered by the Australian Clinical Trials Registry (ACTRN12610001036000).

  • Contributors ND (the guarantor) accepts full responsibility for the work and the conduct of the study, had access to the data, and controlled the decision to publish. ND conceived of the study, contributed to the data interpretation, and drafted the manuscript. MEH, AH, LP and AS recruited participants and coordinated study visits. MEH also managed clinical data entry. MM, MC and APG contributed to data acquisition and genetic data entry. GDG analysed the data. TRM conceived of the study, contributed to the data interpretation, and drafted the manuscript. All authors read and approved the final manuscript.

  • Funding This study was funded by the Health Research Council of New Zealand (grant number 11/1075).

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval The study received ethics approval from the New Zealand Ministry of Health Multiregional Ethics Committee.

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