SLC2A9: A Key Urate Transporter in Humans
Author Information
Author(s): Mark J Caulfield, Patricia B Munroe, Deb O'Neill, Kate Witkowska, Fadi J Charchar, Manuel Doblado, Sarah Evans, Susana Eyheramendy, Abiodun Onipinla, Philip Howard, Sue Shaw-Hawkins, Richard J Dobson, Chris Wallace, Stephen J Newhouse, Morris Brown, John M Connell, Anna Dominiczak, Martin Farrall, G. Mark Lathrop, Nilesh J Samani, Meena Kumari, Michael Marmot, Eric Brunner, John Chambers, Paul Elliott, Jaspal Kooner, Maris Laan, Elin Org, Gudrun Veldre, Margus Viigimaa, Francesco P Cappuccio, Chen Ji, Roberto Iacone, Pasquale Strazzullo, Kelle H Moley, Chris Cheeseman
Primary Institution: William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, London, United Kingdom
Hypothesis
Is SLC2A9 a functional urate transporter that contributes to the association between urate and blood pressure?
Conclusion
SLC2A9 splice variants act as high-capacity urate transporters, but no association with blood pressure was found.
Supporting Evidence
- SLC2A9 splice variants mediate rapid urate fluxes.
- Urate is transported by SLC2A9 at rates 45- to 60-fold faster than glucose.
- Genetic variants of SLC2A9 are associated with reduced urinary urate clearance.
- No association was found between SLC2A9 and hypertension in a large meta-analysis.
- Urate uptake was at least 2-fold greater in cells overexpressing SLC2A9.
Takeaway
SLC2A9 helps move uric acid in our bodies, but it doesn't seem to affect blood pressure.
Methodology
The study involved expressing SLC2A9 variants in frog eggs and human kidney cells to measure urate transport.
Limitations
The exact causative variant of SLC2A9 responsible for elevated serum urate was not defined.
Participant Demographics
The study included participants from various cohorts, primarily men aged 25-74.
Statistical Information
P-Value
p > 0.33
Confidence Interval
95% CI 0.9 to 1.05
Statistical Significance
p > 0.05
Digital Object Identifier (DOI)
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