Sugar-sweetened beverage consumption: a risk factor for prevalent gout with SLC2A9 genotype-specific effects on serum urate and risk of gout
- Caitlin Batt1,
- Amanda J Phipps-Green1,
- Michael A Black1,
- Murray Cadzow1,
- Marilyn E Merriman1,
- Ruth Topless1,
- Peter Gow2,
- Andrew Harrison3,
- John Highton4,
- Peter Jones5,
- Lisa Stamp6,
- Nicola Dalbeth5,
- Tony R Merriman1
- 1Department of Biochemistry, University of Otago, Dunedin, New Zealand
- 2Department of Rheumatology, Middlemore Hospital, Auckland, New Zealand
- 3Department of Medicine, University of Otago, Wellington, New Zealand
- 4Department of Medicine, University of Otago, Dunedin, New Zealand
- 5Department of Medicine, University of Auckland, Auckland, New Zealand
- 6Department of Medicine, University of Otago, Christchurch, New Zealand
- Correspondence to Dr Tony R Merriman, Department of Biochemistry, University of Otago, Dunedin, 9054, New Zealand;
- Received 11 March 2013
- Revised 25 June 2013
- Accepted 15 July 2013
- Published Online First 11 September 2013
Objective Consumption of high fructose corn syrup (HFCS)-sweetened beverages increases serum urate and risk of incident gout. Genetic variants in SLC2A9, that exchanges uric acid for glucose and fructose, associate with gout. We tested association between sugar (sucrose)-sweetened beverage (SSB) consumption and prevalent gout. We also tested the hypothesis that SLC2A9 genotype and SSB consumption interact to determine gout risk.
Methods Participants were 1634 New Zealand (NZ) European Caucasian, Māori and Pacific Island people and 7075 European Caucasians from the Atherosclerosis Risk in Communities (ARIC) study. NZ samples were genotyped for rs11942223 and ARIC for rs6449173. Effect estimates were multivariate adjusted.
Results SSB consumption increased gout risk. The OR for four drinks/day relative to zero was 6.89 (p=0.045), 5.19 (p=0.010) and 2.84 (p=0.043) for European Caucasian, Māori and Pacific Islanders, respectively. With each extra daily SSB serving, carriage of the gout-protective allele of SLC2A9 associated with a 15% increase in risk (p=0.078), compared with a 12% increase in non-carriers (p=0.002). The interaction term was significant in pooled (pInteraction=0.01) but not meta-analysed (pInteraction=0.99) data. In ARIC, with each extra daily serving, a greater increase in serum urate protective allele carriers (0.005 (p=8.7×10−5) compared with 0.002 (p=0.016) mmol/L) supported the gout data (pInteraction=0.062).
Conclusions Association of SSB consumption with prevalent gout supports reduction of SSB in management. The interaction data suggest that SLC2A9-mediated renal uric acid excretion is physiologically influenced by intake of simple sugars derived from SSB, with SSB exposure negating the gout risk discrimination of SLC2A9.
This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/