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Interaction of the GCKR and A1CF loci with alcohol consumption to influence the risk of gout

Overview of attention for article published in Arthritis Research & Therapy, July 2017
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Title
Interaction of the GCKR and A1CF loci with alcohol consumption to influence the risk of gout
Published in
Arthritis Research & Therapy, July 2017
DOI 10.1186/s13075-017-1369-y
Pubmed ID
Authors

Humaira Rasheed, Lisa K. Stamp, Nicola Dalbeth, Tony R. Merriman

Abstract

Some gout-associated loci interact with dietary exposures to influence outcome. The aim of this study was to systematically investigate interactions between alcohol exposure and urate-associated loci in gout. A total of 2792 New Zealand European and Polynesian (Māori or Pacific) people with or without gout were genotyped for 29 urate-associated genetic variants and tested for a departure from multiplicative interaction with alcohol exposure in the risk of gout. Publicly available data from 6892 European subjects were used to test for a departure from multiplicative interaction between specific loci and alcohol exposure for the risk of hyperuricemia (HU). Multivariate adjusted logistic and linear regression was done, including an interaction term. Interaction of any alcohol exposure with GCKR (rs780094) and A1CF (rs10821905) influenced the risk of gout in Europeans (interaction term 0.28, P = 1.5 × 10(-4); interaction term 0.29, P = 1.4 × 10(-4), respectively). At A1CF, alcohol exposure suppressed the gout risk conferred by the A-positive genotype. At GCKR, alcohol exposure eliminated the genetic effect on gout. In the Polynesian sample set, there was no experiment-wide evidence for interaction with alcohol in the risk of gout (all P > 8.6 × 10(-4)). However, at GCKR, there was nominal evidence for an interaction in a direction consistent the European observation (interaction term 0.62, P = 0.05). There was no evidence for an interaction of A1CF or GCKR with alcohol exposure in determining HU. These data support the hypothesis that alcohol influences the risk of gout via glucose and apolipoprotein metabolism. In the absence of alcohol exposure, genetic variants in the GCKR and A1CF genes have a stronger role in gout.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 3 11%
Student > Doctoral Student 3 11%
Student > Postgraduate 2 7%
Student > Master 2 7%
Student > Ph. D. Student 2 7%
Other 5 19%
Unknown 10 37%
Readers by discipline Count As %
Medicine and Dentistry 6 22%
Biochemistry, Genetics and Molecular Biology 3 11%
Agricultural and Biological Sciences 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Social Sciences 1 4%
Other 3 11%
Unknown 11 41%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 July 2017.
All research outputs
#20,660,571
of 25,382,440 outputs
Outputs from Arthritis Research & Therapy
#2,907
of 3,380 outputs
Outputs of similar age
#251,586
of 325,782 outputs
Outputs of similar age from Arthritis Research & Therapy
#60
of 67 outputs
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