Alcohol cited as risk factor for gout through glucose, apolipoprotein metabolism

 

Tony Merriman
Tony Merriman

Alcohol altered the risk for gout through glucose and apolipoprotein metabolism, according to a recently published study.

“This systematic analysis provides the first evidence for an interaction of alcohol consumption (an established dietary risk factor for gout) with previously identified urate/gout-associated loci GCKR and A1CF that are predominantly involved in glycolysis and lipid homeostasis,” Tony Merriman, PhD, from the University of Otago in New Zealand and colleagues wrote. They added, “Our findings are consistent with alcohol consumption causally contributing to gout via glycolysis and apolipoprotein metabolism.”

Researchers assessed 2,782 patients with or without gout who were genotyped for 29 urate-linked genetic variants. They used additional data from 6,892 patients to test for interaction between loci and alcohol exposure in the risk for hypouricemia.

Among European patients, investigators found interaction of any alcohol exposure with GCKR and A1CF had an influence on the risk for gout, with an interaction term of 0.28 for GCKR and 0.29 for A1CF. At the A1CF loci, alcohol exposure was found to suppress the risk for gout that was conferred by A-positive genotype. At the GCKR loci, alcohol exposure eliminated the effect on gout.

Among Polynesian patients, there was no overall interaction. However, there was evidence for an interaction at the GCKR loci, with an interaction term of 0.62. For all patients, there was no evidence for interaction of A1CF or GCKR with alcohol exposure in the determination of hyperuricemia. – by Will A. Offit

Disclosures: The researchers report no relevant financial disclosures.

 

Tony Merriman
Tony Merriman

Alcohol altered the risk for gout through glucose and apolipoprotein metabolism, according to a recently published study.

“This systematic analysis provides the first evidence for an interaction of alcohol consumption (an established dietary risk factor for gout) with previously identified urate/gout-associated loci GCKR and A1CF that are predominantly involved in glycolysis and lipid homeostasis,” Tony Merriman, PhD, from the University of Otago in New Zealand and colleagues wrote. They added, “Our findings are consistent with alcohol consumption causally contributing to gout via glycolysis and apolipoprotein metabolism.”

Researchers assessed 2,782 patients with or without gout who were genotyped for 29 urate-linked genetic variants. They used additional data from 6,892 patients to test for interaction between loci and alcohol exposure in the risk for hypouricemia.

Among European patients, investigators found interaction of any alcohol exposure with GCKR and A1CF had an influence on the risk for gout, with an interaction term of 0.28 for GCKR and 0.29 for A1CF. At the A1CF loci, alcohol exposure was found to suppress the risk for gout that was conferred by A-positive genotype. At the GCKR loci, alcohol exposure eliminated the effect on gout.

Among Polynesian patients, there was no overall interaction. However, there was evidence for an interaction at the GCKR loci, with an interaction term of 0.62. For all patients, there was no evidence for interaction of A1CF or GCKR with alcohol exposure in the determination of hyperuricemia. – by Will A. Offit

Disclosures: The researchers report no relevant financial disclosures.