Polymorphisms in the uric acid transporter SLC2A9
(GLUT9) are associated with elevated serum urate and
the risk of gout, but SLC2A9 polymorphisms are not associated
with obesity or the metabolic syndrome phenotype.
However, SLC2A9 exports urate out of cells [60,61], in
contrast to the transporter URAT1 (SLC22A12), which
mediates entry (uptake) of urate into cells. URAT1 is located
on adipocytes [62,63] and URAT1 transporter gene
polymorphisms in hypertensive subjects are associated
with body mass index (BMI), waist circumference, HDL
cholesterol, and the metabolic syndrome; - they accounted
for 7% of the variation of BMI in Caucasians. However,
there was no such association in African Americans [64].
In support of an involvement of adipocytes is a study in
obese mice with the metabolic syndrome [65]. These mice
are hyperuricaemic and lowering urate levels with allopurinol
improves their pro-inflammatory phenotype in adipose
tissue, with decreased macrophage infiltration and
reduced insulin resistance.