Failure of beta-cell function to compensate lack of insulin action in hyperuricemic subjects

Background Elevated serum uric acid has been related to insulin resistance, but there are no studies regarding its association with beta-cell function. In this study, we examine the response of beta-cell function to compensate insulin resistance in hyperuricaemic subjects. Methods Population-based cross-sectional study. A total of 212 healthy individuals, men and non-pregnant women, aged 20-65 years, were randomly recruited and allocated into groups with hyperuricaemia or normouricaemia that were matched by value of Belfiore index. Hyperuricaemia was defined by serum uric acid concentration >= 416 mu mol/L in men and >= 357 mu mol/L in women. To evaluate the compensation of insulin secretion to variation of insulin sensitivity, we used a surrogate of the hyperbolic model of beta-cell function based on Belfiore and Homeostasis Model Analysis beta-cell (HOMA-beta) indexes; the area under curves (AUC) was calculated. The association between the uric acid levels and the AUC was estimated using a multivariate regression analysis adjusted by age, sex, and waist circumference. Results Hyperuricaemia was identified in 77 (36.3%) individuals. A total of 39 (50.6%) hyperuricaemic and 44 (32.6%) normouricaemic subjects had diagnosis of impaired glucose tolerance (IGT), p = 0.01. In the total population, the AUCs in the hyperuricaemic and normouricaemic groups were 1.60725 cm(2) and 3.9819 cm(2), respectively (odds ratio [OR] 3.9; CI 95% 1.4-8.9). Among the 83 individuals with IGT, the AUCs in the subgroups with and without hyperuricaemia were 0.8495 cm(2) and 2.42075 cm(2), respectively (OR 2.7; CI 95% 1.3-10.1). Conclusions Our results show the failure of beta-cell function to compensate variation of insulin sensitivity in the hyperuricaemic individuals. Copyright (C) 2009 John Wiley & Sons, Ltd.