Insufficient compensatory pancreatic β-cells function might be closely associated with hyperuricemia in U.S. adults: evidence from the National Health and Nutrition Examination Survey

Abstract

Abstract Background The prevalence of hyperuricemia (HUA) is gradually increasing worldwide. HUA is closely related to diabetes, but the relationship between HUA and pancreatic β-cells function in the population is unclear. The purpose of this article is to investigate the association between pancreatic β-cells and HUA. Methods This cross-sectional study examined the association between pancreatic β-cells and HUA in 1999–2004 using data from the National Health and Nutrition Examination Survey (NHANES). Subjects were divided into two groups: HUA and non-HUA. Pancreatic β-cells function levels were assessed using homeostasis model assessment version 2-%S (HOMA2-%S), homeostasis model assessment version 2-%B (HOMA2-%B) and disposition index (DI). Multivariate logistic regression models and restricted cubic spline models were fitted to assess the association of pancreatic β-cells function with HUA. Results The final analysis included 5496 subjects with a mean age of 46.3 years (standard error (SE), 0.4). The weighted means of HOMA2-%B, HOMA2-%S and DI were 118.1 (SE, 1.0), 69.9(SE, 1.1) and 73.9 (SE, 0.7), respectively. After adjustment for major confounders, participants in the highest quartile of HOMA2-%B had a higher risk of HUA (OR = 2.55, 95% CI: 1.89–3.43) compared to participants in the lowest quartile. In contrast, participants in the lowest quartile of HOMA2-%S were significantly more likely to have HUA than that in the highest quartile (OR = 3.87, 95% CI: 2.74–5.45), and similar results were observed in DI (OR = 1.98, 95% CI: 1.32–2.97). Multivariate adjusted restricted cubic spline analysis found evidence of non-linear associations between HOMA2-%B, HOAM2-%S, DI and the prevalence of HUA. Conclusion Our finding illustrated the indicators of inadequate β-cells compensation might be a new predictor for the presence of HUA in U.S. adults, highlighting a critical role of pancreatic β-cells function on HUA.