Background: Uric acid (UA) has been suggested as a novel risk factor for diabetes. However, its definite role in this
prevalent disease is still the subject of much discussion because it is always accompanied with other major risk
factors such as obesity and high visceral adiposity. In order to clarify the role of UA in diabetes, this study aimed to
investigate the associations between plasma UA and fasting plasma glucose, HbA1c, lipid profile and inflammatory
markers after accounting for the contribution of other diabetes risk factors such as BMI and VAT fat mass.
Methods: In the present cross-sectional study, 100 non-diabetic middle-aged males (n = 48) and females (n = 52)
were recruited. Central fat distribution measures including android to gynoid fat ratio, VAT and subcutaneous adipose
tissue (SAT) fat mass were determined using dual-energy X-ray absorptiometry (DXA). Biochemical analysis was done
using methods well established for clinical and research laboratories. Multiple linear regression analysis was performed
to analyse the association between plasma UA and the biochemical and central fat distribution measures.
Results: UA was positivly associated with body mass index (BMI) (r (98) = 0.42, P ≤ 0.001), android to gynoid fat ratio
(r (98) = 0.62, P ≤ 0.001) and VAT fat mass (r (96) = 0.55, P ≤ 0.001). UA was also positively associated with plasma
glucose (r (98) = 0.33, P ≤ 0.001), hemoglobin A1c (r (93) = 0.25, P = 0.014), plasma triglyceride (rs (95) = 0.40, P ≤ 0.001),
HDL cholesterol (r (98) = − 0.61, P ≤ 0.001) and CRP (rs (98) = 0.23, P = 0.026). However, these associations were no
longer significant after accounting for BMI or/and VAT fat mass. No significant association was observed between UA
and SAT fat mass (r (97) = 0.02, P ≥ 0.05), Total cholesterol (r (98) = 0.03, P ≥ 0.05), LDL cholesterol (r (98) = 0.13, P ≥ 0.
05), TNF-α (r (97) = 0.12, P ≥ 0.05) and IL-6 (r (96) = −0.02, P ≥ 0.05).
Conclusion: Results from this study suggest, for the first time, that the association between plasma UA and glucose in
a non-diabetic population is not direct but rather dependent on VAT fat mass.