UA

Hyperuricemia has been linked to insulin resistance, pancreatic β-cell dysfunction, and the potential development of type 2 diabetes. Although the direct causal relationship between elevated uric acid (UA) levels and diabetes remains debated, growing evidence suggests that hyperuricemia contributes to pancreatic β-cell damage. Mechanistically, UA has been shown to impair glucose-stimulated insulin secretion and promote β-cell apoptosis through oxidative stress and inflammation. Additionally, UA induces the expression of inducible nitric oxide synthase (iNOS), leading to nitric oxide (NO)-mediated β-cell dysfunction. These findings suggest that hyperuricemia may contribute to the pathogenesis of diabetes by impairing β-cell function. Consequently, UA-lowering therapies could hold potential as a preventive strategy for diabetes in hyperuricemic individuals.