Uric acid‐induced pancreatic β-cell dysfunction

• Main Author: Asghar Ghasemi
• Format: Article
• Language: English
• Published: BMC 2021-02-01
• Series: BMC Endocrine Disorders
• Subjects: Uric acid; Pancreatic β-cell; Type 2 diabetes; Nitric oxide
• Online Access: https://doi.org/10.1186/s12902-021-00698-6

Abstract Hyperuricemia is associated with insulin resistance, pancreatic β-cell dysfunction and consequently with development of type 2 diabetes. Although a direct relationship between high levels of uric acid (UA) and the development of diabetes is still a controversial issue, there is some evidence that strongly points to pancreatic β-cells damage as a result of high serum UA levels. Here, the mechanisms underlying UA-induced β-cell damage are discussed. Available literature indicates that UA can decrease glucose-stimulated insulin secretion and cause β-cell death. The mechanisms underlying these effects are UA-induced oxidative stress and inflammation within the β-cells. UA also stimulates inducible nitric oxide (NO) synthase (iNOS) gene expression leading to NO-induced β-cell dysfunction. Thus hyperuricemia may potentially cause β-cell dysfunction, leading to diabetes. It may be hypothesized that in hyperuricemic subjects, UA-lowering drugs may be beneficial in preventing diabetes.