Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, P.O. Box: 19395-4763, No. 24, Parvaneh Street, Velenjak, Tehran, Iran.
BMC Endocr Disord. 2021 Feb 16;21(1):24. doi: 10.1186/s12902-021-00698-6.
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.
高尿酸血症与胰岛素抵抗、胰岛β细胞功能障碍有关，进而导致 2 型糖尿病的发生。虽然高尿酸（UA）水平与糖尿病发展之间存在直接关系仍存在争议，但有一些证据强烈表明高血清 UA 水平会导致胰岛β细胞损伤。在这里，我们讨论了 UA 诱导的β细胞损伤的机制。现有文献表明，UA 可降低葡萄糖刺激的胰岛素分泌并导致β细胞死亡。这些作用的机制是 UA 诱导的β细胞内氧化应激和炎症。UA 还可刺激诱导型一氧化氮合酶（iNOS）基因表达，导致 NO 诱导的β细胞功能障碍。因此，高尿酸血症可能会导致β细胞功能障碍，进而导致糖尿病。可以假设，在高尿酸血症患者中，降低 UA 的药物可能有益于预防糖尿病。
