It has been well established that advanced glycation end-products (AGEs) have a strong correlation with diabetes and its secondary complications. Moreover, dicarbonyls, especially, methylglyoxal (MG) and glyoxal, accelerate AGEs formation and hence, have potential roles in the pathogenesis of diabetes. They can also induce oxidative stress and concomitantly decrease the efficiency of antioxidant enzymes. Increased proinflammatory cytokines (tumor necrosis factor-α and interleukin- 1β) are secreted by monocytes due to the dicarbonyl-modified proteins. High levels of blood dicarbonyls have been identified in diabetes and its associated complications (retinopathy, nephropathy and neuropathy). This review aims to provide a better understanding by including in-depth information about the formation of MG and glyoxal through multiple pathways with a focus on their biological functions and detoxifications. The potential role of these dicarbonyls in secondary diabetic complications is also discussed.

众所周知，晚期糖基化终产物（AGEs）与糖尿病及其继发性并发症有很强的相关性。此外，二羰基化合物，尤其是甲基乙二醛（MG）和乙二醛，可加速AGEs的形成，因此在糖尿病的发病机理中具有潜在作用。它们还可以诱导氧化应激并因此降低抗氧化酶的效率。由于二羰基修饰的蛋白质，单核细胞分泌增加的促炎细胞因子（肿瘤坏死因子-α和白介素-1β）。在糖尿病及其相关并发症（视网膜病变，肾病和神经病）中已发现高水平的血液二羰基化合物。这篇综述旨在通过包含有关MG和乙二醛通过多种途径的形成的深入信息来提供更好的理解，重点在于它们的生物学功能和排毒作用。还讨论了这些二羰基在继发性糖尿病并发症中的潜在作用。