糖尿病性周围神经病变（DPN）是糖尿病常见的并发症之一。DPN 的发病机制尚未明确，是由多因素互相作用的综合结果。 以高糖参与的异常代谢通路为基础，其中包括多元醇通路、己糖胺通路、蛋白激酶 C 通路及糖基化终末产物堆积 。这些代谢通路最 终都会引起细胞内氧化应激反应，诱导免疫反应。另外、脂代谢、生长因子、胰岛素抵抗及神经营养不足等因素直接或间接地参与和 影响了代谢通路。通过对 DPN 发生机制的进一步研究，有利于探索新的治疗方向。文章主要系统阐述 DPN 发生机制，对已知的机制 进行补充和完善。

 Diabetic peripheral neuropathy is one of the most common complication of diabetes, which causes pain and inconvenience to the patients and reduces the quality of life. The pathogenesis of DPN is not yet clear, which is the result of multi-factor interaction. Hyperglycemia is clearly an important factor for its pathogenesis and development. Several metabolic pathways have been identified that may relate to the cellular metabolic including glucose flux through the polyol pathway, the hexosamine pathway, production of the protein kinase C isoforms and accumulation of advanced glycation end products. The additive imbalance of these pathways alters the mito-chondrial redox state of the cell and results in oxidative stress. It also causes inflammation. Additionally, growth factors, insulin resistance and lipid abnormality may participate in the metabolic pathway. This review is aimed to elaborate the pathogenesis and complement the known mechanism.