丙型肝炎病毒感染者糖代谢异常的发病率有不同程度的升高。除了肝源性糖尿病共有的发病机制外,胰岛β细胞功能的减低和胰岛素抵抗(IR)在丙型肝炎病毒感染者糖代谢异常的发病机制中起着重要作用。但IR可能更为重要,而肝脂肪变性、肿瘤坏死因子-α过表达、脂联素水平下降、细胞因子信号抑制因子合成以及铁代谢异常等都可能参与了IR的形成。 Hepatitis C virus infection, the incidence of abnormal glucose metabolism increased to varying degrees. In addition to the common pathogenesis of liver-derived diabetes, the reduction of pancreatic β-cell function and insulin resistance (IR) play an important role in the pathogenesis of abnormal glucose metabolism in HCV-infected individuals. However, IR may be more important, and hepatic steatosis, TNF-α overexpression, decreased adiponectin, cytokine signaling inhibitors and iron metabolism may be involved in the formation of IR.