丙型肝炎病毒感染致糖代谢异常的相关机制研究进展

Progress in mechanisms of abnormal glucose metabolism in patients with hepatitis C virus infection

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。

The morbidity of abnormal glucose metabolism in patients with hepatitis C infection increases gradually. In addition to the common pathogenesis similar to hepatogenous diabetes,malfunciton in pancreaticβ-cell and insulin resistance （IR） play important roles in the pathogenesis of abnormal glucose metabolism in pa-tients with hepatitis C virus infection. IR may be more important,and hepatic steatosis, tumor necrosis factor-αoverexpression,decreased adiponectin, abnormality in synthesis of cytokine signaling inhibitory factors and in iron metabolism may all be involved in IR.