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Insulin resistance and sustained virological response in hepatitis C: from bench to bedside.

机译:丙型肝炎的胰岛素抵抗和持续的病毒学应答:从板凳到床边。

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摘要

Insulin resistance is the main feature of metabolic syndrome and is characterised by hyperinsulinaemia in patients with normal fasting glucose. It has been associated with an increased risk of developing diabetes mellitus, cardiovascular disease and non-alcoholic fatty liver disease (1). In recent years, a large body of literature, including molecular, epidemiological, randomised-con-trolled trials and observational studies, has highlighted the interaction between hepatitis C and insulin resistance (2). Molecular studies demonstrated the ability of hepatitis C virus (HCV) to promote insulin resistance by interfering with the intracellular signalling of insulin. Transgenic mice expressing core protein developed stea-tosis, insulin resistance and type 2 diabetes mellitus.
机译:胰岛素抵抗是代谢综合征的主要特征,其特征是空腹血糖正常的患者出现高胰岛素血症。它与患糖尿病,心血管疾病和非酒精性脂肪肝疾病的风险增加有关(1)。近年来,大量文献,包括分子,流行病学,随机对照试验和观察性研究,都强调了丙型肝炎与胰岛素抵抗之间的相互作用(2)。分子研究表明,丙型肝炎病毒(HCV)通过干扰胰岛素的细胞内信号传导来增强胰岛素抵抗的能力。表达核心蛋白的转基因小鼠发展为脂肪变性,胰岛素抵抗和2型糖尿病。

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