Kawaguchi Yasunori, Mizuta Toshihiko
Yasunori Kawaguchi, Toshihiko Mizuta, Department of Internal Medicine, Saga Medical School, Saga 849-8501, Japan.
World J Gastroenterol. 2014 Mar 21;20(11):2888-901. doi: 10.3748/wjg.v20.i11.2888.
Hepatitis C virus (HCV) infection disrupts the normal metabolism processes, but is also influenced by several of the host's metabolic factors. An obvious and significantly detrimental pathophysiological feature of HCV infection is insulin resistance in hepatic and peripheral tissues. Substantial research efforts have been put forth recently to elucidate the molecular mechanism of HCV-induced insulin resistance, and several cytokines, such as tumor necrosis factor-α, have been identified as important contributors to the development of insulin resistance in the distant peripheral tissues of HCV-infected patients and animal models. The demonstrated etiologies of HCV-induced whole-body insulin resistance include oxidative stress, lipid metabolism abnormalities, hepatic steatosis and iron overload. In addition, myriad effects of this condition have been characterized, including glucose intolerance, resistance to antiviral therapy, progression of hepatic fibrosis, development of hepatocellular carcinoma, and general decrease in quality of life. Metabolic-related conditions and disorders, such as visceral obesity and diabetes mellitus, have been shown to synergistically enhance HCV-induced metabolic disturbance, and are associated with worse prognosis. Yet, the molecular interactions between HCV-induced metabolic disturbance and host-associated metabolic factors remain largely unknown. The diet and lifestyle recommendations for chronic hepatitis C are basically the same as those for obesity, diabetes, and metabolic syndrome. Specifically, patients are suggested to restrict their dietary iron intake, abstain from alcohol and tobacco, and increase their intake of green tea and coffee (to attain the beneficial effects of caffeine and polyphenols). While successful clinical management of HCV-infected patients with metabolic disorders has also been achieved with some anti-diabetic (i.e., metformin) and anti-lipid (i.e., statins) medications, it is recommended that sulfonylurea and insulin be avoided.
丙型肝炎病毒（HCV）感染会扰乱正常的代谢过程，但也受到宿主多种代谢因素的影响。HCV感染一个明显且极为有害的病理生理特征是肝脏和外周组织中的胰岛素抵抗。最近人们投入了大量研究精力来阐明HCV诱导胰岛素抵抗的分子机制，并且已确定几种细胞因子，如肿瘤坏死因子-α，是HCV感染患者和动物模型远处外周组织中胰岛素抵抗发展的重要促成因素。已证实的HCV诱导全身胰岛素抵抗的病因包括氧化应激、脂质代谢异常、肝脂肪变性和铁过载。此外，这种情况的多种影响已得到描述，包括葡萄糖不耐受、对抗病毒治疗的抵抗、肝纤维化进展、肝细胞癌的发展以及生活质量普遍下降。内脏肥胖和糖尿病等与代谢相关的状况和疾病已被证明会协同增强HCV诱导的代谢紊乱，并与更差的预后相关。然而，HCV诱导的代谢紊乱与宿主相关代谢因素之间的分子相互作用在很大程度上仍然未知。慢性丙型肝炎的饮食和生活方式建议与肥胖、糖尿病和代谢综合征的基本相同。具体而言，建议患者限制饮食中铁的摄入量，戒酒戒烟，并增加绿茶和咖啡的摄入量（以获得咖啡因和多酚的有益效果）。虽然使用一些抗糖尿病药物（即二甲双胍）和抗脂质药物（即他汀类药物）也成功实现了对患有代谢紊乱的HCV感染患者的临床管理，但建议避免使用磺脲类药物和胰岛素。
