Badar Sadaf, Khubaib Bushra, Idrees Muhammad, Hussain Abrar, Awan Zunaira, Butt Sadia, Afzal Samia, Akram Madeeha, Fatima Zareen, Aftab Mahwish, Saleem Sana, Munir Sara, Rauff Bisma, Naudhani Mahrukh, Ali Liaquat, Ali Muhammaad, Rehman Irshadul
National Centre of Excellence in Molecular Biology, University of the Punjab, Lahore, Pakistan.
Hepat Mon. 2012 Jan;12(1):11-5. Epub 2012 Jan 20.
HCV infection is strongly associated with development of insulin resistance and type-2 diabetes, however molecular mechanism of these associations is not known. The aim of this review was to conduct a comprehensive literature search to understand the nature of the association between hepatitis C virus (HCV) infection and insulin resistance (IR). We also explored the role of HCV core protein and NS5a in modulating the course of the insulin-signaling pathway.
We searched Directory of Open Access Journals (DOAJ) Google Scholar, Pubmed (NLM), LISTA (EBSCO), Web of Science (TS and PakMediNet).
Emerging evidence suggests an association between HCV infection and carotid/coronary vascular disease. IR appears to be a dominant underlying cause of accelerated atherosclerosis in patients with chronic hepatitis C (CHC). HCV can induce IR directly through the stimulation of SOCS3 and PPA2, and both of these molecules have been shown to inhibit interferon-α signaling. Improvement of insulin sensitivity may increase the response rate to antiviral treatment and prevent IR complications, including vascular diseases. The results of several clinical trials that have used insulin sensitizers (metformin and PPAR-γ agonists) have been inconclusive.
Beside the association between HCV and IR, the published data also have showed the possible association of HCV core and NS5A protein with IR.
丙型肝炎病毒(HCV)感染与胰岛素抵抗及2型糖尿病的发生密切相关,然而这些关联的分子机制尚不清楚。本综述的目的是进行全面的文献检索,以了解丙型肝炎病毒(HCV)感染与胰岛素抵抗(IR)之间关联的本质。我们还探讨了HCV核心蛋白和NS5a在调节胰岛素信号通路进程中的作用。
我们检索了开放获取期刊目录(DOAJ)、谷歌学术、PubMed(美国国立医学图书馆)、LISTA(EBSCO)、科学引文索引(SCI)和巴基斯坦医学网。
新出现的证据表明HCV感染与颈动脉/冠状动脉血管疾病之间存在关联。胰岛素抵抗似乎是慢性丙型肝炎(CHC)患者动脉粥样硬化加速的主要潜在原因。HCV可通过刺激细胞因子信号抑制因子3(SOCS3)和蛋白磷酸酶2A(PPA2)直接诱导胰岛素抵抗,并且这两种分子均已被证明可抑制干扰素-α信号传导。改善胰岛素敏感性可能会提高抗病毒治疗的反应率,并预防包括血管疾病在内的胰岛素抵抗并发症。几项使用胰岛素增敏剂(二甲双胍和过氧化物酶体增殖物激活受体γ激动剂)的临床试验结果尚无定论。
除了HCV与胰岛素抵抗之间的关联外,已发表的数据还显示HCV核心蛋白和NS5A蛋白与胰岛素抵抗可能存在关联。