丙型肝炎病毒所致胰岛素抵抗相关分子的研究进展

李静; 陈红; 张立婷; 刘鹏

丙型肝炎病毒所致胰岛素抵抗相关分子的研究进展

兰州大学第一医院感染科

详细信息

中图分类号: R512.63
计量
- 文章访问数: 3424
- HTML全文浏览量: 21
- PDF下载量: 1038
- 被引次数: 0
出版历程
- 出版日期: 2011-05-20

Progress in molecular research related to insulin resistance in chronic hepatitis C

摘要

摘要: 慢性丙型肝炎(CHC)患者易发生胰岛素抵抗(IR)。实验表明CHC相关IR不但与肝脂肪变性、肝纤维化、食管静脉曲张、肝细胞肝癌、肝癌扩散及一些肝外临床表现有关,还降低了以干扰素(IFN)联合利巴韦林为基础的抗病毒治疗早期及持续应答率。已有较多实验利用各种模型分析了丙型肝炎病毒(CHV)导致IR的发病机制,现对当前研究已知的几个分子及其机制做一综述。
- 胰岛素抗药性 /
- 肝炎,丙型,慢性 /
- 肝炎病毒属
Abstract: Patients with chronic hepatitis C are liable to insulin resistance.Evidence suggests that insulin resistance is not only related with steatosis, hepatic fibrosis, esophageal varices, hepatocarcinogenesis, proliferation of hepatocellular carcinoma and some extrahepatic manifestations but also related with the reduction of the early and sustained virological response to the interferon-alpha-based therapy.The effect of HCV on insulin signaling has been analyzed in some experiments using kinds of models.The authors review the current understanding of the Molecular mechanisms of insulin resistance in chronic hepatitis C.
- insulin resistance /
- hepatitis C /
- chronic

HTML全文

参考文献(23)

[1]Hui JM, Sud A, Farrell GC, et al.Insulin resistance is associated with chronic hepatitis C virus infection and fibrosis progression[J].Gastroenterology, 2003, 125 (6) :1695-1704.

[2]Moucari R, Asselah T, Cazals-Hatem D, et al.Insulin resistance in chronic hepatitis C:association with genotypes 1 and 4, serum HCV RNA level, and liver fibrosis[J].Gastroenterology, 2008, 134 (2) :416-423.

[3]Leandro G, Mangia A, Hui J, et al.Relationship between J Clini Hepatol, May 2011, Vol.27, No.5steatosis, inflammation, and fibrosis in chronic hepatitis C:a meta-analysis of individual patient data[J].Gastroenterology, 2006, 130 (6) :1636-1642.

[4]Kawaguchi Y, Mizuta T, Oza N, et al.Eradication of hepatitis C virus by interferon improves whole-body insulin resistance and hyperinsulinaemia in patients with chronic hepatitis C[J].Liver Int, 2009, 29 (6) :871-877.

[5]Khattab M, Emad M, Abdelaleem A, et al.Pioglitazone improves virological response to peginterferon alpha-2b/ribavirin combination therapy in hepatitis C genotype 4 patients with insulin resistance[J].2010, Liver Int, 30 (3) :447-454.

[6]Miyaaki H, Ichikawa T, Nakao K, et al.Predictive value of the phosphorylation of signal transducers and activators of transcription in the outcome of interferon therapy for chronic hepatitis C[J].Intervirology, 2008, 51 (6) :394-399.

[7]Pazienza V, Clement S, Pugnale P, et al.The hepatitis C virus core protein of genotypes 3a and 1b downregulates insulin receptor substrate 1 through genotype-specific mechanisms[J].Hepatology, 2007, 45 (5) :1164-1171.

[8]Miyamoto H, Moriishi K, Moriya K, et al.Involvement of the PA28gamma-dependent pathway in insulin resistance induced by hepatitis C virus core protein[J].Virol, 2007, 81 (4) :1727-1735.

[9]Moriishi K, Shoji I, Mori Y, et al.Involvement of PA-28gamma in the propagation of hepatitis C virus[J].Hepatology, 2010, 52 (2) :411-420.

[10]Bernsmeier C, Duong FH, Christen V, et al.Virus-induced over-expression of protein phosphatase 2A inhibits insulin signalling in chronic hepatitis C[J].Hepatol, 2008, 49 (3) :429-440.

[11]Qiu Y, Ting Mao, Zhang Y, et al.A crucial role for RACK1 in the regulation of glucose-stimulated IRE1alpha activation in pancreatic beta cells[J].Sci Signal, 2010, 3 (106) :ra7.

[12]PersicoM, Svelto M, Andolfo I, et al.SOCS3 and IRS-1 gene expression differs between genotype 1 and genotype 2 hepatitis C virus-infected HepG2 cells[J].Clin Chem Lab Med, 2009, 47 (10) :1217-1225.

[13]Miyaaki H, Ichikawa T, Nakao K, et al.Predictive value of suppressor of cytokine signal 3 (SOCS3) in the outcome of interferon therapy in chronic hepatitis C[J].Hepatol Res, 2009, 39 (9) :850-855.

[14]Bensinger SJ, Tontonoz P.Integration of metabolism and inflammation by lipid-activated nuclear receptors[J].Nature, 2008, 454 (7203) :470-477.

[15]Kim K, Ha E, Park JY, et al.Hepatitis C virus NS5A protein increases hepatic lipid accumulation via induction of activation and expression of PPARgamma[J].FEBS Let, 2009, 583 (17) :2720-2726.

[16]Mankouri J, Tedbury PR, Gretton S, et al.Enhanced hepatitis C virus genome replication and lipid accumulation mediated by inhibition of AMP-activated protein kinase[J].Proc Natl Acad Sci U S A, 2010, 107 (25) :11549-11554.

[17]Vidali M, Tripodi MF, Ivaldi A, et al.Interplay between oxidative stress and hepatic steatosis in the progression of chronic hepatitis C[J].J Hepatol, 2008, 48 (3) :399-406.

[18]Evans J, Goldfine I, Maddux B, et al.Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction?[J].Diabetes, 2003, 52 (1) :1-8.

[19]Majano PL, Medina J, Zubía I, et al.N-Acetyl-cysteine modulates inducible nitric oxide synthase gene expression in human hepatocytes[J].J Hepatol, 2004, 40 (4) :632-637.

[20]Guo XQ, Wang YJ, Chang YZ, et al.The role of hepcidin on HCV-induced liver damage[J].Zhonghua GanZangBing ZaZhi, 2010, 18 (4) :318-320.

[21]Takeo M, Kobayashi Y, Fujita N, et al.Upregulation of transferrin receptor 2 and ferroportin 1 mRNA in the liver of patients with chronic hepatitis C[J].Gastroenterol Hepatol, 2005, 20 (4) :562-569.

[22]Arkan MC, Hevener AL, Greten FR, et al.IKK-beta links inflammation to obesity-induced insulin resistance[J].Nat Med, 2005, 11 (2) :191-198.

[23]Aksoz K, Unsal B, Kirci A, et al.The relationship between chronic HCV infection and the level of plasma adiponectin[J].Turk J Gastroenterol, 2008, 19 (4) :254-257.

施引文献

资源附件(0)

访问统计