Hepatitis C Virus Infection: Molecular Pathways to Insulin resistance

被引：28

作者：

Parvaiz, Fahed ^{[1
]}

Manzoor, Sobia ^{[1
]}

Tariq, Huma ^{[1
]}

Javed, Farakh ^{[1
]}

Fatima, Kaneez ^{[1
]}

Qadri, Ishtiaq ^{[1
]}

机构：

[1] Natl Univ Sci & Technol, NUST Ctr Virol & Immunol, Islamabad 44000, Pakistan

来源：

VIROLOGY JOURNAL | 2011年 / 8卷

关键词：

HCV Infection; Molecular Pathways; Insulin Resistance; PROTEIN PHOSPHATASE 2A; CORE PROTEIN; RECEPTOR SUBSTRATE-1; DIABETES-MELLITUS; OXIDATIVE STRESS; HEPATOCELLULAR-CARCINOMA; LIPID-ACCUMULATION; SIGNALING PATHWAY; VIRAL-HEPATITIS; NADPH OXIDASE;

D O I：

10.1186/1743-422X-8-474

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Chronic Hepatitis C virus has the potential of inducing insulin resistance and type 2 Diabetes Mellitus in vitro as well as in vivo. Structural and non-structural proteins of HCV modulate cellular gene expression in such a way that insulin signaling is hampered, concomitantly leads toward diabetes mellitus. A number of mechanisms have been proposed in regard to the HCV induced insulin resistance involving the upregulation of Inflammatory cytokine TNF-alpha, hypophosphorylation of IRS-1 and IRS-2, phosphorylation of Akt, up-regulation of gluconeogenic genes, accumulation of lipids and targeting lipid storage organelles. This review provides an insight of molecular mechanisms by which HCV structural and non-structural proteins can induce insulin resistance.

引用

页数：6

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