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丙型肝炎病毒感染:胰岛素抵抗的分子途径。

Hepatitis C virus infection: molecular pathways to insulin resistance.

机构信息

NUST Center of Virology and Immunology, National University of Sciences and Technology, Islamabad 44000, Pakistan.

出版信息

Virol J. 2011 Oct 18;8:474. doi: 10.1186/1743-422X-8-474.

Abstract

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-α, 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.

摘要

慢性丙型肝炎病毒在体外和体内都有诱导胰岛素抵抗和 2 型糖尿病的潜力。丙型肝炎病毒的结构蛋白和非结构蛋白以这样一种方式调节细胞基因表达,即胰岛素信号受到阻碍,同时导致糖尿病。已经提出了许多与丙型肝炎病毒诱导的胰岛素抵抗有关的机制,包括炎症细胞因子 TNF-α的上调、IRS-1 和 IRS-2 的低磷酸化、Akt 的磷酸化、糖异生基因的上调、脂质积累和靶向脂质储存细胞器。这篇综述提供了丙型肝炎病毒结构蛋白和非结构蛋白诱导胰岛素抵抗的分子机制的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/806d/3206488/9a8ac2ffe12e/1743-422X-8-474-1.jpg

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