1. Hepatitis C virus-induced glucose metabolic disorder.
- Author
-
Shoji I, Deng L, Matsui C, and Hotta H
- Subjects
- Forkhead Box Protein O1 physiology, Gluconeogenesis genetics, Glucose metabolism, Glucose Metabolism Disorders metabolism, Glucose Transporter Type 2 metabolism, Hepatitis C metabolism, Humans, Liver metabolism, Signal Transduction physiology, Glucose Metabolism Disorders etiology, Hepacivirus genetics, Hepatitis C complications, Hepatitis C virology, Viral Nonstructural Proteins physiology
- Abstract
Hepatitis C virus (HCV) infection often causes intrahepatic diseases, such as chronic hepatitis, liver chirrohsis, and hepatocellular carcinoma (HCC). Moreover, HCV infection exhibits various extrahepatic manifestations, such as thyroiditis, glucose and lipid metabolic disorder, and iron metabolic disorder. HCV infection is often associated with type 2 diabetes, involving hepatic fibrosis and poor prognosis. Type 2 diabetes increases the risk of HCC. We have been investigating molecular mechanisms of HCV-induced glucose metabolic disorder and we reported that HCV infection promotes hepatic gluconeogenesis through forkhead box O1 (FoxO1)-dependent pathway and that HCV infection suppresses the cell surface expression of glucose transporter 2 (GLUT2), resulting in suppression of glucose uptake. We have found that HCV NS5A protein plays important roles in these two independent pathways. Here we discuss the roles of HCV NS5A in HCV-induced glucose metabolic disorder.
- Published
- 2015
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