Hepatitis C and Insulin Resistance
DOI:
https://doi.org/10.9771/cmbio.v8i1.4378Keywords:
Virus C Hepatitis – Insulin Resistance – Fibrosis – TreatmentAbstract
Chronic infection hepatitis C virus (HCV) infection affects over 200 million people worldwide. Epidemiological data suggest an association between hepatitis C and type 2 diabetes mellitus; the action of the virus C on the glucose metabolism as well as the fibrosing role of the hyperinsulinism have been studied in the last years. The increased prevalence of the type-2 diabetes in hepatitis C virus infection is not exclusively reported for cirrhotic patients. The HCV infection may promote insulin resistance (IR) due to an increased production of Tumor Necrosis Factor alpha (TNF-α), which causes over-expression of the SOCS-3 (suppressor of cytokines substrate) leading to a blockage of the transactivation of GLUT 4 transporter, thus avoiding the glucose subtraction by the cell. The TNF-α was over-expressed in hepatitis due to C virus associated to a more severe fibrosis and the non-response to treatment. Insulin resistance may be also induced by HCV core protein, leading to an increase on the TNF-α. High levels of insulin may directly stimulate the Ito cells mitogenesis and cause an over-regulation of the Connective Growth Factor. It was demonstrated that overweight, hepatic steatosis and IR influence the response to anti-viral treatment with Interferon and Ribavirin, being responsible for the therapeutic failure.Downloads
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Published
2009-03-02
How to Cite
Schinoni, M. I., & Oliveira, A. (2009). Hepatitis C and Insulin Resistance. Journal of Medical and Biological Sciences, 8(1), 67–74. https://doi.org/10.9771/cmbio.v8i1.4378
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Review Articles
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