Journal List > Korean J Gastroenterol > v.59(4) > 1006934

Chung: Chronic Hepatitis C and Insulin Resistance

Abstract

Insulin resistance is frequently associated with chronic liver disease, and the interaction between hepatitis C virus (HCV) infection and insulin resistance is a major public health issue, bound to increase in the near term. Because of their potential synergism on liver disease severity, a better understanding of the clinical consequences of the relationship between HCV infection and insulin resistance is needed. This translates into accelerated liver disease progression, reduced response to anti-viral agents and, in susceptible individuals, increased risk of developing type 2 diabetes. HCV may also cause hepatic steatosis, especially in patients infected with genotype 3, although the clinical impact of viral steatosis is debated. Little is known regarding the effect of anti-diabetic agents on HCV infection, and a possible association between use of exogenous insulin or a sulfonylurea agents and the development of hepatocellular carcinoma has recently been reported. Thus, modified lifestyle and pharmacological modalities are urgently warranted in chronic hepatitis C with metabolic alterations.

Figures and Tables

Fig. 1
Schematic representation of expected interaction between interferon and insulin at the presence of hepatitis C virus. Dotted lines represent the facts that need more to be identified.
HCV, hepatitis C virus; IFN, interferon; IRS, insulin receptor substrates; PI3K, phosphoinositide 3-kinase; FoxO1, forkhead box protein O 1; PEPCK1, phosphoenolpyruvate carboxykinase 1; JAK1, janus kinase 1; Tyk2, tyrosine kinase 2; STAT1, signal transducers and activators of transcription family of transcription factors 1; Tyr, tyrosine; Ser, serine; ISRE, interferon-sensitive response.
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Fig. 2
Scheme of mechanisms for hepatitis C virus-associated insulin resistance and clinical results. HCC, hepatocellular carcinoma.
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Notes

Financial support: None.

Conflict of interest: None.

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