Korean J Gastroenterol.  2012 Apr;59(4):268-274. 10.4166/kjg.2012.59.4.268.

Chronic Hepatitis C and Insulin Resistance

Affiliations
  • 1Department of Internal Medicine, Keimyung University School of Medicine, Daegu, Korea. chung50@dsmc.or.kr

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.

Keyword

Chronic hepatitis; Hepatitis C virus; Insulin resistance

MeSH Terms

Antiviral Agents/therapeutic use
Diabetes Mellitus, Type 2/complications/drug therapy/metabolism
Genotype
Hepatitis C, Chronic/*drug therapy/etiology/metabolism
Humans
Hypoglycemic Agents/therapeutic use
Insulin/therapeutic use
*Insulin Resistance
Liver Cirrhosis/etiology
Liver Neoplasms/etiology
Sulfonylurea Compounds/therapeutic use

Figure

  • 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.

  • Fig. 2 Scheme of mechanisms for hepatitis C virus-associated insulin resistance and clinical results. HCC, hepatocellular carcinoma.


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