Interaction of IFNL3 with insulin resistance, steatosis and lipid metabolism in chronic hepatitis C virus infection

World J Gastroenterol. 2013 Nov 7;19(41):7055-61. doi: 10.3748/wjg.v19.i41.7055.

Abstract

Metabolic changes are inextricably linked to chronic hepatitis C (CHC). Recently polymorphisms in the IFNL3 (IL28B) region have been shown to be strongly associated with spontaneous and treatment induced recovery from hepatitis C virus (HCV) infection. Further, circumstantial evidence suggests a link between IFNL3 single nucleotide polymorphisms and lipid metabolism, steatosis and insulin resistance in CHC. The emerging picture suggests that the responder genotypes of IFNL3 polymorphisms are associated with a higher serum lipid profile, and less frequent steatosis and insulin resistance. This review analyzes the current data regarding this interaction and its meaning for HCV pathogenesis and disease progression.

Keywords: Chronic hepatitis C; IFNL3; Insulin resistance; Lipids.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers / blood
  • Disease Progression
  • Fatty Liver / genetics*
  • Fatty Liver / metabolism
  • Genetic Predisposition to Disease
  • Hepatitis C, Chronic / complications
  • Hepatitis C, Chronic / genetics*
  • Hepatitis C, Chronic / metabolism
  • Hepatitis C, Chronic / virology
  • Humans
  • Insulin Resistance / genetics*
  • Interferons
  • Interleukins / genetics*
  • Interleukins / metabolism
  • Lipid Metabolism / genetics*
  • Lipids / blood
  • Non-alcoholic Fatty Liver Disease
  • Phenotype
  • Polymorphism, Single Nucleotide*
  • Prognosis
  • Risk Factors

Substances

  • Biomarkers
  • interferon-lambda, human
  • Interleukins
  • Lipids
  • Interferons