title: Hepatitis C virus and metabolic disorder interactions towards liver damage and atherosclerosis.
abstract: Hepatitis C virus (HCV) is one of the main causes of liver disease worldwide, and alterations of glucose metabolism have reached pandemic proportions in western countries. However, the frequent coexistence between these two conditions is more than simply coincidental, since HCV can induce insulin resistance through several mechanisms. Indeed, the virus interferes with insulin signaling both directly and indirectly, inducing the production of pro-inflammatory cytokines. Furthermore, the entire viral life cycle has strict interconnections with lipid metabolism, and HCV is responsible for a "viral" steatosis which is frequently superimposed to a "metabolic" one. Several evidences suggest that HCV-induced metabolic disorders contribute both to the evolution of liver fibrosis and, likely, to the progression of the other disorders which are typically associated with altered metabolism, in particular atherosclerosis. In the present review, we will examine in depth the links between HCV infection and insulin resistance, liver steatosis and diabetes, and analyze the impact of these interactions on the progression of liver fibrosis and atherosclerosis. Special attention will be focused on the highly debated topic of the relationship between HCV infection and cardiovascular disease. The available clinical literature on this item will be broadly reviewed and all the mechanisms possibly implied will be discussed.
authors.affiliation: Umberto Vespasiani-Gentilucci, Paolo Gallo, Antonio De Vincentis, Giovanni Galati, Antonio Picardi, Internal Medicine and Hepatology Unit, University Campus Bio-Medico of Rome, 00128 Rome, Italy.
authors.forename: Umberto
authors.initials: U
authors.lastname: Vespasiani-Gentilucci
authors.affiliation: Umberto Vespasiani-Gentilucci, Paolo Gallo, Antonio De Vincentis, Giovanni Galati, Antonio Picardi, Internal Medicine and Hepatology Unit, University Campus Bio-Medico of Rome, 00128 Rome, Italy.
authors.forename: Paolo
authors.initials: P
authors.lastname: Gallo
authors.affiliation: Umberto Vespasiani-Gentilucci, Paolo Gallo, Antonio De Vincentis, Giovanni Galati, Antonio Picardi, Internal Medicine and Hepatology Unit, University Campus Bio-Medico of Rome, 00128 Rome, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: De Vincentis
authors.affiliation: Umberto Vespasiani-Gentilucci, Paolo Gallo, Antonio De Vincentis, Giovanni Galati, Antonio Picardi, Internal Medicine and Hepatology Unit, University Campus Bio-Medico of Rome, 00128 Rome, Italy.
authors.forename: Giovanni
authors.initials: G
authors.lastname: Galati
authors.affiliation: Umberto Vespasiani-Gentilucci, Paolo Gallo, Antonio De Vincentis, Giovanni Galati, Antonio Picardi, Internal Medicine and Hepatology Unit, University Campus Bio-Medico of Rome, 00128 Rome, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: Picardi
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000209:etiology*; D005234:Fatty Liver / Q000209:etiology*; D006526:Hepatitis C / Q000150:complications* / Q000378:metabolism*; D006801:Humans; D007333:Insulin Resistance; D008103:Liver Cirrhosis / Q000209:etiology
keywords: Atherosclerosis; Cardiovascular risk; Diabetes mellitus; Fibrosis; Hepatitis C virus; Insulin resistance; Metabolism; Steatosis