Insulin resistance, hepatic steatosis and hepatitis C: A complex relationship with relevant clinical implications

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Insulin resistance, hepatic steatosis and hepatitis C: A complex relationship with relevant clinical implications

Journal Title: Annals of Hepatology - Year 2010, Vol 9, Issue 0

Abstract

Insulin resistance (IR) is a common pathophysiological condition where higher-than-normal concentrations of insulin are needed to maintain a normal glycemia and adequate glucose utilization in insulin target tissues. A high proportion (50-80%) of patients chronically infected with the hepatitis C virus (HCV) exhibit evidence of IR. Basic and clinical studies have disclosed a complex bidirectional relationship between IR and HCV infection that has important clinical implications. HCV infection may promote IR through direct viral-dependent mechanisms or due to activation of the inflammatory response resulting in increased production of Tumor Necrosis Factor-a and other cytokine-related molecules. These abnormalities may act synergistically with pre-existing metabolic risk factors and result in the development of hepatic steatosis and type 2 diabetes mellitus (T2DM) which are frequently found in the setting of HCV infection. Moreover, in addition to underlying metabolic abnormalities leading to its development hepatic steatosis also exhibit genotype-specific pathogenic mechanisms. A number of studies have shown that hepatic steatosis is associated to fibrosis progression in patients with HCV and that IR has a negative impact on the response rates to interferon-a-based therapy. Thus, modification of these factors through life-style changes or pharmacological agents may represent an undervalued specific target of therapy aiming to improve sustained virological response rates and reduce HCV related-morbidity and mortality.

Authors and Affiliations

Arnoldo Riquelme, Alejandro Soza

Keywords

Fatty Liver Insulin diabetes metabolic syndrome

EP ID EP77974
DOI -
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