PMID- 20714007 OWN - NLM STAT- MEDLINE DCOM- 20101213 LR - 20130516 IS - 1665-2681 (Print) IS - 1665-2681 (Linking) VI - 9 Suppl DP - 2010 TI - Insulin resistance, hepatic steatosis and hepatitis C: a complex relationship with relevant clinical implications. PG - 112-8 AB - 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. FAU - Arrese, Marco AU - Arrese M AD - School of Medicine, Pontificia Universidad Catolica de Chile, Marcoleta #367, Santiago, Chile. marrese@med.puc.cl FAU - Riquelme, Arnoldo AU - Riquelme A FAU - Soza, Alejandro AU - Soza A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review PL - Mexico TA - Ann Hepatol JT - Annals of hepatology JID - 101155885 RN - 0 (Antiviral Agents) RN - 0 (Hypoglycemic Agents) SB - IM MH - Antiviral Agents/therapeutic use MH - Energy Intake MH - Fatty Liver/epidemiology/metabolism/*physiopathology/therapy MH - Hepatitis C/drug therapy/epidemiology/metabolism/*physiopathology MH - Humans MH - Hypoglycemic Agents/therapeutic use MH - *Insulin Resistance MH - Risk Reduction Behavior MH - Treatment Outcome MH - Viral Load MH - Weight Loss EDAT- 2010/08/28 06:00 MHDA- 2010/12/14 06:00 CRDT- 2010/08/18 06:00 PHST- 2010/08/18 06:00 [entrez] PHST- 2010/08/28 06:00 [pubmed] PHST- 2010/12/14 06:00 [medline] AID - 916036 [pii] PST - ppublish SO - Ann Hepatol. 2010;9 Suppl:112-8.