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

dc.contributor.authorArrese, Marco
dc.contributor.authorRiquelme, Arnoldo
dc.contributor.authorSoza, Alejandro
dc.date.accessioned2024-01-10T13:13:55Z
dc.date.available2024-01-10T13:13:55Z
dc.date.issued2010
dc.description.abstractInsulin 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-alpha 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.
dc.description.funderFondo Nacional De Ciencia y Tecnologia de Chile (Fondecyt)
dc.fechaingreso.objetodigital2024-04-16
dc.format.extent7 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1016/S1665-2681(19)31735-1
dc.identifier.issn1665-2681
dc.identifier.pubmedidMEDLINE:20714007
dc.identifier.urihttps://doi.org/10.1016/S1665-2681(19)31735-1
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/78354
dc.identifier.wosidWOS:000280885700019
dc.information.autorucMedicina;Arrese M;S/I;76095
dc.information.autorucMedicina;Riquelme A;S/I;3538
dc.information.autorucMedicina;Soza A;S/I;461
dc.language.isoen
dc.nota.accesocontenido completo
dc.publisherELSEVIER ESPANA
dc.revistaANNALS OF HEPATOLOGY
dc.rightsacceso abierto
dc.subjectFatty liver
dc.subjectInsulin
dc.subjectDiabetes
dc.subjectMetabolic syndrome
dc.subjectSUSTAINED VIROLOGICAL RESPONSE
dc.subjectFATTY LIVER-DISEASE
dc.subjectCOMBINATION THERAPY
dc.subjectVIRUS-INFECTION
dc.subjectHEPATOCELLULAR-CARCINOMA
dc.subjectPEGYLATED INTERFERON
dc.subjectPEGINTERFERON
dc.subjectFIBROSIS
dc.subjectPIOGLITAZONE
dc.subjectIMPACT
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleInsulin resistance, hepatic steatosis and hepatitis C: A complex relationship with relevant clinical implications
dc.typeartículo
dc.volumen9
sipa.codpersvinculados76095
sipa.codpersvinculados3538
sipa.codpersvinculados461
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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