NAFLD (non-alcoholic fatty liver disease) is one of the most frequent chronic liver diseases worldwide. The metabolic factors associated with NAFLD are also determinants of liver disease progression in chronic HCV (hepatitis C virus) infection. It has been reported that, besides inducing hepatic fatty acid biosynthesis, LXR (liver X receptor) regulates a set of inflammatory genes. We aimed to evaluate the hepatic expression of LXRα and its lipogenic and inflammatory targets in 43 patients with NAFLD, 44 with chronic HCV infection and in 22 with histologically normal liver. Real-time PCR and Western blot analysis were used to determine hepatic expression levels of LXRα and related lipogenic and inflammatory mediators in the study population. We found that the LXRα gene and its lipogenic targets PPAR-γ (peroxisome-proliferator-activated receptor-γ), SREBP (sterol-regulatory-element-binding protein)-1c, SREBP-2 and FAS (fatty acid synthase) were overexpressed in the liver of NAFLD and HCV patients who had steatosis. Moreover, up-regulation of inflammatory genes, such as TNF (tumour necrosis factor)-α, IL (interleukin)-6, OPN (osteopontin), iNOS (inducible NO synthase), COX (cyclo-oxygenase)-2 and SOCS (suppressors of cytokine signalling)-3, was observed in NAFLD and HCV patients. Interestingly, TNF-α, IL-6 and osteopontin gene expression was lower in patients with steatohepatitis than in those with steatosis. In conclusion, hepatic expression of LXRα and its related lipogenic and inflammatory genes is abnormally increased in NAFLD and HCV patients with steatosis, suggesting a potential role of LXRα in the pathogenesis of hepatic steatosis in these chronic liver diseases.
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Research Article|
December 03 2010
Enhanced expression of pro-inflammatory mediators and liver X-receptor-regulated lipogenic genes in non-alcoholic fatty liver disease and hepatitis C
Elena Lima-Cabello;
Elena Lima-Cabello
*Institute of Biomedicine (IBIOMED), University of León, León, Spain
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María Victoria García-Mediavilla;
María Victoria García-Mediavilla
*Institute of Biomedicine (IBIOMED), University of León, León, Spain
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
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María E. Miquilena-Colina;
María E. Miquilena-Colina
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
‡Liver Research Unit, University Hospital Santa Cristina, Instituto de Investigación Sanitaria Princesa, Madrid, Spain
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Javier Vargas-Castrillón;
Javier Vargas-Castrillón
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
‡Liver Research Unit, University Hospital Santa Cristina, Instituto de Investigación Sanitaria Princesa, Madrid, Spain
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Tamara Lozano-Rodríguez;
Tamara Lozano-Rodríguez
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
‡Liver Research Unit, University Hospital Santa Cristina, Instituto de Investigación Sanitaria Princesa, Madrid, Spain
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Miguel Fernández-Bermejo;
Miguel Fernández-Bermejo
§Gastroenterology Service, San Pedro de Alcántara Hospital, Cáceres, Spain
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José Luis Olcoz;
José Luis Olcoz
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
∥Department of Gastroenterology, Complejo Asistencial de León, León, Spain
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Javier González-Gallego;
Javier González-Gallego
*Institute of Biomedicine (IBIOMED), University of León, León, Spain
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
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Carmelo García-Monzón;
Carmelo García-Monzón
1
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
‡Liver Research Unit, University Hospital Santa Cristina, Instituto de Investigación Sanitaria Princesa, Madrid, Spain
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Sonia Sánchez-Campos
Sonia Sánchez-Campos
1
*Institute of Biomedicine (IBIOMED), University of León, León, Spain
†Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain
Correspondence: Dr Sonia Sánchez-Campos (email ssanc@unileon.es).
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Clin Sci (Lond) (2011) 120 (6): 239–250.
Article history
Received:
July 22 2010
Revision Received:
September 20 2010
Accepted:
October 08 2010
Accepted Manuscript online:
October 08 2010
Citation
Elena Lima-Cabello, María Victoria García-Mediavilla, María E. Miquilena-Colina, Javier Vargas-Castrillón, Tamara Lozano-Rodríguez, Miguel Fernández-Bermejo, José Luis Olcoz, Javier González-Gallego, Carmelo García-Monzón, Sonia Sánchez-Campos; Enhanced expression of pro-inflammatory mediators and liver X-receptor-regulated lipogenic genes in non-alcoholic fatty liver disease and hepatitis C. Clin Sci (Lond) 1 March 2011; 120 (6): 239–250. doi: https://doi.org/10.1042/CS20100387
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