Articles producció científica> Medicina i Cirurgia

Endocannabinoid receptors gene expression in morbidly obese with non alcoholic fatty liver disease

  • Dades identificatives

    Identificador: PC:807
    Autors:
    Richart, C.Del Castillo, D.Hernández, M.Sabench, F.Alibalic, A.Filiu, E.Aguilar, C.Martinez, S.Terra, X.Guiu-Jurado, E.Berlanga, A.Auguet, T.
    Resum:
    Background. Recent reports suggest a role for the endocannabinoid system in the pathology of nonalcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the relationship between liver expression of cannabinoid (CB) receptor subtypes, CB1 and CB2, in morbidly obese (MO) women with different histological stages of NAFLD. Methods. We analysed hepatic CB1 and CB2 mRNA expression, and the expression of genes involved in lipid metabolism in 72 MO women, subclassified by liver histology into MO with normal liver (NL, n=16), simple steatosis (SS, n=28), and nonalcoholic steatohepatitis (NASH, n=28) by enzyme-linked immunosorbent assay and RT-PCR. Results. We found that CB1 mRNA expression was significantly higher in NASH compared with SS and correlated negatively with PPARa. Regarding CB2, CB2 mRNA expression correlated positively with ACC1, PPAR?, IL6, TNFa, resistin, and adiponectin. Conclusions. The increased expression of CB1 in NASH and the negative correlation with PPARa suggest a deleterious role of CB1 in NAFLD. Regarding CB2, its positive correlation with the anti-inflammatory molecule adiponectin and, paradoxically, with inflammatory genes suggests that this receptor has a dual role. Taken together, our results suggest that endocannabinoid receptors might be involved in the pathogenesis of NAFLD, a finding which justifies further study.
  • Altres:

    Autor segons l'article: Richart, C. Del Castillo, D. Hernández, M. Sabench, F. Alibalic, A. Filiu, E. Aguilar, C. Martinez, S. Terra, X. Guiu-Jurado, E. Berlanga, A. Auguet, T.
    Departament: Medicina i Cirurgia
    e-ISSN: 2314-6141
    Autor/s de la URV: Teresa Auguet, Alba Berlanga, Esther Guiu-Jurado, Ximena Terra, Salomé Martinez, Carmen Aguilar, Elisa Filiu, Ajla Alibalic, Fàtima Sabench, Mercé Hernández, Daniel Del Castillo, and Cristóbal Richart
    Resum: Background. Recent reports suggest a role for the endocannabinoid system in the pathology of nonalcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the relationship between liver expression of cannabinoid (CB) receptor subtypes, CB1 and CB2, in morbidly obese (MO) women with different histological stages of NAFLD. Methods. We analysed hepatic CB1 and CB2 mRNA expression, and the expression of genes involved in lipid metabolism in 72 MO women, subclassified by liver histology into MO with normal liver (NL, n=16), simple steatosis (SS, n=28), and nonalcoholic steatohepatitis (NASH, n=28) by enzyme-linked immunosorbent assay and RT-PCR. Results. We found that CB1 mRNA expression was significantly higher in NASH compared with SS and correlated negatively with PPARa. Regarding CB2, CB2 mRNA expression correlated positively with ACC1, PPAR?, IL6, TNFa, resistin, and adiponectin. Conclusions. The increased expression of CB1 in NASH and the negative correlation with PPARa suggest a deleterious role of CB1 in NAFLD. Regarding CB2, its positive correlation with the anti-inflammatory molecule adiponectin and, paradoxically, with inflammatory genes suggests that this receptor has a dual role. Taken together, our results suggest that endocannabinoid receptors might be involved in the pathogenesis of NAFLD, a finding which justifies further study.
    Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 2314-6133
    Pàgina final: 7
    Volum de revista: 2014
    Versió de l'article dipositat: info:eu-repo/semantics/publishedVersion
    URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
    Entitat: Universitat Rovira i Virgili.
    Any de publicació de la revista: 2014
    Pàgina inicial: 1
  • Paraules clau:

    Cannabinoides -- Receptors
    2314-6133
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