Pasarín Castellanos, MarcosLa Mura, VincenzoGracia-Sancho, JorgeGarcía Calderó, HéctorRodríguez Vilarrupla, AinaGarcía Pagán, Juan CarlosBosch i Genover, JaumeGonzález-Abraldes Iglesias, Juan2013-05-222013-05-222012-04-031932-6203https://hdl.handle.net/2445/43658Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Most morbidity associated with the metabolic syndrome is related to vascular complications, in which endothelial dysfunction is a major pathogenic factor. However, whether NAFLD is associated with endothelial dysfunction within the hepatic vasculature is unknown. The aims of this study were to explore, in a model of diet-induced overweight that expresses most features of the metabolic syndrome, whether early NAFLD is associated with liver endothelial dysfunction. Wistar Kyoto rats were fed a cafeteria diet (CafD; 65% of fat, mostly saturated) or a control diet (CD) for 1 month. CafD rats developed features of the metabolic syndrome (overweight, arterial hypertension, hypertryglyceridemia, hyperglucemia and insulin resistance) and liver steatosis without inflammation or fibrosis. CafD rats had a significantly higher in vivo hepatic vascular resistance than CD. In liver perfusion livers from CafD rats had an increased portal perfusion pressure and decreased endothelium-dependent vasodilation. This was associated with a decreased Akt-dependent eNOS phosphorylation and NOS activity. In summary, we demonstrate in a rat model of the metabolic syndrome that shows features of NAFLD, that liver endothelial dysfunction occurs before the development of fibrosis or inflammation.9 p.application/pdfengcc-by (c) Pasarín, M. et al., 2012http://creativecommons.org/licenses/by/3.0/esMalalties del fetgeEndoteliFibrosi pulmonarLiver diseasesEndotheliumPulmonary fibrosisinfo:eu-repo/semantics/article6241962013-05-22info:eu-repo/semantics/openAccess22509248