Abstract Introduction: the excessive consumption of fructose can cause liver damage, characteristic of non-alcoholic fatty liver disease (NAFLD) associated with changes in lipid metabolism and antioxidant defenses. Açai, the fruit of Euterpe oleracea Mart., has demonstrated numerous biological activities, including anti-inflammatory, antioxidant, and lipid metabolism modulating action. Objective: we evaluated the benefits of açai supplementation on liver damage caused by replacing starch with fructose in rats. Methods: thirty male Fischer rats were divided into two groups, the control group (C, 10 animals), which consumed a standard diet (AIN-93M), and the fructose (F, 20 animals) group, which consumed a diet containing 60% of fructose. After eight weeks, 10 animals from the fructose group received 2% of lyophilized açai, and were called the açai fructose group (FA). The animals were fed ad libitum with these diets for another ten weeks. Serum, hepatic and fecal lipid profile, antioxidant enzymes and carbonylated protein were assessed and histopathological characterization of the liver was performed. Results: açai promoted the reduction of ALT activity in relation to the fructose group (F), reduced alkaline phosphatase to a level similar to that of the control group (C) in relation to the fructose group (F), and reduced catalase activity. The fruit also increased the ratio of total/oxidized glutathione (GSH/GSSG) and reduced the degree of macrovesicular steatosis and the number of inflammatory cells. Conclusion: the replacement of starch by fructose during this period was effective in promoting NAFLD. Açai showed attenuating effects on some markers of hepatic steatosis and inflammation.

Resumen Introducción: el consumo excesivo de fructosa puede causar daño hepático, característico de la enfermedad hepática grasa no alcohólica (EHGNA), asociada con cambios en el metabolismo de los lípidos y defensas antioxidantes. El açai, fruto del Euterpe oleracea Mart., ha demostrado desempeñar numerosas actividades biológicas, incluidas acciones antiinflamatorias, antioxidantes y moduladoras del metabolismo lipídico. Objetivo: se evaluaron los beneficios de la suplementación con açai en el daño hepático causado por la sustitución del almidón por fructosa en ratas. Métodos: se distribuyeron 30 ratas Fischer macho en dos grupos: 10 ratas en el grupo control (C), que consumía una dieta estándar (AIN-93M), y 20 ratas en el grupo fructosa (F), que consumía una dieta que contenía un 60% de fructosa. Después de ocho semanas, diez animales del grupo fructosa recibieron un 2% de açai liofilizado, por lo que pasaron a integrar el grupo açai fructosa (FA). Los animales fueron alimentados ad libitum con estas dietas durante otras diez semanas. Se analizaron el perfil lipídico hepático y fecal, las enzimas antioxidantes y la proteína carbonilada, y se realizó la caracterización histopatológica del hígado. Resultados: el açai promovió la reducción de la actividad de ALT en relación al grupo de fructosa (F) y la reducción de la fosfatasa alcalina a niveles similares a los hallados en el grupo control (C) en relación con el grupo de fructosa (F). El fruto también aumentó la proporción de glutatión total/oxidado (GSH/GSSG) y redujo el grado de esteatosis macrovesicular y el número de células inflamatorias. Conclusión: la sustitución de almidón por fructosa durante este periodo fue eficaz en la promoción de NAFLD. El açai mostró efectos atenuantes en algunos marcadores de esteatosis hepática y de inflamación.

Objetivo Determinar se uma dieta hipercolesterolemiante induz esteatose hepática, alterações na expressão de mRNA da NADPH oxidase e nas defesas antioxidantes.Materiais e métodos : Ratas Fischer foram divididas em dois grupos de oito animais de acordo com o tratamento recebido, controle (C) e hipercolesterolêmico (H). Aquelas do grupo C foram alimentadas com dieta padrão (AIN-93M) e as do grupo H foram alimentadas com dieta hipercolesterolemiante (25% de óleo de soja e 1% de colesterol). As dietas foram oferecidas por oito semanas.Resultados : O grupo H apresentou acúmulo de lipídios no fígado, aumento das atividades de ALT e AST e da concentração de colesterol no soro comparado ao grupo C. O marcador da peroxidação lipídica (TBARS) e os níveis de mRNA das subunidades p47phox da NADPH-oxidase e p22phox foram aumentados no fígado de animais do grupo H, além de alteração da atividade e expressão de enzimas antioxidantes.Conclusão : Os resultados mostram um aumento na expressão de subunidades da NADPH oxidase e alterações na atividade das enzimas antioxidantes na esteatose hepática induzida por dieta hipercolesterolemiante. Arq Bras Endocrinol Metab. 2014;58(3):251-9

Objective : This study aimed to determine whether a hypercholesterolemic diet induces hepatic steatosis, alterations in mRNA expression of NADPH oxidase subunits, and antioxidant defenses.Materials and methods : Fischer rats were divided into two groups of eight animals according to the treatment, control (C) and hypercholesterolemic diet (H). Those in group C were fed a standard diet (AIN-93M), and those of the group H were fed a hypercholesterolemic diet (25% soybean oil and 1% cholesterol).Results : The hypercholesterolemic diet did not affect body weight, but resulted in the accumulation of lipids in the liver, increased serum activities of aminotransferases and cholesterol levels. Biomarker of lipid peroxidation (TBARS) and mRNA expression of NADPH oxidase subunits p22phox and p47phox were increased in the liver of animals in group H. Besides, the activity and expression of antioxidant enzymes were altered.Conclusion : The results show increased mRNA expression of NADPH oxidase subunits and changes in antioxidant enzyme activities in diet-induced hepatic steatosis. Arq Bras Endocrinol Metab. 2014;58(3):251-9