ABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is directly associated with insulin resistance and oxidative stress. In NAFLD is established a reduction in n-3 LCPUFA (EPA + DHA) levels and hepatic activity of transcription factor PPAR-alpha. EPA and DHA inhibit lipogenesis and stimulate fatty acid oxidation in the liver. Extra virgin olive oil (EVOO) has important antioxidant properties. This study evaluated the prevention of insulin resistance and prevention of depletion of hepatic antioxidant defense inC57BL/6J mice fed high-fat diet (HFD), supplemented with n-3 LCPUFA plus EVOO. HFD generated insulin resistance and hepatic steatosis, together with significant reduction in i) n-3 LCPUFA hepatic levels, ii) DNA binding activity of PPAR-alpha, iii) activity of antioxidant enzymes (catalase and superoxide dismutase), respect to control group (fed with control diet). Supplementation with n-3 LCPUFA plus EVOO prevent development insulin resistance and attenuate increased of fat in liver (p < 0.05), together with a normalization of i) DNA binding activity of PPAR-á, ii) activity of antioxidant enzymes (catalase and superoxide dismutase) and iii) reducing depletion of n-3 LCPUFA levels in liver tissue, compared to the control group (p < 0.05). Supplementation with n-3 LCPUFA plus EVOO reduced hepatic steatosis and prevent development of insulin resistance, along with preserving the antioxidant defense in liver. Projecting the use of this mixture of AGPICL n-3 plus EVOO as a potential treatment of NAFLD.
Subject(s)
Male , Animals , Mice , Olive Oil/therapeutic use , /therapeutic use , Diet, High-Fat , Dietary Supplements , Non-alcoholic Fatty Liver Disease/diet therapy , Olive Oil/pharmacology , /pharmacology , Catalase , Catalase/physiology , Liver , Oxidative Stress , Superoxide DismutaseABSTRACT
Polyunsaturated Omega-3 fatty acids (ω-3 PUFA), particularly docosahexaenoic acid (C22:6 ω-3, DHA), are critical nutrients during pregnancy with a key role for visual and brain development. Fish, especially oily fish, is an excellent dietary source of DHA. However, its dietary consumption is low. Bioconversion from alpha-linolenic acid (C18: 3 ω-3, ALA) to DHA is a limited metabolic pathway in humans, however, it increases during fertility and pregnancy. The chia seed oil (Salvia hispanica) is a good vegetal source of ω-3 PUFA, containing a large proportion (60-65% of total fatty acids) as ALA. The aim of this study was to compare the acceptability of two different commercial oils: chia oil (63% ALA) and canola oil (10% ALA) in a group of Chilean pregnant women. A sample of 41 women was included. Each participant performed: a) an assessment of the acceptability of two commercial oils (hedonic scale), b) a dietary intake questionnaire and, c) a test of knowledge related to ω-3 PUFAs. Main results indicated that 57% of the participants properly recognized food sources of ω-3 PUFA, and 12.2% met their dietary requirements. The characteristics that had the highest scores were the appearance of chia oil and the taste of canola oil. However, there were no significant differences between the overall acceptability of both evaluated oils. It is concluded that chia oil could be a new and useful alternative to increase dietary ALA intake in pregnant women.
Los ácidos grasos (AG) poliinsaturados omega 3 (AGPI ω-3), y especialmente el ácido docosahexaenoico (C22:6 ω-3, DHA) participan en el desarrollo cerebral y visual del feto y del lactante, constituyendo nutrientes críticos durante el embarazo. Los pescados grasos, representan una excelente fuente de consumo de DHA, sin embargo, su consumo a nivel poblacional es bajo. El ácido alfa-linolénico (C18:3 ω-3, ALA) es el precursor del DHA, vía metabólica limitada en el ser humano, pero que aumenta en mujeres en edad fértil y embarazadas. El aceite de semilla de chía (Salvia hispánica) contiene en una gran cantidad de AGPI ω-3 (60-65% del total de AG) y su aceite podría representar una nueva fuente de este tipo de AG. El objetivo de este estudio fue comparar la aceptabilidad de un aceite de canola (10% ALA) y chía (63% ALA) en embarazadas chilenas. Se estudió una muestra de 41 embarazadas quienes respondieron una encuesta de aceptabilidad (escala hedónica), una encuesta de tendencia de consumo modificada y una prueba de conocimiento respecto a los AGPI ω-3. Los resultados indicaron que el 57% de las embarazadas reconoció correctamente los alimentos fuentes de AGPI ω-3 y 12.2% de ellas cumplió con sus requerimientos dietarios. Las características que presentaron los mayores puntajes fueron la apariencia del aceite de chía, y el sabor del aceite de canola. Sin embargo, no existió diferencia significativa entre la aceptabilidad de ambos aceites evaluados. Se concluye que el aceite de chía podría ser utilizado como una alternativa dietaria de buena fuente de ALA en embarazadas.
Subject(s)
Humans , Sensation , Plant Oils , Linoleic Acids , Eating , Pregnant Women , Diet, HealthyABSTRACT
Non-alcoholic fatty liver disease (NAFLD) is triggered by a nutritional-metabolic alteration characterized by triacylglicerides acumulation, insulin resistance (IR), oxidative stress and depletion of polyunsaturated fatty acid (PUFA). The n-3 PUFA, such as eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, would be hepatoprotective against the development of NAFLD by stimulating lipolysis and inhibit lipogenesis. So, fish oil supplementation (EPA + DHA) prevents HFDinduced NAFLD. In this context, the aim of this study is to evaluate the correlation between liver oxidative stress with IR and levels of PUFA in supplemented mice. Male mice C57BL/6J (n=9) were fed for 12th week: a) control diet (20% protein, 70% carbohydrate, 10% lipids), b) control diet and fish oil supplementation (200 mg EPA+DHA/kg/day), c) high fat diet (20% protein, 20% carbohydrate, 60% lipids), and d) high fat diet and fish oil supplementation. Liver steatosis (histology), insulin resistance (HOMA), liver oxidative stress (GSH/GSSG, carbonyl protein and 8-isoprostanes) and liver fatty acid content were evaluated. The significant decrease in liver oxidative stress parameters (p<0.05, ANOVA followed by Newman Keuls test) were correlated (Pearson test) with HOMA and levels of PUFA, along with the hepatoprotection observed. It concludes that prevention of NAFLD by supplementation with fish oil (EPA+DHA) is dependent of the prevention of liver oxidative stress, IR and PUFA depletion.
La enfermedad por hígado graso no alcohólica (EHGNA) está provocada por una alteración metabólico- nutricional caracterizada por la acumulación de triacilglicéridos, resistencia a la insulina, estrés oxidativo y disminución de ácidos grasos poliinsaturados (AGPI). Los AGPI ω-3, como los ácidos eicosapentaenoico (EPA) y docosahexaenoico (DHA), serían hepatoprotectores contra la EHGNA al estimular la lipolisis e inhibir la lipogénesis hepática. La suplementación con aceite de pescado (EPA + DHA) previene la esteatosis hepática inducida por una dieta alta en grasas. En este contexto, el objetivo de este estudio es evaluar la correlación entre el estrés oxidativo hepático, la resistencia a la insulina y los niveles de AGPI ω-3 en ratones suplementados. Ratones machos C57BL/6J (n=9) alimentados durante 12 semanas con: a) dieta control (20% proteína, 70% hidratos de carbono, 10% lípidos), b) dieta control y suplementación con 200 mg de EPA+DHA/kg/día, c) dieta alta en grasa (20% proteína, 20% hidratos de carbono, 60% lípidos), y d) dieta alta en grasas más EPA+DHA. Se evaluaron la esteatosis hepática (histología), resistencia a la insulina (HOMA), estrés oxidativo hepático (GSH/GSSG, proteínas carboniladas y 8-isoprostanos) y el contenido de ácidos grasos hepáticos. La disminución significativa en los parámetros hepáticos de estrés oxidativo (p <0,05, ANOVA seguido de Newman-Keuls) se correlacionó positivamente (test de Pearson) con el HOMA y los niveles de AGPI ω-3, junto con la hepatoprotección observada. Se concluye que la prevención de EHGNA por suplementación con EPA+DHA, se acompaña de una correlación inversa entre el estrés oxidativo y la resistencia a la insulina y la disminución de AGPI ω-3 hepáticos.