Eficácia e segurança de mudanças no estilo de vida na Esteatose Hepática não Alcoólica: revisão rápida de evidências / Effectiveness and safety of lifestyle modifications for Nonalcoholic Hepatic Steatosis: rapid response review of evidence

Tecnologia: Intervenção de mudança no estilo de vida (dieta, exercícios). Indicação: doença hepática gordurosa não alcoólica (DHGNA). Pergunta clínica: Intervenções de mudança no estilo de vida, comparados a nenhum tratamento ou placebo, são eficazes no tratamento de DHGNA para modificar indicadores metabólicos, reduzir mortalidade e prevenir complicações relacionadas à esteatose hepática? Métodos: Foi feito levantamento bibliográfico na base de dados PUBMED, seguindo estratégias de buscas predefinidas. As revisões sistemáticas foram avaliadas com a ferramenta "AMSTAR 2 - Assessing the Methodological Quality of Systematic Reviews version 2". Resultados: Foram selecionadas 4 revisões sistemáticas, que atendiam aos critérios de inclusão. Conclusão: As evidências disponíveis não são suficientes para confirmar ou refutar que as modificações do estilo de vida têm efeitos benéficos de longo prazo sobre a DHGNA. Protocolos com dieta mediterrânea, jejum intermitente ou exercícios aeróbicos são benéficos para reduzir parâmetros metabólicos em pessoas com DHGNA

Technology: Lifestyle change intervention (diet, exercise). Indication: Non-alcoholic fatty liver disease (NAFLD). Clinical question: Are lifestyle change interventions, compared to no treatment or placebo, effective in NAFLD treatment to modify metabolic indicators, reduce mortality and prevent complications related to hepatic steatosis? Methods: A bibliographic survey was carried out in the PUBMED database, following predefined search strategies. Systematic reviews were evaluated using the tool "AMSTAR 2 - Assessing the Methodological Quality of Systematic Reviews version 2". Results: 4 systematic reviews that met the inclusion criteria were selected. Conclusion: The available evidence is not sufficient to confirm or refute that lifestyle modifications have long-term beneficial effects on NAFLD. Protocols such as a Mediterranean diet, intermittent fasting, or aerobic exercise are beneficial in reducing metabolic parameters in people with NAFLD

Efecto del extracto purificado rico en antocianinas del fruto del maqui (Aristotelia chilensis) en un modelo experimental de hígado graso no alcohólico / Effect of a purified anthocyanin-rich extract of maqui (Aristotelia chilensis) on experimental model of nonalcoholic fatty liver disease

Background: Non-alcoholic fatty liver disease (NAFLD) is a spectrum of hepatic lesions, ranging from benign intrahepatic lipid accumulation (steatosis) to progressive non-alcoholic steatohepatitis, in absence of other known secondary causes. Both insulin resistance and oxidative stress have been involved in NAFLD development and progression and, therefore, insulin-sensitizers and/or antioxidants have been targets of different therapeutic agents. Some natural compounds such as Aristotelia chilensis have a high content of polyphenols, which are known for their antioxidant and anti-inflammatory properties. Objective: To assess the effect of a purified anthocyanin-rich extract of maqui (Aristotelia chilensis) on experimental model of NAFLD. Methods: C57BL6 mice were separated in four experimental groups (n = 4-10) and fed a control diet (chow) or a high fat diet (HFD) with or without a purified anthocyanin-rich extract of Aristotelia chilensis (ACnE) (400 mg/kg/day diluted in drinking water). The hepatic effects of HFD were assessed measuring serum levels of glucose and aminotransferases, hepatic histology and triglycerides. Results: HFD diet induced an increase in hepatic triglycerides and histological NAFLD. Administration of ACnE did not affect serum aminotransferases, hepatic triglycerides, liver weight or histological NAFLD. Conclusion: Administration of an ACnE showed no effects on NAFLD in the HFD experimental model.

Introducción: El hígado graso no alcohólico (HGNA) constituye un espectro de lesiones hepáticas, desde la acumulación lipídica intrahepática benigna (esteatosis) hasta la esteatohepatitis no-alcohólica progresiva, en ausencia de causas secundarias conocidas. En el desarrollo y la progresión del HGNA se ha involucrado la resistencia a insulina y el estrés oxidativo y, por lo tanto, insulino-sensibilizantes y antioxidantes han sido blancos de diferentes agentes terapéuticos. Algunos compuestos naturales como la Aristotelia chilensis (maqui) tienen un alto contenido de polifenoles, los que presentan propiedades antiinflamatorias y antioxidantes. Objetivo: Evaluar el efecto de un extracto purificado rico en antocianinas (EACn) del fruto del maqui (Aristotelia chilensis) sobre la esteatosis, en un modelo experimental de HGNA. Métodos: Los ratones fueron distribuidos en 4 grupos (n = 4-10). Dos alimentados con una dieta estándar (grupo control) y dos con una dieta alta en grasa- high fat diet (grupo HFD). Un grupo control y uno HFD recibieron además 400 mg/kg/día de EACn (grupo EACn). Se determinaron los niveles séricos de aminotransferasas y glucosa; se evaluó la histología hepática y el contenido hepático de triglicéridos. Resultados: HFD indujo aumento de triglicéridos hepáticos e HGNA histológico. La administración de EACn no modificó las transaminasas séricas, los triglicéridos hepáticos, el peso del hígado ni el HGNA histológico. Conclusiones: La administración de un EACn no mostró efectos en el modelo experimental de HGNA inducido por una dieta alta en grasa.

Reducción de la esteatosis hepática, insulino resistencia y pérdida de la defensa antioxidante en ratones alimentados con dieta alta en grasa suplementados con AGPICL n-3 más aceite de oliva extra virgen / Reduction of hepatic steatosis, insulin resistance and loss of antioxidant defense in high fat diet fed mice suplemented with n-3 LCPUFA more extra virgin olive oil

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.

Dietas ricas em gordura, frutose e sacarose: alterações no fígado / Diets high in fat, fructose and sucrose: changes in liver

Hábitos inadequados no estilo de vida, pelo consumo exacerbado de dietas ricas em gorduras e açúcares (frutose e sacarose), correlacionam-se positivamente com o desenvolvimento da obesidade, da resistência à insulina (RI) e da esteatose hepática não alcoólica (NAFLD). O estudo teve como objetivo avaliar a magnitude dos efeitos da administração crônica de dietas ricas em gordura e/ou frutose, e ainda, comparar os efeitos dos açúcares isoladamente (frutose e sacarose) sob as alterações bioquímicas, o perfil inflamatório, as respostas morfofuncionais e as expressões proteicas e gênicas de fatores de transcrição envolvidos na lipogênese, na beta-oxidação, na gliconeogênese e no estresse oxidativo no fígado. Camundongos machos C57BL/6 foram divididos em dois experimentos: 1) Dieta controle/standard chow (SC), dieta high fat (HF – 42%), dieta high frutose (HFr – 34%) e dieta high fat + high frutose (HFHFr - 42% fat + 34% frutose) por 16 semanas; 2) Dieta controle/standard chow (SC), dieta high frutose (HFru – 50%) e dieta high sacarose (HSu – 50%) por 15 semanas. Ao final dos experimentos foram observados: 1) Não houve diferença na massa corporal entre os animais HFr e SC, só foi observado ganho de peso nos grupos HF e HFHFr. Houve ainda aumento do colesterol total, dos triglicerídeos plasmáticos e hepáticos e RI nos grupos HF, HFr e HFHFr. No fígado, foi observado NAFLD com aumento na expressão de SREBP-1c e PPAR-γ, e redução de PPAR-α. A gliconeogênese mediada pelo GLUT-2 e PEPCK também foi aumentada nos grupos HF, HFr e HFHFr em relação ao grupo SC. Áreas de necroinflamação também foram observadas nos animais HFr e HFHFr; 2) Não houve diferença na massa corporal entre os grupos SC, HFru e HSu. Porém, houve aumento do colesterol total, dos triglicerídeos plasmáticos e hepáticos, da RI, das adipocinas (IL-6, resistina, MCP-1 e leptina), e redução da adiponectina...

Habits unsuitable lifestyle, exacerbated by consumption of diets rich in fat and sugars (sucrose and fructose) are positively correlated with the development of obesity, insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD). The study aimed to evaluate the magnitude of the effects of chronic administration of diets rich in fat and/or fructose, and also compare the effects of sugars alone (fructose and sucrose) in the biochemical changes, the inflammatory profile, and the morphological and functional responses the protein and gene expression of transcription factors involved in lipogenesis, beta-oxidation, gluconeogenesis and oxidative stress in the liver. Male C57BL / 6 mice were divided into two experiments: 1) Diet control/standard chow (SC), high fat diet (HF - 42%), high-fructose diet (HFr - 34%) and high fat + high fructose diet (HFHFr - 42% fat + 34% fructose) for 16 weeks; 2) Diet control/standard chow (SC), high-fructose diet (HFru - 50%) and high sucrose diet (HSu - 50%) for 15 weeks. At the end of the experiments were observed: 1) There was no difference in body mass between HFr and SC groups, only weight gain was observed in the HF group and HFHFr. There was also an increase in total cholesterol, plasma and hepatic triglycerides and IR in HF, HFr, HFHFr groups. In the liver, NAFLD was observed with increased expression of SREBP-1c, PPAR-γ and PPAR-α reduction. The gluconeogenesis mediated by GLUT-2 and PEPCK was also increased in HF, HFr and HFHFr groups compared to SC. Areas of necroinflammation were also observed in HFr and HFHFr; 2) There was no difference in body mass between the SC, HFru and HSu groups. However, there was an increase in total cholesterol, plasma and hepatic triglycerides, IR, adipokines (IL-6, resistin, leptin and MCP-1), and decreased of adiponectin...