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1.
Food Funct ; 10(4): 2148-2160, 2019 Apr 17.
Artigo em Inglês | MEDLINE | ID: mdl-30938723

RESUMO

Non-alcoholic fatty liver disease (NAFLD) is defined as the accumulation of fat in liver cells, which causes serious health consequences. Animal and human studies suggest that the gut microbiota plays a role in the pathogenesis of NAFLD. Here, we investigated whether spinach consumption could ameliorate high-fat-diet-induced disturbances in certain intestinal bacterial groups and products derived from their metabolism, such as short-chain fatty acids (SCFAs) and microbial phenolic catabolites. Attention is also paid to blood lipids and glucose. In the study, a rat model of high-fat-diet-induced NAFLD was used. There were six experimental groups: NC (normal diet), NB (normal diet + 2.5% spinach), NA (normal diet + 5% spinach), HC (high-fat diet), HB (high-fat diet + 2.5% spinach) and HA (high-fat diet + 5% spinach). The rats consumed these diets for five weeks, and after that, they were sacrificed and plasma, urine, intestinal content, faeces and liver samples were taken. Biochemical parameters were analyzed in plasma, phenolic catabolites were quantified in the faeces, urine, plasma and liver by UPLC-ESI-MS/MS, and the analysis of the microbiota and SCFAs in the intestinal content was performed by qPCR and GLC. Consumption of a high-fat diet caused NAFLD and dislipaemia and altered the gut microbiota and the pattern of SCFAs and phenolic gut microbial catabolites. Supplementation with spinach partially ameliorated some alterations induced by the high-fat diet, in particular by increasing the Lactobacillus counts, reducing the fasting glucose and total and LDL-cholesterol and preventing excess liver cholesterol accumulation, thereby improving the values of the steatosis biomarkers.


Assuntos
Dieta Hiperlipídica/efeitos adversos , Microbioma Gastrointestinal , Metabolismo dos Lipídeos , Hepatopatia Gordurosa não Alcoólica/dietoterapia , Spinacia oleracea/metabolismo , Animais , Bactérias/classificação , Bactérias/genética , Bactérias/isolamento & purificação , Bactérias/metabolismo , LDL-Colesterol/metabolismo , Ácidos Graxos Voláteis/metabolismo , Humanos , Fígado/metabolismo , Masculino , Hepatopatia Gordurosa não Alcoólica/etiologia , Hepatopatia Gordurosa não Alcoólica/metabolismo , Hepatopatia Gordurosa não Alcoólica/microbiologia , Ratos , Ratos Sprague-Dawley
2.
Food Funct ; 8(10): 3542-3552, 2017 Oct 18.
Artigo em Inglês | MEDLINE | ID: mdl-28876011

RESUMO

Gut microbiota may play a role in the pathogenesis of NAFLD. We investigated whether tomato juice consumption for 5 weeks could ameliorate high-fat diet-induced alterations in certain intestinal bacterial groups and products arising from their metabolism (short-chain fatty acids and microbial phenolic catabolites). For this, we used a rat model with NAFLD induced by a high-fat diet, involving four experimental groups: NA (standard diet and water), NL (standard diet and tomato juice), HA (high-fat diet and water) and HL (high-fat diet and tomato juice). The onset of NAFLD impacted the gut microbiota profile, reducing the abundance of Bifidobacterium and Lactobacillus and increasing that of Enterobacteriaceae. Also, reduced concentrations of propionate, butyrate and phenolic catabolites and an increased acetate to propionate (Ac : Pr) ratio were observed. Tomato juice intake partially ameliorated high-fat diet-induced disturbances, particularly by increasing Lactobacillus abundance and diminishing the Ac : Pr ratio, suggesting a potential improvement of the metabolic pattern of NAFLD.


Assuntos
Bactérias/metabolismo , Sucos de Frutas e Vegetais/análise , Microbioma Gastrointestinal , Hepatopatia Gordurosa não Alcoólica/dietoterapia , Hepatopatia Gordurosa não Alcoólica/microbiologia , Prebióticos/análise , Solanum lycopersicum/metabolismo , Animais , Bactérias/classificação , Bactérias/genética , Bactérias/isolamento & purificação , Ácidos Graxos Voláteis/metabolismo , Trato Gastrointestinal/metabolismo , Trato Gastrointestinal/microbiologia , Humanos , Masculino , Hepatopatia Gordurosa não Alcoólica/metabolismo , Ratos , Ratos Sprague-Dawley
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