Microbiota Modulation With Synbiotic Decreases Liver Fibrosis in a High Fat Choline Deficient Diet Mice Model of Non-Alcoholic Steatohepatitis (NASH)

Cortez-Pinto, Helena; Borralho, Paula; Machado, Jorge; Lopes, Maria Denise; Gato, Inês Vale de; Santos, António Mário; Guerreiro, António

doi:10.1016/j.jpge.2016.01.004

Cited by 20 publications

(13 citation statements)

References 46 publications

(43 reference statements)

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“…In addition to body weight, the weight of adipose tissue is often used as an index of obesity and IR is strongly correlated these factors, influencing directly in the hepatic lipid metabolism. Higher adiposity is a common finding in experimental nutritional models, similar to the data obtained in this study, 13 , 14 , 37 , 38 although there are some disagreements in the literature probably due to different animal models and feeding protocols. 39 , 40 …”

Section: Discussionsupporting

confidence: 88%

“…Our histological data are in accordance with experimental studies of NAFLD developed through caloric excess, with simple steatosis usually being demonstrated in 8 weeks of experiment, NASH with progressive fibrosis between 16 and 24 weeks and hepatocellular carcinoma in 52 weeks. 13 , 38 The study of HCC through dietary models can be performed by adding inducing carcinogenic substances, reducing the experiment time by 16 weeks and consequently decreasing the cost of maintaining the animals. 31 …”

Section: Discussionmentioning

confidence: 99%

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<p>Gut Dysbiosis and Increased Intestinal Permeability Drive microRNAs, NLRP-3 Inflammasome and Liver Fibrosis in a Nutritional Model of Non-Alcoholic Steatohepatitis in Adult Male Sprague Dawley Rats</p>

Longo

Ferrari²,

Rampelotto

et al. 2020

CEGHas erratum 2020-10

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Background/Aim The interactions between the gut and liver have been described in the progression of non-alcoholic steatohepatitis (NASH). The aim of this study was to develop an experimental nutritional model of NASH simulating metabolic changes occurring in humans. Materials and Methods Adult male Sprague Dawley rats were randomized into two groups: controls (standard diet) and intervention (high-fat and choline-deficient diet) for 16 weeks, each experimental group with 10 animals. Biochemical analysis, hepatic lipid content, microRNAs, inflammatory, gut permeability markers and gut microbiota were measured. Results Animals in the intervention group showed significantly higher delta Lee index ( p =0.017), abdominal circumference ( p <0.001), abdominal adipose tissue ( p <0.001) and fresh liver weight ( p <0.001), as well as higher serum levels of alanine aminotransferase ( p =0.010), glucose ( p =0.013), total cholesterol ( p =0.033), LDL cholesterol ( p =0.011), and triglycerides ( p =0.011), and lower HDL cholesterol ( p =0.006) compared to the control group. Higher TLR4 ( p =0.041), TLR9 ( p =0.033), MyD88 ( p =0.001), Casp1 ( p <0.001), NLPR3 ( p =0.019), liver inflammation index interleukin (IL)-1β/IL10 ( p <0.001), IL6/IL10 ( p =0.002) and TNFα/IL10 ( p =0.001) were observed in the intervention group, and also lower permeability markers Ocln ( p =0.003) and F11r ( p =0.041). Gene expression of miR-122 increased ( p =0.041) and miR-145 ( p =0.010) decreased in the intervention group. Liver steatosis, inflammation and fibrosis, along with collagen fiber deposition increment ( p <0.001), were seen in the intervention group. Regarding gut microbiota, Bray-Curtis dissimilarity index and number of operational taxonomic units were significantly different ( p <0.001) between the groups. Composition of the gut microbiota showed a significant correlation with histopathological score of NAFLD (r=0.694) and index IL-1β/IL-10 (r=0.522). Conclusion This experimental model mimicking human NASH demonstrated gut and liver interaction, with gut microbiota and intestinal permeability changes occurring in parallel with systemic and liver inflammation, miRNAs regulation and liver tissue damage.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

<p>Gut Dysbiosis and Increased Intestinal Permeability Drive microRNAs, NLRP-3 Inflammasome and Liver Fibrosis in a Nutritional Model of Non-Alcoholic Steatohepatitis in Adult Male Sprague Dawley Rats</p>

Longo

Ferrari²,

Rampelotto

et al. 2020

CEGHas erratum 2020-10

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“…Additionally, mice fed methionine-choline diet, a model of severe NASH not associated with obesity or the metabolic syndrome, developed less liver fibrosis when treated with VSL#3 [ 130 ]. Other probiotics also showed beneficial effects in animal models of NAFLD/NASH [ 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 ].…”

Section: Microbiota As a Therapeutic Targetmentioning

confidence: 99%

Diet, Microbiota, Obesity, and NAFLD: A Dangerous Quartet

Machado¹,

Cortez-Pinto

2016

IJMS

Self Cite

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Recently, the importance of the gut-liver-adipose tissue axis has become evident. Nonalcoholic fatty liver disease (NAFLD) is the hepatic disease of a systemic metabolic disorder that radiates from energy-surplus induced adiposopathy. The gut microbiota has tremendous influences in our whole-body metabolism, and is crucial for our well-being and health. Microorganisms precede humans in more than 400 million years and our guest flora evolved with us in order to help us face aggressor microorganisms, to help us maximize the energy that can be extracted from nutrients, and to produce essential nutrients/vitamins that we are not equipped to produce. However, our gut microbiota can be disturbed, dysbiota, and become itself a source of stress and injury. Dysbiota may adversely impact metabolism and immune responses favoring obesity and obesity-related disorders such as insulin resistance/diabetes mellitus and NAFLD. In this review, we will summarize the latest evidence of the role of microbiota/dysbiota in diet-induced obesity and NAFLD, as well as the potential therapeutic role of targeting the microbiota in this set.

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“…Probiotics supplementation can prevent the occurrence and development of fatty liver disease, improve liver steatosis and brosis in mice fed with high-fat diet (HFD) [13,14]. The protective effects of probiotics on fatty liver disease by many pathways including reducing hepatic lipid deposition, endotoxemia and oxidative stress [15]. It's reported that Parabacteroides distasonis can alleviate the disorder of lipid metabolism dysfunction in ob/ob mice and HFD mice, indicating that weight loss, a decrease in hyperglycemia and hyperlipidemia, and the improvement of hepatic steatosis [16].Ritze reported that Lactobacillus rhamnosus GG attenuated liver in ammation and steatosis in high glucose diet-induced NAFLD model mice [17].…”

Section: Introductionmentioning

confidence: 99%

Probiotics Supplementation Alleviate Corticosterone-induced Fatty Liver Disease Related With the Changes of Hepatic Lipogenesis and Gut Microbiota Profile in Broiler

Mei

Feng

Yao

et al. 2020

Preprint

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Background:Emerging evidencesindicate a close relationship between gut microbiotaand fatty liver disease.It has been suggested that gut microbiota modulation with probiotics improved fatty liver disease in rodents and human, yet it still remains unclear in poultry.Results: Ninety six one-day-old green-legged chicken were divided into control group (CON) and probiotic group (PB), respectively. Probiotics were administrated throughdrinking water for two weeks from 1-day-old. At 28 d of age,16 broilers selectedfromCON or PB group randomly, and receivedvehicle(15% ethanol) or CORT(4.0 mg/kg)treatmentdaily viasubcutaneous injection for a week to induce fatty liver. At the end of the experiment, broilers from 4 groups,control group(CON), corticosterone group (CORT), probiotic group (PB), PB plusCORT group(CORT&PB),were slaughtered for sampling and analysis.The results showed that probiotics administration significantly prevented CORT-induced body weight loss(P<0.05), but did not alleviate the reduction of immune organs weight caused by CORT. Compared to CON,broilers in CORT group exhibited a significant increase of triglyceride (TG) levelin both plasma and liver(P< 0.01), as well as severe hepatocytic steatosis and hepatocellular ballooning, and accompanied with the up-regulation of hepatic lipogenesis genes expression. However, probiotics supplementation markedly decreased the intrahepatic lipid accumulation and steatosis histological score, which was associated withthedown-regulation of sterol regulatory element-binding protein-1 (SREBP1) and acetyl-CoA carboxylase (ACC) mRNA (P< 0.05)as well as it protein (P= 0.06) expression.Cecal microbiota composition was determined by 16S rRNA high-throughput sequencing. Results showed that CORT treatment induced distinct gut microbiota alterations with a decrease of microbial diversity, and anincrease of proteobacteriaabundance (P<0.05). On the contrary, probiotic supplementation increased the beta diversity and increased community richness and diversity index(P> 0.05), as well as the abundance of Intestinimonas(P<0.05).Conclusion: Our results indicate that CORT treatment induced serious fatty liver disease and altered the gut microbiota composition in broilers, however,probiotics supplementation from post-hatching had a beneficial effect on alleviatingfatty liver disease through regulating lipogenic genes expression and increasing gut microbiota diversity andbeneficial bacteria abundanceimbalance.

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Microbiota Modulation With Synbiotic Decreases Liver Fibrosis in a High Fat Choline Deficient Diet Mice Model of Non-Alcoholic Steatohepatitis (NASH)

Cited by 20 publications

References 46 publications

<p>Gut Dysbiosis and Increased Intestinal Permeability Drive microRNAs, NLRP-3 Inflammasome and Liver Fibrosis in a Nutritional Model of Non-Alcoholic Steatohepatitis in Adult Male Sprague Dawley Rats</p>

<p>Gut Dysbiosis and Increased Intestinal Permeability Drive microRNAs, NLRP-3 Inflammasome and Liver Fibrosis in a Nutritional Model of Non-Alcoholic Steatohepatitis in Adult Male Sprague Dawley Rats</p>

Diet, Microbiota, Obesity, and NAFLD: A Dangerous Quartet

Probiotics Supplementation Alleviate Corticosterone-induced Fatty Liver Disease Related With the Changes of Hepatic Lipogenesis and Gut Microbiota Profile in Broiler

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