scholarly journals Role of Probiotics in Non-alcoholic Fatty Liver Disease: Does Gut Microbiota Matter?

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2837 ◽  
Author(s):  
Chencheng Xie ◽  
Dina Halegoua-DeMarzio
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Randomized Clinical Trials ◽  
Short Chain Fatty Acids ◽  
Energy Harvest ◽  
Hepatic Inflammation ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is the hepatic consequence of metabolic syndrome, which often also includes obesity, diabetes, and dyslipidemia. The connection between gut microbiota (GM) and NAFLD has attracted significant attention in recent years. Data has shown that GM affects hepatic lipid metabolism and influences the balance between pro/anti-inflammatory effectors in the liver. Although studies reveal the association between GM dysbiosis and NAFLD, decoding the mechanisms of gut dysbiosis resulting in NAFLD remains challenging. The potential pathophysiology that links GM dysbiosis to NAFLD can be summarized as: (1) disrupting the balance between energy harvest and expenditure, (2) promoting hepatic inflammation (impairing intestinal integrity, facilitating endotoxemia, and initiating inflammatory cascades with cytokines releasing), and (3) altered biochemistry metabolism and GM-related metabolites (i.e., bile acid, short-chain fatty acids, aromatic amino acid derivatives, branched-chain amino acids, choline, ethanol). Due to the hypothesis that probiotics/synbiotics could normalize GM and reverse dysbiosis, there have been efforts to investigate the therapeutic effect of probiotics/synbiotics in patients with NAFLD. Recent randomized clinical trials suggest that probiotics/synbiotics could improve transaminases, hepatic steatosis, and reduce hepatic inflammation. Despite these promising results, future studies are necessary to understand the full role GM plays in NAFLD development and progression. Additionally, further data is needed to unravel probiotics/synbiotics efficacy, safety, and sustainability as a novel pharmacologic approaches to NAFLD.

scholarly journals Gut Microbiota-Derived Components and Metabolites in the Progression of Non-Alcoholic Fatty Liver Disease (NAFLD)

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1712 ◽  
Author(s):  
Yun Ji ◽  
Yue Yin ◽  
Ziru Li ◽  
Weizhen Zhang
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Redox Homeostasis ◽  
Short Chain Fatty Acids ◽  
Pathological Process ◽  
Bioactive Substances ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Human gut microbiota has been increasingly recognized as a pivotal determinant of non-alcoholic fatty liver disease (NAFLD). Apart from the changes in the composition of gut microbiota, the components and metabolites derived from intestinal microbiota have emerged as key factors in modulating the pathological process of NAFLD. Compelling evidences have revealed that gut microbiota generates a variety of bioactive substances that interact with the host liver cells through the portal vein. These substances include the components derived from bacteria such as lipopolysaccharides, peptidoglycan, DNA, and extracellular vesicles, as well as the metabolites ranging from short-chain fatty acids, indole and its derivatives, trimethylamine, secondary bile acids, to carotenoids and phenolic compounds. The mechanisms underlying the hepatic responses to the bioactive substances from gut bacteria have been associated with the regulation of glycolipid metabolism, immune signaling response, and redox homeostasis. Illuminating the interplay between the unique factors produced from gut microbiome and the liver will provide a novel therapeutical target for NAFLD. The current review highlights the recent advances on the mechanisms by which the key ingredients and metabolites from gut microbiota modulate the development and progression of NAFLD.

Resveratrol Supplementation in Patients with Non-Alcoholic Fatty Liver Disease: Systematic Review and Meta-analysis

2017 ◽  
Vol 26 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Ahmed Elgebaly ◽  
Ibrahim A. I. Radwan ◽  
Mohamed M. AboElnas ◽  
Hamza H. Ibrahim ◽  
Moutaz F. M. Eltoomy ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Randomized Clinical Trials ◽  
Controlled Trial ◽  
Antioxidant Properties ◽  
Density Lipoprotein ◽  
Current Evidence ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Background: Resveratrol is a potential treatment option for management of non-alcoholic fatty liver disease (NAFLD) due to its anti-inflammatory, antioxidant properties, and calorie restriction-like effects. We aimed to synthesise evidence from published randomized clinical trials (RCTs) about the efficacy of resveratrol in the management of NAFLD.Methods: A computer literature search of PubMed, Scopus, Web of Science, and Cochrane Central was conducted using relevant keywords. Records were screened for eligible studies and data were extracted and synthesized using Review Manager Version 5.3 for windows. Subgroup analysis and sensitivity analysis were conducted.Results: Four RCTs (n=158 patients) were included in the final analysis. The overall effect estimates did not favor resveratrol group in terms of: serum ALT (MD -2.89, 95%CI [-15.66, 9.88], p=0.66), serum AST (MD -3.59, 95%CI [-13.82, 6.63], p=0.49), weight (MD -0.18, 95%CI [-0.92, 0.55], p=0.63), BMI (MD -0.10, 95 %CI [-0.43, 0.24], p=0.57), blood glucose level (MD -0.27, 95%CI [-0.55, 0.01], p=0.05), insulin level (MD -0.12, 95%CI [-0.69, 0.46], p=0.69), triglyceride level (MD 0.04, 95%CI [-0.45, 0.53], p=0.87), and LDL level (MD 0.21, 95%CI [-0.41, 0.83], p=0.51). Pooled studies were heterogeneous.Conclusion: Current evidence is insufficient to support the efficacy of resveratrol in the management of NAFLD. Resveratrol does not attenuate the degree of liver fibrosis or show a significant decrease in any of its parameters.Abbreviations: ALT: Alanine aminotransferase; AMPK: AMP-activated protein kinase; AST: Aspartate aminotransferase; BMI: Body mass index; CK-18: Cytokeratin-18; CRP: C-reactive protein; HC: Head circumference; HDL: High density lipoprotein; IL-6: Interleukin-6; LDL: Low density lipoprotein; MD: Mean difference; NAFLD: Non-alcoholic fatty liver disease; NASH: Non-alcoholic steatohepatitis; RCT: Randomized Controlled Trial; RR: Relative risk; SIRT1: Silent information regulation 2 homologue 1; TNF-α: Tumor necrosis factor α; WC: Waist circumference; WHR: Waist hip ratio.

scholarly journals Probiotics and Prebiotics as a Strategy for Non-Alcoholic Fatty Liver Disease, a Narrative Review

Foods ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1719
Author(s):  
Valentina Castillo ◽  
Fernanda Figueroa ◽  
Karoll González-Pizarro ◽  
Paz Jopia ◽  
Claudia Ibacache-Quiroga
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Communicable Disease ◽  
Anthropometric Parameters ◽  
Alcoholic Fatty Liver ◽  
Risks Factors ◽  
Alcoholic Fatty Liver Disease ◽  
Non Communicable Disease

Non-alcoholic fatty liver disease (NAFLD) is a chronic non-communicable disease, with a prevalence of 25% worldwide. This pathology is a multifactorial illness, and is associated with different risks factors, including hypertension, hyperglycemia, dyslipidemia, and obesity. Beside these predisposing features, NAFLD has been related to changes in the microbiota, which favor the disease progression. In this context, the modulation of the gut microbiota has emerged as a new therapeutic target for the prophylaxis and treatment of NAFLD. This review describes the changes in the gut microbiota associated with NAFLD and the effect of probiotics, prebiotics, and synbiotics on the gut microbiota, liver damage, anthropometric parameters, blood lipids, inflammation markers and insulin resistance in these patients.

scholarly journals Addressing the liver progenitor cell response and hepatic oxidative stress in experimental non-alcoholic fatty liver disease/non-alcoholic steatohepatitis using amniotic epithelial cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mihiri Goonetilleke ◽  
Nathan Kuk ◽  
Jeanne Correia ◽  
Alex Hodge ◽  
Gregory Moore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Epithelial Cells ◽  
Fatty Liver ◽  
Progenitor Cells ◽  
Fatty Liver Disease ◽  
Hepatic Inflammation ◽  
Alcoholic Fatty Liver ◽  
And Oxidative Stress ◽  
Alcoholic Fatty Liver Disease

Abstract Background Non-alcoholic fatty liver disease is the most common liver disease globally and in its inflammatory form, non-alcoholic steatohepatitis (NASH), can progress to cirrhosis and hepatocellular carcinoma (HCC). Currently, patient education and lifestyle changes are the major tools to prevent the continued progression of NASH. Emerging therapies in NASH target known pathological processes involved in the progression of the disease including inflammation, fibrosis, oxidative stress and hepatocyte apoptosis. Human amniotic epithelial cells (hAECs) were previously shown to be beneficial in experimental models of chronic liver injury, reducing hepatic inflammation and fibrosis. Previous studies have shown that liver progenitor cells (LPCs) response plays a significant role in the development of fibrosis and HCC in mouse models of fatty liver disease. In this study, we examined the effect hAECs have on the LPC response and hepatic oxidative stress in an experimental model of NASH. Methods Experimental NASH was induced in C57BL/6 J male mice using a high-fat, high fructose diet for 42 weeks. Mice received either a single intraperitoneal injection of 2 × 106 hAECs at week 34 or an additional hAEC dose at week 38. Changes to the LPC response and oxidative stress regulators were measured. Results hAEC administration significantly reduced the expansion of LPCs and their mitogens, IL-6, IFNγ and TWEAK. hAEC administration also reduced neutrophil infiltration and myeloperoxidase production with a concurrent increase in heme oxygenase-1 production. These observations were accompanied by a significant increase in total levels of anti-fibrotic IFNβ in mice treated with a single dose of hAECs, which appeared to be independent of c-GAS-STING activation. Conclusions Expansion of liver progenitor cells, hepatic inflammation and oxidative stress associated with experimental NASH were attenuated by hAEC administration. Given that repeated doses did not significantly increase efficacy, future studies assessing the impact of dose escalation and/or timing of dose may provide insights into clinical translation.

Gut microbiota and non-alcoholic fatty liver disease: a narrative review

2021 ◽  
Author(s):  
Ludovico Abenavoli ◽  
Anna C. Procopio ◽  
Emidio Scarpellini ◽  
Natale Polimeni ◽  
Isabella Aquila ◽  
...  
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Narrative Review ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals Correlation of Gut Firmicutes/Bacteroidetes Ratio with Fibrosis and Steatosis in Patients with Non-alcoholic Fatty Liver Disease

2020 ◽  
Author(s):  
Chyntia Olivia Maurine Jasirwan ◽  
Akhmadu Muradi ◽  
Irsan Hasan ◽  
Marcellus Simadibrata ◽  
Ikhwan Rinaldi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Central Obesity ◽  
Gastrointestinal Microbiota ◽  
Alcoholic Fatty Liver ◽  
Microbiota Diversity ◽  
Alcoholic Fatty Liver Disease ◽  
High Triglyceride

Abstract Background : We investigated the gut microbiota in patients with non-alcoholic fatty liver disease (NAFLD) and its correlation with fibrosis and steatosis as reflected in the controlled attenuation parameter and transient elastography valuesMethods : A cross-sectional study was performed on 37 patients with NAFLD at Cipto Mangunkusumo National General Hospital from December 2018 to March 2019. The gut microbiota was investigated in fecal samples with 16S RNA sequencing using the next-generation sequencing platform MiSeq (Illumina).Results : NAFLD was more common in patients with metabolic syndrome. Firmicutes, Bacteroidetes, and Proteobacteria were the predominant phyla. Bacteroides was more dominant than Prevotella, contrary to the results in previous studies on normal populations in Indonesia. Microbiota dysbiosis was observed in most samples. The gastrointestinal microbiota diversity was significantly decreased in patients with NAFLD with high triglyceride levels and central obesity. The Firmicutes/Bacteroidetes ratio correlated with steatosis and obesity, whereas some other species in the lower taxonomy were mostly correlated with steatosis and obesity without fibrosis. Proteobacteria is the only phylum strongly correlated with fibrosis in patients with normal body mass index.Conclusions : The gut microbiota diversity was decreased in patients with NAFLD with high triglyceride levels and central obesity, and certain gut microbes were correlated with fibrosis and steatosis.

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