scholarly journals Intestinal Dysbiosis and Non-Alcoholic Fatty Liver Disease

2021 ◽  
Author(s):  
Teresa Auguet ◽  
Laia Bertran ◽  
Jessica Binetti
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Immune Cell ◽  
Specific Treatment ◽  
Short Chain Fatty Acids ◽  
Hepatocellular Injury ◽  
Alcoholic Fatty Liver ◽  
Intestinal Dysbiosis ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) affects 20–30% of the population, with an increased prevalence in industrialized regions. Some patients with NAFLD develop an inflammatory condition termed non-alcoholic steatohepatitis (NASH) that is characterized by hepatocellular injury, innate immune cell-mediated inflammation, and progressive liver fibrosis. In clinical practice, abdominal imaging, which reveals hepatic steatosis, is sufficient for NAFLD diagnosis if other diseases have been rejected. However, a liver biopsy is needed to differentiate NASH from simple steatosis. Therapeutic strategies used to treat obesity and metabolic syndrome improve NAFLD, but there is no specific treatment effective for NASH. The gut microbiota (GM) is composed of millions of microorganisms. Changes in the GM have a significant impact on host health. Intestinal dysbiosis is an imbalance in the GM that can induce increased permeability of the epithelial barrier, with migration of GM-derived mediators through portal vein to the liver. These mediators, such as lipopolysaccharides, short-chain fatty acids, bile acids (BAs), choline, and endogenous ethanol, seem to be involved in NAFLD pathogenesis. Given this evidence, it would be interesting to consider GM-derived mediator determination through omics techniques as a noninvasive diagnostic tool for NASH and to focus research on microbiota modulation as a possible treatment for NASH.

Sinapine reduces non-alcoholic fatty liver disease in mice by modulating the composition of the gut microbiota

2019 ◽  
Vol 10 (6) ◽  
pp. 3637-3649 ◽  
Author(s):  
Youdong Li ◽  
Jinwei Li ◽  
Qingfeng Su ◽  
Yuanfa Liu
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Chronic Inflammation ◽  
Fatty Liver Disease ◽  
Low Grade ◽  
Alcoholic Fatty Liver ◽  
Intestinal Dysbiosis ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is associated with low-grade chronic inflammation and intestinal dysbiosis.

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.

Characteristics of intestinal dysbiosis in patients with non-alcoholic fatty liver disease

2020 ◽  
Vol 0 (6) ◽  
pp. 5-13
Author(s):  
G. D. Fadieienko ◽  
A. Y. Gridnyev ◽  
I. E. Kushnir ◽  
O. G. Kurinna ◽  
V. M. Chernova ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Intestinal Dysbiosis ◽  
Alcoholic Fatty Liver Disease

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.

Hepatocyte and immune cell crosstalk in non-alcoholic fatty liver disease

2021 ◽  
pp. 1-14
Author(s):  
Azalia Mariel Carranza-Trejo ◽  
Vaclav Vetvicka ◽  
Lucie Vistejnova ◽  
Milena Kralickova ◽  
Edgar B. Montufar
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Immune Cell ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease ◽  
Cell Crosstalk

scholarly journals Gut-Microbial and -Metabolomic Signatures in the Prevention of Non-Alcoholic Fatty Liver Disease by Lactobacillus Lactis and Pediococcus Pentosaceus

2020 ◽  
Author(s):  
Gi Soo Youn ◽  
Jeong Seok Yu ◽  
Jieun Choi ◽  
Yujin Kang ◽  
Byung Yong Kim ◽  
...  
Keyword(s):  
Liver Disease ◽  
Mouse Model ◽  
Fatty Liver ◽  
Bile Acids ◽  
Fatty Liver Disease ◽  
Area Under The Curve ◽  
Short Chain Fatty Acids ◽  
Alcoholic Fatty Liver ◽  
Tryptophan Metabolites ◽  
Alcoholic Fatty Liver Disease

Abstract Background: Despite a recent preventive evidence of Lactobacillus and Pediococcus on non-alcoholic fatty liver disease (NAFLD) progression, the underlying mechanistic is less understood. We explored the causality of L. lactis and P. pentosaceus on the gut-metabolomic modulation in the prevention of NAFLD progression in mouse model and subsequently discovered metabolic biomarkers based on NAFLD patients.Results: Six-week-old male C57BL/6J mice were divided into 4 groups (control, Western diet [WD], and 2 WD with strains [L. lactis and P. pentosaceus]). Given completely reproduced data (liver/body ratio, pathology, and metagenomic profiles), comorbid etiologies including inflammation and diabetes were significantly amended by 2 strains. The comprehensive metabolomic profiles of the mouse cecum revealed unique compositional characteristic according to the groups. L. lactis and P. pentosaceus supplementation restored the dysregulation in short chain fatty acids (SCFAs), bile acids, and tryptophan metabolites. Indole derivatives (indole-3-acetic acid, indole-3-propionic acid, and indole-3-acrylic acid) showed anti-inflammatory activities by suppressing pro-inflammation cytokines. Human data (healthy control [n=30] and NAFLD patients [n=74]) were analyzed for clinical association and biomarker. The Fermicutes/Bacteroidetes ratio of NAFLD (4.3) was significantly higher compared with control (0.6)(p<0.05), accompanied by the dysregulation in the key metabolic signatures identified in mouse model. Metabolic panel with 5 stool metabolites (indole, bile acids, and SCFAs) revealed 0.868 (area under the curve; 95% CI 0.773-0.933) in the diagnosis of NAFLD.Conclusion: L. lactis and P. pentosaceus ameliorate NAFLD by modulating gut metabolic environment, particularly the indole pathway, of the gut-liver axis. NAFLD progression was associated with metabolic deterioration in the SCFAs, bile acid, and indole pathways. ClinicalTrials.gov: NCT04339725

scholarly journals Excessive Consumption of the Sugar Rich Longan Fruit Promoted the Development of Non-alcoholic Fatty Liver Disease via Mediating Gut Dysbiosis

2021 ◽  
Author(s):  
Huimin Huang ◽  
Mingxing Li ◽  
Yi Wang ◽  
Xiaoxiao Wu ◽  
Qin Wang ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Alcoholic Fatty Liver ◽  
Free Sugars ◽  
Gut Dysbiosis ◽  
Alcoholic Fatty Liver Disease

Abstract Background: Controversy exists as towards the association of excessive fruits intake and certain disease risks. Longan is an edible fruit rich in high levels of fructose, glucose and sucrose. The aim of this study was to provide direct evidence on the effect of the sugar rich longan fruit on the development of non-alcoholic fatty liver disease (NAFLD). Chemical profiling of longan fruit was conducted using LC-HRMS and HPLC-ELSD.Results: Longan extracts at the doses of 4.0 g/kg, 8.0 and 16.0 g/kg were orally administered for 4 weeks to healthy C57BL/6J mice or to C57BL/6J mice fed with a HFD diet. Fecal microbiome was analyzed by 16S rRNA sequencing. The amounts of short chain fatty acids (SCFAs) in colonic contents were determined by GC-MS. Colon and liver tissues were used for histopathological examination after H&E, Masson’s trichrome, and Oil-red O staining. ELISA method was used for biochemical analysis in serum. In mice fed a normal diet, repeated longan intake for 4 weeks at excess doses (8 or 16 g/kg), but not the normal dose (4 g/kg), promoted inflammation and gut dysbiosis-like status and reduced short-chain fatty acids (SCFAs) production. In high-fat diet (HFD)-fed mice, longan intake at 4 g/kg hardly influenced the NAFLD development. In contrast, excess longan intake (8 or 16 g/kg) promoted NAFLD pathogenesis, including increased abnormality in hepatic indices, elevated inflammation, and gut permeability associated with more severe liver steatosis and fibrosis. Moreover, the exacerbated pathogenic markers were positively correlated with increased blood sugar, aggravated HFD-associated microbial dysbiosis. Conclusions: Effects mediated by excess longan intake resembled that of equivalent free sugars supplementation, suggesting that high level of free sugars in fruits contributed to the promotion of NAFLD development as demonstrated in case of excessive longan intake.

scholarly journals Predicting Non-Alcoholic Fatty Liver Disease Progression and Immune Deregulations by Specific Gene Expression Patterns

2021 ◽  
Vol 11 ◽  
Author(s):  
Fanhong Zeng ◽  
Yue Zhang ◽  
Xu Han ◽  
Min Zeng ◽  
Yi Gao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Immune Cell ◽  
Expression Patterns ◽  
Disease Status ◽  
Gene Signature ◽  
Specific Gene ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide with rising rates in parallel to obesity, type 2 diabetes, and metabolic syndrome. NAFLD includes pathologies ranging from simple steatosis (NAFL) to non-alcoholic steatohepatitis and cirrhosis (NASH), which may eventually develop into hepatocellular carcinoma (HCC). Mechanically, lipids accumulation and insulin resistance act as the first hit, inflammation and fibrosis serve as the second hit. Currently, the diagnosis of NAFLD mainly depends on pathology examination and medical imaging, whereas proper gene signature classifiers are necessary for the evaluation of disease status. Here, we developed three signature classifiers to distinguish different NAFLD disease states (NAFL and NASH). Moreover, we found that B cells, DCs, and MAIT cells are key deregulated immune cells in NAFLD, which are associated with NAFLD and NAFLD-HCC progression. Meanwhile, AKR1B10 and SPP1 are closely related to the above three immune cell infiltrations and immunosuppressive cytokines expressions in NAFLD and NAFLD-HCC. Subsequently, we screened out AKR1B10 and SPP1 sensitive molecules TGX-221, which may provide a possible therapy for NAFLD and NAFLD-HCC.

Gut microbiota as an emerging therapeutic avenue for the treatment of non-alcoholic fatty liver disease

2021 ◽  
Vol 27 ◽  
Author(s):  
Tanya Ralli ◽  
Yub Raj Neupane ◽  
Zoya Saifi ◽  
Kanchan Kohli
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Dietary Fibre ◽  
Fatty Liver Disease ◽  
Intestinal Inflammation ◽  
Specific Treatment ◽  
Hepatoprotective Activity ◽  
Alcoholic Fatty Liver ◽  
Therapeutic Avenue ◽  
Alcoholic Fatty Liver Disease

: Non-alcoholic fatty liver disease (NAFLD) is one of the leading causes of death related to liver diseases worldwide. Despite this, there is no specific treatment that is approved for the disease till now, which could be due to a poor understanding of the pathophysiology of this disease. In the past few decades, several scientists have speculated the root cause of NAFLD to be dysbalance in the gut microbiome resulting in a susceptibility totheinflammatory cascade in the liver. Herein, we hypothesize to fabricate a novel formulation containing prebiotic with probiotics, which, thereby would help in maintaining the gut homeostasis, and used for the treatment of NAFLD. The proposed novel formulation would contain a Bifidobacteriumsp. with Faecalibacteriumprausnitzii in the presence of a dietary fibre having hepatoprotective activity. These two strains of probiotics would help in increasing the concentration of butyrate in the gut, which in turn would inhibit intestinal inflammation and maintain gut integrity. The dietary fibre would serve a dual mechanism; firstly they would act as a prebiotic, which helps in the proliferation of administered probiotics and secondly, would protect the liver via own hepatoprotective action. This combinatorial approach would pave a new therapeutic avenue for the treatment of NAFLD.

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