scholarly journals The Role of the Gut-Liver Axis in Metabolic Dysfunction-Associated Fatty Liver Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Rosa Martín-Mateos ◽  
Agustín Albillos
Keyword(s):  
Immune System ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Structural Changes ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Intercellular Junctions ◽  
Metabolic Dysfunction ◽  
Non Invasive

The complex interplay between the gut microbiota, the intestinal barrier, the immune system and the liver is strongly influenced by environmental and genetic factors that can disrupt the homeostasis leading to disease. Among the modulable factors, diet has been identified as a key regulator of microbiota composition in patients with metabolic syndrome and related diseases, including the metabolic dysfunction-associated fatty liver disease (MAFLD). The altered microbiota disrupts the intestinal barrier at different levels inducing functional and structural changes at the mucus lining, the intercellular junctions on the epithelial layer, or at the recently characterized vascular barrier. Barrier disruption leads to an increased gut permeability to bacteria and derived products which challenge the immune system and promote inflammation. All these alterations contribute to the pathogenesis of MAFLD, and thus, therapeutic approaches targeting the gut-liver-axis are increasingly being explored. In addition, the specific changes induced in the intestinal flora may allow to characterize distinctive microbial signatures for non-invasive diagnosis, severity stratification and disease monitoring.

Long‐term prognosis of patients with metabolic (dysfunction)‐associated fatty liver disease by non‐invasive methods

2022 ◽  
Author(s):  
Marie Decraecker ◽  
Dan Dutartre ◽  
Jean‐Baptiste Hiriart ◽  
Marie Irles‐Depé ◽  
Faiza Chermak ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Metabolic Dysfunction ◽  
Non Invasive ◽  
Long Term Prognosis

scholarly journals Ultrasound Elastography—Cornerstone of Non-Invasive Metabolic Dysfunction-Associated Fatty Liver Disease Assessment

Medicina ◽  
2021 ◽  
Vol 57 (6) ◽  
pp. 516
Author(s):  
Andrej Hari
Keyword(s):  
Liver Disease ◽  
Liver Fibrosis ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Ultrasound Elastography ◽  
Disease Assessment ◽  
Metabolic Dysfunction ◽  
Common Cause ◽  
Non Invasive ◽  
Invasive Evaluation

Metabolic dysfunction-associated fatty liver disease has become the most common chronic liver disease as well as the most common cause for liver transplantation. With its different methods types, elastography of the liver can be used for non-invasive evaluation of the liver fibrosis and steatosis degree. The article focuses on the description, use, advantages, and limitations of the currently known elastographic techniques. It proposes a simple risk assessment algorithm for the liver fibrosis progress evaluation. The following is an overview of the use of liver and spleen elastography in the detection of clinically relevant portal hypertension. It concludes with research and technological possibilities that could be important to the field in the upcoming years.

scholarly journals Pediatric Non-Alcoholic Fatty Liver Disease: Nutritional Origins and Potential Molecular Mechanisms

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3166 ◽  
Author(s):  
Ashok Mandala ◽  
Rachel C. Janssen ◽  
Sirish Palle ◽  
Kevin R. Short ◽  
Jacob E. Friedman
Keyword(s):  
Immune System ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Molecular Mechanisms ◽  
Rapid Progression ◽  
Alcoholic Fatty Liver ◽  
Non Invasive ◽  
Immune System Development ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is the number one chronic liver disease worldwide and is estimated to affect nearly 40% of obese youth and up to 10% of the general pediatric population without any obvious signs or symptoms. Although the early stages of NAFLD are reversible with diet and lifestyle modifications, detecting such stages is hindered by a lack of non-invasive methods of risk assessment and diagnosis. This absence of non-invasive means of diagnosis is directly related to the scarcity of long-term prospective studies of pediatric NAFLD in children and adolescents. In the majority of pediatric NAFLD cases, the mechanisms driving the origin and rapid progression of NAFLD remain unknown. The progression from NAFLD to non-alcoholic steatohepatitis (NASH) in youth is associated with unique histological features and possible immune processes and metabolic pathways that may reflect different mechanisms compared with adults. Recent data suggest that circulating microRNAs (miRNAs) are important new biomarkers underlying pathways of liver injury. Several factors may contribute to pediatric NAFLD development, including high-sugar diets, in utero exposures via epigenetic alterations, changes in the neonatal microbiome, and altered immune system development and mitochondrial function. This review focuses on the unique aspects of pediatric NAFLD and how nutritional exposures impact the immune system, mitochondria, and liver/gastrointestinal metabolic health. These factors highlight the need for answers to how NAFLD develops in children and for early stage-specific interventions.

scholarly journals Inflammation and Fibrogenesis in MAFLD: Role of the Hepatic Immune System

2021 ◽  
Vol 8 ◽  
Author(s):  
Pietro Torre ◽  
Benedetta Maria Motta ◽  
Roberta Sciorio ◽  
Mario Masarone ◽  
Marcello Persico
Keyword(s):  
Immune System ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Diseases ◽  
Metabolic Dysfunction ◽  
Therapeutic Approaches ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Metabolic (dysfunction)-associated fatty liver disease (MAFLD) is the definition recently proposed to better circumscribe the spectrum of conditions long known as non-alcoholic fatty liver disease (NAFLD) that range from simple steatosis without inflammation to more advanced liver diseases. The progression of MAFLD, as well as other chronic liver diseases, toward cirrhosis, is driven by hepatic inflammation and fibrogenesis. The latter, result of a “chronic wound healing reaction,” is a dynamic process, and the understanding of its underlying pathophysiological events has increased in recent years. Fibrosis progresses in a microenvironment where it takes part an interplay between fibrogenic cells and many other elements, including some cells of the immune system with an underexplored or still unclear role in liver diseases. Some therapeutic approaches, also acting on the immune system, have been probed over time to evaluate their ability to improve inflammation and fibrosis in NAFLD, but to date no drug has been approved to treat this condition. In this review, we will focus on the contribution of the liver immune system in the progression of NAFLD, and on therapies under study that aim to counter the immune substrate of the disease.

Non-Invasive Distinction of Non-Alcoholic Fatty Liver Disease using Urinary Volatile Organic Compound Analysis: Early Results

2015 ◽  
Vol 24 (2) ◽  
pp. 197-201 ◽  
Author(s):  
Ramesh P. Arasaradnam ◽  
Michael McFarlane ◽  
Emma Daulton ◽  
Erik Westenbrink ◽  
Nicola O’Connell ◽  
...  
Keyword(s):  
Liver Disease ◽  
Pilot Study ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Diagnostic Methods ◽  
Screening Methods ◽  
Alcoholic Fatty Liver ◽  
Non Invasive ◽  
Volatile Organic ◽  
Alcoholic Fatty Liver Disease

Background & Aims: Non-Alcoholic Fatty Liver Disease (NAFLD) is the commonest cause of chronic liver disease in the western world. Current diagnostic methods including Fibroscan have limitations, thus there is a need for more robust non-invasive screening methods. The gut microbiome is altered in several gastrointestinal and hepatic disorders resulting in altered, unique gut fermentation patterns, detectable by analysis of volatile organic compounds (VOCs) in urine, breath and faeces. We performed a proof of principle pilot study to determine if progressive fatty liver disease produced an altered urinary VOC pattern; specifically NAFLD and Non-Alcoholic Steatohepatitis (NASH).Methods: 34 patients were recruited: 8 NASH cirrhotics (NASH-C); 7 non-cirrhotic NASH; 4 NAFLD and 15 controls. Urine was collected and stored frozen. For assay, the samples were defrosted and aliquoted into vials, which were heated to 40±0.1°C and the headspace analyzed by FAIMS (Field Asymmetric Ion Mobility Spectroscopy). A previously used data processing pipeline employing a Random Forrest classification algorithm and using a 10 fold cross validation method was applied.Results: Urinary VOC results demonstrated sensitivity of 0.58 (0.33 - 0.88), but specificity of 0.93 (0.68 - 1.00) and an Area Under Curve (AUC) 0.73 (0.55 -0.90) to distinguish between liver disease and controls. However, NASH/NASH-C was separated from the NAFLD/controls with a sensitivity of 0.73 (0.45 - 0.92), specificity of 0.79 (0.54 - 0.94) and AUC of 0.79 (0.64 - 0.95), respectively.Conclusions: This pilot study suggests that urinary VOCs detection may offer the potential for early non-invasive characterisation of liver disease using 'smell prints' to distinguish between NASH and NAFLD.

scholarly journals Targeting the GPR119/incretin axis: a promising new therapy for metabolic-associated fatty liver disease

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Jianan Zhao ◽  
Yu Zhao ◽  
Yiyang Hu ◽  
Jinghua Peng
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Drug Targets ◽  
Metabolic Dysfunction ◽  
Multiple Organs ◽  
Glucose And Lipid Metabolism ◽  
Potential Therapeutic Role ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

AbstractIn the past decade, G protein-coupled receptors have emerged as drug targets, and their physiological and pathological effects have been extensively studied. Among these receptors, GPR119 is expressed in multiple organs, including the liver. It can be activated by a variety of endogenous and exogenous ligands. After GPR119 is activated, the cell secretes a variety of incretins, including glucagon-like peptide-1 and glucagon-like peptide-2, which may attenuate the metabolic dysfunction associated with fatty liver disease, including improving glucose and lipid metabolism, inhibiting inflammation, reducing appetite, and regulating the intestinal microbial system. GPR119 has been a potential therapeutic target for diabetes mellitus type 2 for many years, but its role in metabolic dysfunction associated fatty liver disease deserves further attention. In this review, we discuss relevant research and current progress in the physiology and pharmacology of the GPR119/incretin axis and speculate on the potential therapeutic role of this axis in metabolic dysfunction associated with fatty liver disease, which provides guidance for transforming experimental research into clinical applications.

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