Abstract
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.
Highlights
Metabolic dysfunction-associated fatty liver disease (MAFLD), previously known as non-alcoholic fatty liver disease (NAFLD), is a major cause of liver-related morbimortality, with an estimated global prevalence of 25.24% [1]
The term reflects the wide spectrum of the disease, which ranges from simple steatosis, to liver inflammation, fibrosis and cirrhosis
The diagnostic criteria for MAFLD have been reformulated, and are based on the evidence of hepatic steatosis, in addition to one of the following criteria: overweight/obesity, type 2 diabetes mellitus, or metabolic dysregulation defined by the presence of at least two metabolic risk factors [4]
Summary
Metabolic dysfunction-associated fatty liver disease (MAFLD), previously known as non-alcoholic fatty liver disease (NAFLD), is a major cause of liver-related morbimortality, with an estimated global prevalence of 25.24% [1]. The interaction between the gut, its microbiome and the liver, is key to the pathogenesis of MAFLD, and a significant number of reviews addressing the role of the gut-liver axis have been published over the past few years [5,6,7]. This evolving field has recently achieved promising therapeutic advances based on microbiota composition manipulation. The disruption of the gutliver axis alters the balance between immune activation and tolerance [9], and the subsequent immune dysfunction critically contributes to the pathogenesis and progression of liver diseases, and in particular, to MAFLD [5]
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