Role of gut-liver axis and glucagon-like peptide-1 receptor agonists in the treatment of metabolic dysfunction-associated fatty liver disease

Figure 1 Intestinal barrier in healthy and metabolic dysfunction-associated fatty liver disease syndrome people. Comparison of the intestinal barrier and mechanisms involved in its disruption. A: Healthy people; B: Metabolic dysfunction-associated fatty liver disease (MAFLD) syndrome people. The composition of the gut microbiota plays a critical role in maintaining the integrity of the intestinal barrier through several mechanisms: regulation of mucus layer thickness produced by goblet cells, production of antimicrobial peptides by Paneth cells, levels of tight junction proteins responsible for epithelial cell integrity, and the activation of immune cells such as macrophages, plasma cells, and T and B lymphocytes. These mechanisms are located in different compartments of the intestinal barrier. In individuals with MAFLD syndrome, dysbiosis results in a reduction in mucous layer thickness, antimicrobial peptides production, and the levels of tight junction proteins. There is also an alteration in the number of immune cells in the lamina propria. Macrophage activation leads to the production of pro-inflammatory cytokines. These factors contribute to increased intestinal permeability and disturbance of the gut-liver axis homeostasis. The figure was created using Servier Medical Art application offered by Servier and licensed under a Creative Commons Attribution 3.0 Unported License.