Gut Microbiota in NAFLD/MASLD: Functional Dysbiosis and the Gut–Liver Axis in Disease Progression

Background: Non-alcoholic fatty liver disease (NAFLD), now largely encompassed by the metabolic dysfunction-associated steatotic liver disease (MASLD) framework, is a leading cause of chronic liver disease worldwide and is closely linked to obesity, insulin resistance, type 2 diabetes (T2D), and cardiometabolic dysfunction. Although hepatic lipid accumulation and metabolic injury remain central to its pathogenesis, increasing evidence implicates the intestinal microbiota as a modulator of disease onset and progression through the gut–liver axis. Objectives: This narrative review summarizes current evidence linking gut microbiota to NAFLD/MASLD, with emphasis on functional microbial alterations relevant to the gut–liver axis, disease severity, microbiota-related biomarkers, and microbiota-targeted interventions. Methods: The literature search for this narrative review was mainly performed using PubMed/MEDLINE (which produced 200 results since 2023). The search addressed the relationship between gut microbiota, NAFLD/MASLD, and gut–liver axis dysfunction. Results: Early studies mainly focused on disease-associated bacterial taxa; however, no consistent microbial signature has been reproduced across populations, disease stages, and methodological platforms. This limitation supports a shift from a taxonomic view of dysbiosis toward a functional interpretation. Different microbial communities may converge on shared pathogenic outputs, including impaired epithelial barrier integrity, microbial translocation, lipopolysaccharide-driven Toll-like receptor 4 activation, bile acid remodelling, altered short-chain fatty acid production, endogenous ethanol generation, choline and trimethylamine-N-oxide metabolism, and tryptophan-derived indole signalling. These mechanisms may influence hepatic steatosis, inflammatory activation, and fibrogenesis. Conclusions: Current data support the microbiota as a biologically plausible disease modifier, but not yet as a standalone diagnostic or therapeutic target; clinical translation will require longitudinal, multi-omics, and function-oriented studies.