Oat beta-glucan modulates gut microbiota to prevent progression of metabolic dysfunction-associated steatotic liver disease (MASLD). In a mouse model of MASLD induced by a western-style diet (WSD), oat beta-glucan did not affect body weight or glucose intolerance but significantly reduced inflammation and fibrosis. This protective effect was mediated by gut microbiota, not bile acid signaling, and was associated with a shift toward beneficial microbial taxa, such as Ruminococcus and Lactobacillus, and reduced translocation of bacterial components. Broad-spectrum antibiotic treatment, which depleted gut microbiota, abolished the protective effects of oat beta-glucan. The study highlights that oat beta-glucan may be a cost-effective and well-tolerated approach to prevent MASLD progression, with potential for clinical application. The findings suggest that oat beta-glucan can reduce liver inflammation and fibrosis by modulating the gut microbiome, thereby protecting against bacterial translocation and fibroinflammatory pathways. The results indicate that oat beta-glucan could be a promising therapeutic option for MASLD, particularly in advanced stages of the disease. The study also underscores the importance of gut microbiota in MASLD progression and the potential of oat beta-glucan as a prebiotic to restore microbial balance and reduce disease severity. Further research is needed to confirm these findings in human trials and to explore the mechanisms underlying the protective effects of oat beta-glucan.Oat beta-glucan modulates gut microbiota to prevent progression of metabolic dysfunction-associated steatotic liver disease (MASLD). In a mouse model of MASLD induced by a western-style diet (WSD), oat beta-glucan did not affect body weight or glucose intolerance but significantly reduced inflammation and fibrosis. This protective effect was mediated by gut microbiota, not bile acid signaling, and was associated with a shift toward beneficial microbial taxa, such as Ruminococcus and Lactobacillus, and reduced translocation of bacterial components. Broad-spectrum antibiotic treatment, which depleted gut microbiota, abolished the protective effects of oat beta-glucan. The study highlights that oat beta-glucan may be a cost-effective and well-tolerated approach to prevent MASLD progression, with potential for clinical application. The findings suggest that oat beta-glucan can reduce liver inflammation and fibrosis by modulating the gut microbiome, thereby protecting against bacterial translocation and fibroinflammatory pathways. The results indicate that oat beta-glucan could be a promising therapeutic option for MASLD, particularly in advanced stages of the disease. The study also underscores the importance of gut microbiota in MASLD progression and the potential of oat beta-glucan as a prebiotic to restore microbial balance and reduce disease severity. Further research is needed to confirm these findings in human trials and to explore the mechanisms underlying the protective effects of oat beta-glucan.