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This review examines the biological mechanisms underlying GLP-1 RA therapy in MASLD/MASH, analyzes the mechanistic distinctions between mono-, dual-, and triple agonists, and synthesizes current clinical evidence supporting their utilization in individuals with this condition.

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Preclinical models, clinical trials and real-world observational studies strongly support the hypothesis that glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and SGLT2 inhibitors may confer neuroprotective benefits