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The ENS communicates with the brain through neuropeptides such as substance P and vasoactive intestinal peptide, which are involved in modulating inflammatory responses (Marsilio, 2019)

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Regarding fibrosis, while direct anti-fibrotic mechanisms are less established, preclinical studies indicate that GLP-1 RAs could suppress fibrogenic cell activation and reduce expression of pro-fibrotic genes encoding extracellular matrix proteins, potentially facilitating fibrosis regression in conjunction with improvements in steatosis and inflammation [29-32]