NFKB1 and short bowel syndrome: GLP-2 is an prominent regulator of intestinal permeability which is secreted by enteroendocrine L cells following meals and enhances intestinal barrier integrity: consistently, GLP-2 analogues26 are currently used in short bowel syndrome and may represent an attractive therapeutic tool in MASH by their anti-inflammatory effects, which are both indirect, mediated through amelioration of intestinal permeability and metabolic endotoxemia, and direct, by inhibition of NF-kB activation by LPS and NEFAs in MNCs.7,26,27