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In a lipopolysaccharide (LPS)-induced mouse model, GLP-1 expression was reduced in peripheral blood and increased in alveolar lavage fluid and lung tissues, which was inhibited by liraglutide, a GLP-1RA, and was able to suppress LPS-induced lung injury in mice, inhibit polymorphonuclear neutrophil (PMN) extravasation, reduce the number of apoptotic cells in the lung, inhibit macrophage accumulation 48 and Liraglutide also has anti-inflammatory and airway-protective effects by modulating the PKA/NF-B signaling pathway to improve histopathological changes and airway inflammation in mice, inhibiting E-selectin overexpression and reducing mucus secretion and cupped cell proliferation

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-KG is considered a key hub linking Gln metabolism to phenotypic remodeling (38, 59)