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For example, in alveolar macrophages, GLP-1 receptor agonism suppressed activation of the NLRP3 inflammasome and reduced production of IL-1β [65], an effect in part mediated by the disruption of histone lactylation, a recognised regulator of pro-fibrotic gene expression [65]

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Similarly, DPP-IV inhibitor Gramcyclin A treatment in a recent APP/PS1/tau triple transgenic mouse model of AD stimulated GLP-1R signaling, promoted glucose uptake in the brain, decreased levels of activated microglia and neuroinflammation in the hippocampus, and reduced amyloid-β plaques, soluble amyloid-β–40, and soluble amyloid-β–42 levels (246)