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Nonetheless, the aforementioned animal models, although extremely useful in investigating specific molecular mechanisms in the pathogenesis of ulcerative colitis, do not truly recapitulate disease as observed in patients, as IBD is a multifactorial disease and most clearly is not caused by a single mutation or defect in cellular or molecular pathways

A single administration of sitagliptin 100 mg reduced expression of Toll-like receptor 2, I-kappa-B kinase, C-C chemokine receptor type 2, and CD26 and decreased nuclear factor-B binding in isolated peripheral blood mononuclear cells (210)

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Preclinical and mechanistic studies have suggested potential interactions between GLP-1 signalling and bone metabolism