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Mechanistic work demonstrated that GLP-1 signalling can also modulate intestinal epithelial integrity, mucosal immune responses and the microbiome in pre-clinical colitis models, providing a biologically plausible rationale for a role beyond weight reduction [2]

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[4] Reviews also describe angiogenic effects that the authors argue mirror standard growth factors across multiple tissue types

Both incretins are rapidly clived by the enzyme dipeptidil peptidase 4 (DPP4)

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