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The potential mechanisms (Figure 1) of DPP-4/GLP axis in the IBD may include the following: (1) GLPs promote the tissue repair of injured epithelium

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The intact rat pancreas's GIP perfusion only stimulates glucagon secretion at low glucose levels (4.4 mM) and not at postprandial glucose concentrations (8.9 mM), suggesting that GIP receptor activity in the cell appears to be glucose dependent [18]

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