Abstract
Introduction: The gut born hormones GLP-1 and GIP augment glucose-dependently the postprandial (PP) insulin release from the pancreatic B-cell, mediating the so-called incretin effect. The incretin effect is reduced in T2DM. As synthetic GIP failed to stimulate insulin in T2DM, a defect of GIP effectiveness has been suggested. To compare the contribution of endogenous GLP-1 and non-GLP-1 incretins, we examined the insulinotropic action of a duodenally perfused meal using the specific GLP-1 receptor antagonist exendin(9–39) (Ex-9).
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