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Gastric inhibitory polypeptide and glucagon-like peptide-1 in the pathogenesis of type 2 diabetes Nauck MA; Baller B; Meier JJDiabetes 2004[Dec]; 53 Suppl 3 (ä): S190-6The incretin effect denominates the phenomenon that oral glucose elicits a higher insulin response than does intravenous glucose. The two hormones responsible for the incretin effect, glucose-dependent insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. In patients with type 2 diabetes, the incretin effect is reduced, and there is a moderate degree of GLP-1 hyposecretion. However, the insulinotropic response to GLP-1 is well maintained in type 2 diabetes. GIP is secreted normally or hypersecreted in type 2 diabetes; however, the responsiveness of the endocrine pancreas to GIP is greatly reduced. In approximately 50% of first-degree relatives of patients with type 2 diabetes, similarly reduced insulinotropic responses toward exogenous GIP can be observed, without significantly changed secretion of GIP or GLP-1 after oral glucose. This opens the possibility that a reduced responsiveness to GIP is an early step in the pathogenesis of type 2 diabetes. On the other hand, this provides a basis to use incretin hormones, especially GLP-1 and its derivatives, to replace a deficiency in incretin-mediated insulin secretion in the treatment of type 2 diabetes.|Animals[MESH]|Blood Glucose/drug effects/metabolism[MESH]|Diabetes Mellitus, Type 2/*physiopathology[MESH]|Gastric Inhibitory Polypeptide/pharmacology/*physiology[MESH]|Glucagon-Like Peptide 1[MESH]|Glucagon/*physiology[MESH]|Humans[MESH]|Insulin Secretion[MESH]|Insulin/metabolism[MESH]|Peptide Fragments/*physiology[MESH]|Protein Precursors/*physiology[MESH] |
