Incretin hormones are defined as intestinal hormones released in response to nutrient ingestion, which potentiate the glucose-induced insulin response. The strongest candidates for the incretin effect are glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). The aim of the present study is to investigate the incretin effect in obese and lean women with PCOS. Before and after the intervention, all volunteers underwent an oral glucose tolerance test (OGTT) followed by an intravenous glucose infusion (IVGI) on the following day to mimic the blood glucose profile from the OGTT. In studies of the mechanism of the impaired incretin effect in Type 2 diabetic patients, it has been found that the secretion of GIP is generally normal, whereas the secretion of GLP-1 is reduced, presumably as a consequence of the diabetic state. Equal and progressively delayed gastric emptying due to the increasing loads was found in both groups. These drugs therefore do not restore the defective incretin effect in patients.
The two most common forms result from mutations in the genes encoding glucokinase (GCK) (GCK-diabetes: MODY2; 10–20% of all MODY patients [4,5]) and hepatocyte nuclear factor 1α (HNF1A) (HNF1A-diabetes: MODY3; 36–60% of all MODY patients [4,5]). 27 +/- 8%). Other adverse events include hypoglycemia, particularly when GLP-1RA are used in conjunction with other OAD, especially secretagogs.