Abstract
The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are released in response to nutrient ingestion and potentiate glucose-stimulated insulin secretion from pancreatic beta cells. The augmentation of postprandial insulin secretion by such gastrointestinal hormones is called the incretin effect. The incretin effect is almost completely absent in patients with type 2 diabetes. This is due to 1) an approximate 15% reduction in postprandial GLP-1 secretion and 2) a near total loss of insulinotropic activity of GIP. This review article summarizes clinical studies on abnormalities in the secretion and insulinotropic effects of GIP and GLP-1 in patients with type 2 diabetes as well as in individuals at high risk. A significant proportion of first-degree relatives are characterized by a reduced insulinotropic response to exogenous GIP. Nevertheless, this phenomenon does not predispose to a more rapid deterioration in glucose tolerance or conversion to impaired glucose tolerance or diabetes. Therefore, although there are hints of early abnormalities in incretin secretion and action in prediabetic populations, it has not been proven that such phenomena are central to the pathogenesis of type 2 diabetes.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
