In this study, we evaluate possible impairments in the overall incretin secretion from normal glucose tolerance to overt diabetes, as well as their association with impaired insulin secretion.
Pancreatic GLP-1, independent of gut sources, plays a novel role in regulating insulin secretion. A number of studies have suggested that pancreatic cells produce intact GLP-1, thereby constituting a gut-independent paracrine incretin system.
We tested this model using data from a mixed meal test (MMT), thereby measuring GLP-1-induced potentiation of insulin secretion in response to a meal. Following meal ingestion, the gut-derived incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are released by intestinal L and K cells, respectively. Glucagon-like peptide-1 (GLP-1) was discovered as an incretin hormone, which is released from the intestine upon nutrient intake and stimulates insulin secretion from the pancreatic islet -cells. Subsequently, its ability to suppress appetite was recognized. bstract Gastrointestinal hormones that potentiate insulin secretion from pancreatic -cells are called incretins. Glucose-dependent insulinotropic polypeptide/gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the major incretins. Our data show that development of glucose intolerance and beta cell dysfunction are significantly associated with increased levels of intra-islet intact GLP-1, a potentially beneficial adaptation of the paracrine regulation of insulin secretion in type 2 diabetes.
Following meal ingestion, the gut-derived incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are released by intestinal L and K cells, respectively.
Furthermore, visual representations like the one above help us fully grasp the concept of Glp-1 And Insulin Secretion In Humans With Impaired Glucose Tolerance.
Glucagon-like peptide-1 (GLP-1) was discovered as an incretin hormone, which is released from the intestine upon nutrient intake and stimulates insulin secretion from the pancreatic islet -cells. Subsequently, its ability to suppress appetite was recognized.
Our data show that development of glucose intolerance and beta cell dysfunction are significantly associated with increased levels of intra-islet intact GLP-1, a potentially beneficial adaptation of the paracrine regulation of insulin secretion in type 2 diabetes.
