Glucose dependent insulinotropic polypeptide (GIP) is a 42 amino acid hormone synthesized in duodenal and jejunal enteroendocrine k cells in the proximal small bowel.
The two most important incretins are GIP and GLP-1.
Neuroendocrine cells, called L cells, mostly in large intestine produce GIP.
Gastrointestinal peptides that affect glycemic control.
Incretins include amylin, gastric inhibitory peptide (GIP), and glucagon-like peptide 1 (GLP-1).
GIP levels increase minutes after eating.
GLP-1 causes insulin release from beta cell, but only when blood glucose levels are elevated.
Drugs that work through GLP-1 are less likely to cause hypoglycemia, unlike sulfonylureas which release insulin from the beta cells no matter the blood glucose levels.
Glucagon-like peptide-1 (GLP-1) is an incretin hormone that stimulates release following oral intake of glucose.
The effects of incretin hormones are diminished in patients with type II diabetes.
GLP-1 function is retained in type II diabetes and administration of GLP-one receptor agonists can restore the incretin effect in these patients.
Glucagon like peptide-1 (GLP-1) exists in two circulating equipotent molecular forms, GLP-1(&-37) and GLP-1(&-36)amide.
GLP-1 made in enteroendocrine L cells of the distal ileum and colon, and plasma levels increase in minutes after eating.
Hormones are released by the intestine throughout the day and are increased in response to a meal.
Hormones increase insulin secretion, suppress glucagon release, delay gastric emptying and cause satiety.
GLP-1 decreases glucagon, which normally antagonizes insulin.
GLP-1 amplifies the effect of secreted insulin by decreasing glucagon.
GLP-1 slows gastric motility.
GLP-1 has a central effect on the hypothalamus on satiety and helps account for weight loss with incretins.
Incretin based medications are available in two families: DPP-4 inhibitors and GLP-1 receptor antagonists.