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.

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