The most significant incretin which is deficient in type 2 diabetics.
Suppresses glucagon production, physiologically releases insulin and in animal studies increased beta cell mass from pancreatic duct stem cells.
Increases within minutes.
Glucagon-like peptide-1 (GLP-1) is an incretin released by the duodenum that inhibits relaxation of the stomach.
This inhibition causes increased stretch of the stomach, increasing activation of proximal gastric stretch receptors.
It also slows overall gut motility, increasing the duration of satiety.
This effect is used to increase weight loss and treat obesity through GLP-1 agonists.
Increase release following gastric bypass when large volumes of chyme presented to the hindgut and results in improvement in diabetes.
Most made in enteroendocrine L cells in the distal ileum and colon and plasma levels increase within minutes of eating.
Has a short half-life when released from the gastrointestinal tract so it is given as an injection where it is bound to albumin and slowly released.
A combination of endocrine and neural signals promote secretion before digested food transits via the gut to directly stimulate L cells in the small bowel and colon.
Proximately located L cells in duodenum and jejunum exist but their contributions of such cell in the rapid increase in plasma GLP-1 is not clear.
Plasma levels low in fasting state in the range of 5-10 pmol/L and reach 15-50 pmol/L after eating.
Circulating levels decrease rapidly because of enzymatic inactivation mainly by dipeptyl peptidase-4 (DDP-4) and renal clearance.
GLP-1 based therapies for DM include mimetic exenatide, and a dipeptidyl peptidase 4 inhibitor, sitagliptin phosphate.
A product of pro glucagon processing in the gut and CNS.
Secreted by L-cells of the intestine postprandially.
A gut-derived peptide with glucose and immune modulatory function.
It is secreted in response to nutritional and inflammatory stimuli from intestinal L-Cells and pancreatic alpha cells.
Regulates blood glucose levels via the stimulation of glucose-dependent insulin secretion from pancreatic beta cells and inhibition of glucagon release from pancreatic alpha cells.
Has 36-37 amino acids.
Synthesized in brainstem and projects to the brain including PVN.
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.
Incretin effect is reduced in patients with type 2 diabetes.
Postprandial GLP-1 levels are decreased in patients with type two diabetes.
GLP-1 inhibits food intake.
Half life is short due to rapid inactivation via dipeptidyl peptidase 4.
GLP-1 indirectly effects fullness and satiety by delaying gastric emptying and distention of the stomach and directly effects receptors in CNS to regulate appetite
Stimulates insulin production when glucose levels are elevated.
Blunts glucagon when glucose levels are elevated, preserving appropriate glucagon responses to hypoglycemia.
Modulates gastric emptying with decreased entry of caloric content into small intestine per unit time.
GLP-1 analogs such as exenatide and liraglutide have long half-lives unlike GLP-1 which is broken down in 2 minutes.
GLP_1 analogs require subcutaneous injection.
GLP_1 analogs are associated with a 1% reduction in HgbA1C and are associated with weight loss.
GLP_1 analogues are associated with nausea in 10-15% of cases.
GLP-1 analogs are associated with pancreatitis.