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 of eating.
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.