Where it comes from
- Made in
- L cells of the lower gut
- Sent out by
- After meals, with GLP-1
- Acts on
- Stomach (acid secretion)
- Gut lining
What it does
- Weakly suppresses gastric acid in animals, the effect it was first noticed for
- Activates the GIP, GLP-1 and glucagon receptors in cell assays, but only at concentrations far above those in blood, so it is unlikely to be a signal in its own right 2
- Mostly a marker of how much the L cells secrete, measured beside the other proglucagon products 3
In medicine
- Measured in research, where its blood level tracks L-cell output and rises steeply after bariatric surgery 3
- No medicine and no clinical test is built on it, and no routine laboratory reports it
- Its 69 residues contain glucagon end to end, so antibodies raised against glucagon can read it by mistake; that cross-reaction is why the older “enteroglucagon” numbers are hard to interpret 1
Beyond the body’s own use
- Not in trials, and no analogue of it has been made. The dual and triple agonists now in obesity trials were built from oxyntomodulin and glucagon, not from this longer piece 1
- The question actually asked of it is whether it is more than a leftover of processing. Screening 42 peptides against the GIP receptor in 2026 found glicentin the only non-GIP ligand that switched it on, at about a thousand times the concentration that circulates 2
- Nobody has raised a person’s glicentin and watched what happens, so the negative reading of that cell work is an inference, not a result
Sources
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.