Glicentin
The longest proglucagon peptide released by the gut, what its blood level tracks after meals and surgery, and what it does in animals
Glicentin is the 69-amino-acid peptide that intestinal L cells release when they process proglucagon, the same precursor that yields GLP-1, GLP-2 and oxyntomodulin. It holds the whole oxyntomodulin and glucagon sequences inside it. In people it has been measured, not given: it rises after meals, is higher in infancy, lower in severe obesity, and roughly doubles after gastric bypass. In animals it feeds the growth of the small intestine and slows gut motility, and in cells it weakly activates the GIP, GLP-1 and glucagon receptors.
No established human dose Details ↓
Recommended Dosing
No established human dose
Glicentin has not been given to people in any study we found. Every human study measured it: in blood after glucose or meals, in newborns, in obesity and diabetes, and before and after weight-loss surgery, plus experiments on gut tissue removed at operation.
What is it?
Proglucagon is one precursor cut in different ways in different tissues. In the pancreas it mostly yields glucagon. In the L cells of the small and large intestine it is cut into GLP-1, GLP-2, oxyntomodulin and glicentin. Glicentin is the longest of the gut products, residues 1 to 69 of proglucagon, and its tail end is oxyntomodulin, which in turn contains glucagon. Older papers sometimes call these gut peptides together enteroglucagon or gut glucagon-like immunoreactivity.
That overlap is why glicentin has been the least studied of the family: antibodies against glucagon or oxyntomodulin also catch glicentin, so early measurements could not tell them apart. Specific sandwich assays from the late 1990s, and commercial ones more recently, made it possible to measure glicentin on its own. With them, studies found it rising after oral glucose, peaking higher and sooner after gastrectomy, and absent in a patient with short bowel syndrome, all consistent with release from the small intestine.
Most of what is known about glicentin in people comes from measuring it. Levels are high in infancy and rise with the first feeds; in premature babies, starting breast milk within a day of birth brought that rise forward. In adults, fasting glicentin was about half as high in severe obesity as in normal weight, and lower in adolescents with impaired glucose tolerance. After gastric bypass or sleeve gastrectomy it climbs over the following year, and higher fasting levels after bypass were seen in patients prone to low blood sugar after meals.
What glicentin does is less settled. In rats it promoted growth of the small-intestinal lining but not the colon, and it shortened the post-meal pattern of intestinal contractions. In dogs it released insulin from the pancreas. In human tissue it contracted colon muscle cells. A 2026 cell study found it activates the GIP, GLP-1 and glucagon receptors, but only weakly, so it may act partly through receptors best known for other hormones.
Glicentin is not a drug. No study has given it to people, and its relatives have their own entries: oxyntomodulin, glucagon and GLP-2, and the drugs built on GLP-1. Associations between glicentin levels and weight loss, food preference or blood sugar after surgery are leads, not tests that have changed care.
Mechanism of Action
Glicentin is released from intestinal L cells after meals along with GLP-1 and oxyntomodulin; its own receptor has not been identified, and in cells it acts weakly on the receptors of related hormones.
Proglucagon processing
Intestinal L cells cut proglucagon into glicentin, oxyntomodulin, GLP-1 and GLP-2; the pancreas makes mostly glucagon from the same precursor.
Released after meals
Blood glicentin rises after oral glucose and meals, sooner and higher when food reaches the small intestine quickly, as after gastrectomy or bypass.
Gut growth and motility
In rats it stimulated the small-intestinal lining and shortened the after-meal contraction pattern; it contracts human colon muscle cells.
Shared receptors
In cell assays it activated GIP, GLP-1 and glucagon receptors with low potency.
Published Research
These are studies of glicentin read from their PubMed abstracts: human measurement studies in adults, adolescents, newborns and surgical patients, experiments on donated human gut tissue, a receptor screen, animal studies of gut growth, motility and insulin release, and a review. No study gave glicentin to people.
A specific assay shows it rising after glucose
With a new sandwich ELISA built on synthetic human glicentin, fasting plasma glicentin was about 19 pM in healthy people and in people with diabetes, and above 100 pM in diabetic patients with kidney failure. After an oral glucose load it peaked near 130 pM at 60 minutes in healthy people and near 300 pM at 30 minutes after gastrectomy, while one patient with short bowel syndrome showed no rise, consistent with secretion from the small intestine.
High in infancy and rising after the first feeds
Basal plasma glicentin was higher in children under one year than in children aged 1 to 15. In term and low-birthweight newborns it rose between day 1-2 and day 5-6 and rose after feeds from the first days of life; in very-low-birthweight infants the feeding response did not appear until day 14. Breast-fed and formula-fed infants had similar levels.
Very early feeding brings on glicentin sooner in premature babies
Twenty-one very-low-birthweight infants were randomised to breast milk within 24 hours of birth or later. In the early-fed group basal glicentin rose by day 5-6 and was higher than in the late-fed group at day 5-6 and day 14, and feeds raised it from day 5-6 rather than only at day 14.
Lower in obese adolescents with impaired glucose tolerance
Among 46 adolescents with obesity and 19 lean peers given an oral glucose tolerance test, those with impaired glucose tolerance had lower fasting glicentin (18.2 versus 23.6 pM) and lower GLP-1 than those with normal tolerance. The ratio of glicentin to glucagon during the test fell stepwise from lean to obese to impaired tolerance to type 2 diabetes, suggesting a shift from gut-type to pancreas-type processing of proglucagon.
Halved in severe obesity
Fasting serum glicentin was 12 pmol/L in 39 adults with severe or morbid obesity against 24 pmol/L in 52 adults of normal weight. Across the whole group it did not correlate with body mass index, glucose, insulin, insulin resistance or blood lipids.
Doubles in the year after bariatric surgery
In 30 patients followed after Roux-en-Y gastric bypass (18) or sleeve gastrectomy (12), fasting glicentin rose from six months and by 12 months had about doubled after bypass (fold change 2.0) and risen 1.6-fold after sleeve gastrectomy. The rise did not track changes in weight, glucose or lipids.
A possible warning sign for hypoglycaemia after gastric bypass
In 20 bypass patients with symptoms of low blood sugar after meals, the seven whose glucose fell to 3 mmol/L or less in a mixed-meal test had higher fasting glicentin (22.6 versus 14.0 pM). A cutoff of 17.2 pM flagged them with 86% sensitivity but only 54% specificity; meal responses of GLP-1, glucagon and glicentin rose together in all patients.
Meal response predicts weight loss after surgery
In 42 people with severe obesity, meal-time glicentin and oxyntomodulin responses differed between bypass and sleeve gastrectomy six months after surgery. Larger rises in either hormone predicted more weight lost at 18 months and a stronger move away from energy-dense foods; GLP-1, PYY and ghrelin showed no such link.
Tied to which fuel the body burns overnight
In 192 lean and obese adults measured after an overnight fast, fasting glicentin and GIP were each positively associated with the respiratory quotient, meaning relatively more carbohydrate burning, while free fatty acids were the strongest determinant in the other direction. GLP-1 showed no association.
Linked to reward-area brain responses to food pictures
In 36 adults with obesity scanned while fasting, higher fasting glicentin and oxyntomodulin went with lower activation of reward-related brain areas, including the insula, putamen, caudate and, for glicentin, the orbitofrontal cortex, when they viewed highly desirable foods. The authors call for studies to confirm the link and its bearing on eating.
Contracts human colon muscle cells
In circular smooth muscle cells isolated from colon resections of 22 patients, glicentin caused contraction that grew with concentration, while GLP-1 gave only weak contraction. Exendin(9-39), known as a GLP-1 receptor blocker, abolished the glicentin response, and in rabbit stomach cells glicentin acted at picomolar concentrations.
Acts on nerves in human jejunum strips
Using normal jejunal muscle strips from 14 patients operated on for gastric cancer, recombinant human glicentin relaxed contractions in a concentration-dependent way once adrenergic and cholinergic nerves were blocked, in up to 44% of strips at the highest concentration. Blocking all nerve signalling with tetrodotoxin did not stop the effect, so the authors concluded it acts partly through non-adrenergic non-cholinergic nerves and partly directly on the muscle.
A weak partner at the GIP, GLP-1 and glucagon receptors
Of 42 peptides screened at the human GIP receptor, glicentin was the only one not derived from the GIP precursor to raise cAMP, with low potency (EC50 877 nM). It also activated the human GLP-1 and glucagon receptors; receptor-specific antibodies cut its potency 10- to 20-fold at all three, and the activity carried over to rodent GIP receptors.
Trophic to the rat jejunum
Recombinant rat glicentin injected under the skin daily for two weeks increased the weight, protein and DNA content and alkaline phosphatase activity of the jejunal lining in rats, with no change in the ileum. It also stimulated an intestinal epithelial cell line (IEC-6) to divide in culture.
Grows the small intestine, not the colon, in fed-by-vein rats
In rats kept on intravenous nutrition for six days, daily intravenous glicentin increased cell division in the small-intestinal crypts in a dose-dependent way, most clearly in the ileum, and reduced crypt fission there. It had no effect on proliferation or fission in the colon.
Releases insulin from the dog pancreas
Synthetic human glicentin injected into the artery supplying the pancreas of anaesthetised dogs raised insulin output at the higher of two amounts tested during a glucose infusion, and at both amounts during an arginine infusion, with little change in blood glucose.
Shortens the fed motility pattern in rat intestine
Intravenous glicentin or oxyntomodulin given around a meal raised their blood level three- to fourfold in rats without changing food intake. Glicentin cut the duration of the after-meal electrical activity pattern in the duodenum and jejunum by about two thirds, though it was weaker than oxyntomodulin in the ileum.
Less understood than its proglucagon siblings
This review covers how glicentin is cut from proglucagon in intestinal L cells, its roles in gut physiology and glucose metabolism from experimental and clinical work, and why it has been hard to measure: it shares most of its sequence with oxyntomodulin and glucagon. Newly available specific assays, it says, open the way to clinical uses.
No Established Human Dose
Glicentin has not been given to people in any study we found. Every human study measured it: in blood after glucose or meals, in newborns, in obesity and diabetes, and before and after weight-loss surgery, plus experiments on gut tissue removed at operation. It was given only to rats, dogs and cultured cells, so there is no human amount to report.
What this rests on: PMID 9930583, PMID 27987137, PMID 26745255.
Educational information, not medical advice. The doses on this page come from approved labels, published studies and, where no study exists, amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.
What a Buyer Needs to Know
What is sold, how it is mixed, stored and taken, and what is known about its safety, quality and legal status. Each part names its source. Where we have none, it says unknown.
What is sold
Unknown: we hold no label and no published test that says what forms or vial sizes Glicentin is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
Unknown: no human dose of Glicentin has been established (see No Established Human Dose below), so there is no amount to work out. The reconstitution calculator does the arithmetic for any vial, water and dose.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Glicentin, before or after mixing. The mixing guide sets out the general rules, with their sources: keep a mixed vial in the fridge, and use it promptly, as the bacteriostatic water label says of any drug dissolved in it. The 28 days often quoted is the limit for an opened multiple-dose vial from a manufacturer, an outer limit set for sterility, not a time a mixed solution has been shown to keep. Nobody has published how long Glicentin stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Glicentin. What the human studies gave and how is set out under No Established Human Dose.
What to expect, and when
Unknown: no cited half-life and no label or trial duration on this page says how long Glicentin lasts or how long it was given. Results reported in the studies are under Published Research.
Side effects, and when to stop or get help
From the Side Effects section: In dogs it raised insulin release from the pancreas (PMID 7854165); In rats it slowed the after-meal pattern of intestinal contractions (PMID 15306001). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Glicentin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Glicentin has never been given to people, so it has no human side effect record”).
Interactions
Unknown: a PubMed search for human interaction studies of Glicentin (reviewed 2026-10-28) found none. Unknown is not the same as safe to combine.
Every peptide's record, with its source: the interaction matrix.
Checking what you bought
Unknown: no published independent test of Glicentin products is in our lab-results database yet, so how products sold under this name measure up is not known.
To read a certificate of analysis, paste it into the COA decoder; it checks the measured mass against Glicentin's expected mass, 8,100.8 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not a medicine anywhere: Drugs@FDA (openFDA) and EMA's Article 57 product data return no record (October 29, 2026)). Sport: Prohibited (S0 catch-all).
Country by country ↓ · Regulatory tracker
Source: this entry's approval status and the WADA Prohibited List, as in Legal Status below.
Side Effects & Contraindications
Reported Side Effects
Glicentin has never been given to people, so it has no human side effect record.
Contraindications & Cautions
There is no glicentin product.
Legal Status
Glicentin is a natural gut peptide studied as a research marker; it has no approval anywhere.
Frequently Asked Questions
?What is glicentin?
A 69-amino-acid peptide that intestinal L cells cut from proglucagon. It contains the full sequences of oxyntomodulin and glucagon.
?How is it related to GLP-1?
Both come from proglucagon in the same gut cells and are released together after meals. Glicentin is a different stretch of the precursor, and in cells it activates the GLP-1 receptor only weakly.
?Why does glicentin rise after bariatric surgery?
After bypass or sleeve gastrectomy, food reaches the small intestine faster, stimulating L cells. Fasting glicentin roughly doubled in the year after bypass in one study.
?Is glicentin a drug?
No. It has never been given to people. It is measured in research studies of obesity, diabetes, surgery and infant feeding.
?Is glicentin the same as enteroglucagon?
Enteroglucagon is an older umbrella term for the glucagon-like peptides of the gut, which include glicentin and oxyntomodulin. Specific assays now measure glicentin on its own.
?Can a glicentin test predict anything?
In small studies, higher fasting glicentin after gastric bypass went with low blood sugar after meals, and larger meal responses predicted more weight loss. These are research findings, not established clinical tests.
References
- [other] UniProt P01275: GLUC_HUMAN, pro-glucagon; peptide 21-89 is glicentin, containing glicentin-related polypeptide (21-50) and oxyntomodulin (53-89). Read October 28, 2026. https://www.uniprot.org/uniprotkb/P01275/entry
- [pubmed] Naito H, et al. "Plasma glicentin in diabetic and gastrectomized patients." Regul Pept, 1999;79(1):55-61. PMID: 9930583.
- [pubmed] Tadokoro R, et al. "Postnatal and postprandial changes in plasma concentrations of glicentin in term and preterm infants." Acta Paediatr, 2003;92(10):1175-9. PMID: 14632334.
- [clinical-trial] Shimizu T, et al. "Effects of extremely early enteral feeding on plasma glicentin levels in very-low-birthweight infants." J Paediatr Child Health, 2006;42(10):636-9. PMID: 16972972.
- [pubmed] Manell H, et al. "Altered Plasma Levels of Glucagon, GLP-1 and Glicentin During OGTT in Adolescents With Obesity and Type 2 Diabetes." J Clin Endocrinol Metab, 2016;101(3):1181-9. PMID: 26745255.
- [pubmed] Raffort J, et al. "Decreased serum glicentin concentration in patients with severe and morbid obesity." Ann Clin Biochem, 2018;55(2):198-204. PMID: 28661200.
- [pubmed] Raffort J, et al. "Fasting Circulating Glicentin Increases After Bariatric Surgery." Obes Surg, 2017;27(6):1581-1588. PMID: 27987137.
- [pubmed] Poitou C, et al. "Fasting levels of glicentin are higher in Roux-en-Y gastric bypass patients exhibiting postprandial hypoglycemia during a meal test." Surg Obes Relat Dis, 2018;14(7):929-935. PMID: 29703503.
- [pubmed] Nielsen MS, et al. "Oxyntomodulin and Glicentin May Predict the Effect of Bariatric Surgery on Food Preferences and Weight Loss." J Clin Endocrinol Metab, 2020;105(4). PMID: 32016415.
- [pubmed] Hummel J, et al. "Free fatty acids, glicentin and glucose-dependent insulinotropic polypeptide as potential major determinants of fasting substrate oxidation." Sci Rep, 2021;11(1):16642. PMID: 34404813.
- [pubmed] Perakakis N, et al. "Fasting oxyntomodulin, glicentin, and gastric inhibitory polypeptide levels are associated with activation of reward- and attention-related brain centres in response to visual food cues in adults with obesity: A cross-sectional functional MRI study." Diabetes Obes Metab, 2021;23(5):1202-1207. PMID: 33417264.
- [pubmed] Ayachi SE, et al. "Contraction induced by glicentin on smooth muscle cells from the human colon is abolished by exendin (9-39)." Neurogastroenterol Motil, 2005;17(2):302-9. PMID: 15787950.
- [pubmed] Tomita R, et al. "Role of recombinant human glicentin in the normal human jejunum: an in vitro study." Hepatogastroenterology, 2005;52(65):1459-62. PMID: 16201096.
- [pubmed] James-Okoro PP, et al. "Identification of glicentin as a low-potency glucose-dependent insulinotropic polypeptide receptor agonist." Peptides, 2026;199:171507. PMID: 42425317.
- [pubmed] Myojo S, et al. "Trophic effects of glicentin on rat small-intestinal mucosa in vivo and in vitro." J Gastroenterol, 1997;32(3):300-5. PMID: 9213241.
- [pubmed] Sasaki M, et al. "Glicentin, an active enteroglucagon, has a significant trophic role on the small intestine but not on the colon in the rat." Aliment Pharmacol Ther, 2001;15(10):1681-6. PMID: 11564010.
- [pubmed] Ohneda A, et al. "Insulinotropic action of human glicentin in dogs." Metabolism, 1995;44(1):47-51. PMID: 7854165.
- [pubmed] Pellissier S, et al. "Oxyntomodulin and glicentin are potent inhibitors of the fed motility pattern in small intestine." Neurogastroenterol Motil, 2004;16(4):455-63. PMID: 15306001.
- [review] Raffort J, et al. "Insights on glicentin, a promising peptide of the proglucagon family." Biochem Med (Zagreb), 2017;27(2):308-324. PMID: 28736498.
Sources & Citations
Every study on this page was read from its PubMed record on October 29, 2026. Status comes from Drugs@FDA (openFDA) and EMA's Article 57 product data, read the same day. Grey Peptides sells nothing and links to no vendor.
Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.