Gastrin
The stomach hormone that turns on acid after a meal, measured to find gastrin-making tumours
Gastrin is made by G cells in the lower stomach and upper duodenum and released into the blood after a meal, where it drives acid secretion and the growth of the acid-making lining. Its blood level is measured to diagnose gastrinomas, the tumours behind Zollinger-Ellison syndrome, and it rises with long-term acid-suppressing drugs. Researchers have infused gastrin-17 into volunteers to study acid and gut motility, but it has never been a medicine.
Used in human trials: 5 then 15 pmol/kg/h, Continuous infusion, 60 minutes at each rate, Intravenous (Acid output study (7 healthy volunteers)) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
What is it?
Gastrin is the hormone that tells the stomach to make acid. It is produced mainly by G cells in the antrum, the lower part of the stomach, and the duodenum, and released into the blood. Like the gut hormone cholecystokinin, with which it shares a receptor, it is cut from a larger precursor, progastrin, and every active form ends in the same amidated sequence, -Tyr-Gly-Trp-Met-Asp-Phe-NH2. The main forms in blood and tissue are gastrin-34, or big gastrin, and gastrin-17, or little gastrin; smaller amounts of other lengths exist.
Gastrin works on acid largely through a relay. It makes enterochromaffin-like (ECL) cells release histamine, and histamine turns on the parietal cells. In 14 healthy volunteers, a histamine H2 blocker completely blocked the acid response to infused gastrin-17, and atropine cut it by 73%. Gastrin is also a growth factor for the acid-making lining of the stomach, increasing stem cells and ECL and parietal cell mass, while evidence that the amidated hormone drives growth elsewhere in the gut is thin.
Most of what is known about gastrin in people comes from infusing synthetic gastrin-17 into volunteers at rates chosen to reproduce the levels after a meal. Acid output rose step by step with the infusion rate. Its plasma half-life was about six minutes in both healthy people and people with duodenal ulcers, though ulcer patients cleared it about half as fast and made more acid at any given gastrin level. Matching infusions to each person's meal response showed that gastrin explained 89% of the acid made after a meal on average, ranging from 51% to 162% between individuals. Acute high blood sugar cut gastrin-stimulated acid output by about 40 to 50%. Gastrin infusion also suppressed the fasting contractions of the stomach and duodenum, an effect that disappeared when acid was blocked. Two studies of the lower oesophageal sphincter disagree: one found gastrin lowered its pressure and increased reflux, the other found it raised the pressure.
The main clinical use of gastrin is as a blood test. In the US National Institutes of Health series of 309 people with Zollinger-Ellison syndrome, a normal fasting gastrin was very rare, but two thirds had levels below ten times normal, overlapping with common causes of high gastrin such as Helicobacter pylori infection. In those patients a provocative test is needed, and secretin stimulation diagnosed 94% using a rise of 120 pg/mL. A 2012 review warned that more than half of commercial gastrin kits were unsuited for diagnosis because they measure only one gastrin form or cross-react with others, giving falsely low or high results.
Gastrin also rises when stomach acid is suppressed, because acid normally restrains its release. In 16 studies of people on proton pump inhibitors for more than three years, gastrin rose to one to three times the upper limit of normal and ECL cell hyperplasia became more common, with no neuroendocrine tumours or gastric cancers found. A 2021 review argues that such moderate hypergastrinaemia, from long-term acid suppression or Helicobacter infection, deserves more attention. Gastrin-17 is also one component of serum panels used to screen for atrophic gastritis, listed under References.
Gastrin itself has never been a medicine. Pentagastrin, a synthetic five-residue fragment once used to test acid secretion, has its own entry.
Mechanism of Action
Gastrin is released from antral and duodenal G cells, travels in the blood and acts on the gastrin/CCK-B receptor, the receptor it shares with cholecystokinin.
Acid through histamine
It makes ECL cells release histamine, which drives parietal-cell acid secretion; an H2 blocker abolished the acid response to gastrin-17 in volunteers.
Growth of the acid-making lining
Amidated gastrin increases stem cells and ECL and parietal cell mass in the stomach body; its growth effect on the rest of the gut is unproven.
Feedback from acid
Acid restrains its release, so blocking acid raises gastrin: in volunteers a single H2 blocker dose raised endogenous gastrin, and long-term proton pump inhibitors raise it one to three times above normal.
One receptor, two hormones
Gastrin and cholecystokinin share the C-terminal sequence and the gastrin/CCK-B receptor; only cholecystokinin binds the CCK-A receptor.
Published Research
Studies of gastrin itself, read from their PubMed abstracts: infusions of synthetic gastrin-17 in volunteers, the large NIH series on gastrin as a tumour test, and reviews. Trials of gastrin-blocking drugs and of pentagastrin study other molecules and are not carded here.
High blood sugar blunts the acid response
In seven healthy volunteers, gastrin-17 infused at 5 then 15 pmol/kg/h raised acid output at each step; acute hyperglycaemia reduced basal, low-dose and high-dose gastrin-stimulated acid output (for the high dose, 11.7 against 19.4 mmol/h).
Dose-response and half-life
Graded gastrin-17 infusions (7 to 700 pmol/kg/h) in 15 duodenal ulcer patients and 15 controls gave a plasma half-time of about 6 minutes in both; ulcer patients cleared it nearly twice as slowly and made more acid, but responses matched once corrected for peak acid output.
How much meal acid gastrin explains
In 12 healthy people, relating gastrin-17 infusion levels to acid output showed the average post-meal gastrin concentration could account for 89% of meal-stimulated acid, but from 51% to 162% in individuals.
Histamine is needed for the acid response
In 14 volunteers, synthetic human gastrin-17 at 0.75 and 1.5 ng/kg/min raised acid secretion; famotidine completely blocked the response and atropine reduced it by 72.9%, so histamine and muscarinic pathways mediate it.
Lower oesophageal sphincter: pressure fell
In nine healthy volunteers, gastrin-17 at 15 pmol/kg/h, giving post-meal levels, lowered sphincter pressure and increased reflux and the share of transient relaxations with reflux, without changing how often relaxations occurred.
Lower oesophageal sphincter: pressure rose
In 17 volunteers, human gastrin-17 at 0.75 or 1.5 ng/kg/min raised sphincter pressure (19.0 to 25.8 mmHg at the lower dose), and did so again after acid was fully blocked with famotidine.
Fasting gut contractions
In seven healthy subjects, gastrin-17 at 20 pmol/kg/h acidified the stomach and duodenum and suppressed phase II and III fasting contractions; blocking acid with famotidine abolished the effect.
Fasting gastrin in Zollinger-Ellison syndrome
In 309 NIH patients and 2,229 from the literature, normal fasting gastrin was rare (0.3% to 3%) and levels over 100 times normal uncommon; two thirds had levels below 10 times normal, overlapping with H. pylori infection and G-cell hyperplasia.
Provocative tests for gastrinoma
In 293 NIH patients, a gastrin rise after secretin of at least 120 pg/mL gave 94% sensitivity and 100% specificity; secretin testing was more sensitive than calcium testing (94% against 62%) and is recommended first.
Long-term proton pump inhibitors
Across 16 studies of 1,920 patients on more than 3 years of treatment, gastrin rose to one to three times the upper limit of normal and ECL cell hyperplasia increased; no neuroendocrine tumours or gastric cancers were found.
Pitfalls in measuring it
Because gastrin circulates as several bioactive forms, assays must measure all of them; more than half of the commercial kits tested measured falsely low or high and were unsuited for gastrinoma diagnosis.
Moderate hypergastrinaemia
Reviews gastrin's production, its forms and levels in plasma, and assays, and argues that the moderate rises caused by H. pylori infection and proton pump inhibitors are health issues needing serious attention.
The gastrin and CCK family
Gastrin peptides come from progastrin, share the C-terminal bioactive sequence with cholecystokinin and act on the gastrin/CCK-B receptor; gastrin-34 and gastrin-17 dominate, and gastrinomas secrete excess amounts.
Gastrin as a growth factor
Amidated gastrin's main growth target is the acid-making mucosa of the stomach, where it increases stem cells and ECL and parietal cell mass; less processed forms such as glycine-extended gastrin appear to act on the colon instead.
Dosing Data
The amounts below are the intravenous infusion rates of synthetic gastrin-17 used in the volunteer studies carded above. Gastrin has no treatment use and no label.
Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or 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 Gastrin is sold in. A vial's own label is a seller's claim, not a source.
Mixing a vial: a worked example
No worked example: none of the doses on this page is a fixed amount in mg or mcg injected under the skin or into a muscle (the routes given are: intravenous). There is no home-mixing step to show. The reconstitution calculator does the arithmetic for any vial.
Source: the route and amount of each dose row in Dosing Data below.
Storage before and after mixing
Unknown: no label or published stability study on file says how to store Gastrin, 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 Gastrin stays intact once mixed.
How it is taken
As it was given in human studies: Intravenous (Continuous infusion, 60 minutes at each rate; Acid output study (7 healthy volunteers)).
For injection technique, sites and needle disposal, see the mixing guide.
Source: Used in human trials: the route and frequency of each row in Dosing Data below.
What to expect, and when
How long it stays in the body: a half-life of 6.0 to 6.1 minutes (plasma elimination half-time of infused gastrin-17). After about five half-lives almost none is left.
How long the doses were given: Acid output study (7 healthy volunteers): One session; Acid secretion and mediators (14 volunteers): 60 minutes; Sphincter and reflux study (9 volunteers): One session.
When effects appear: unknown; no source on this page gives a time to effect for Gastrin. Results reported in the studies are under Published Research.
Source: half-life: PMID 3745438; Used in human trials, the duration of each row in Dosing Data below.
Side effects, and when to stop or get help
From the Side Effects section: More stomach acid, the hormone's main effect; Lower oesophageal sphincter pressure and more reflux in one study (another found the opposite); Suppressed fasting contractions of the stomach and duodenum. Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Gastrin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“From the volunteer studies above, which report physiological effects rather than safety”).
Interactions
Unknown: a PubMed search for human interaction studies of Gastrin (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 Gastrin 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 Gastrin's expected mass, 2,098.2 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 in the sources read). 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
From the volunteer studies above, which report physiological effects rather than safety.
Contraindications & Cautions
Not a medicine.
Legal Status
Gastrin is a laboratory test and a research reagent, not a drug.
Frequently Asked Questions
?What does gastrin do?
It makes the stomach produce acid after a meal, mainly by making ECL cells release histamine, and it keeps the acid-making lining of the stomach growing.
?Why would a doctor test my gastrin?
To look for a gastrinoma, the tumour behind Zollinger-Ellison syndrome, which causes severe ulcers. Mildly high gastrin is much more often due to H. pylori or acid-suppressing drugs, so a secretin test is used when the result is borderline.
?Do proton pump inhibitors raise gastrin?
Yes. In studies of more than three years of use, gastrin rose to one to three times the upper limit of normal and ECL cell hyperplasia became more common, without tumours or gastric cancer found.
?Is gastrin used as a drug?
No. Gastrin-17 has been infused in research volunteers. Pentagastrin, a short synthetic fragment, was once used to test acid secretion and has its own entry.
References
- [clinical-trial] Lam WF, et al. "Hyperglycaemia reduces gastrin-stimulated gastric acid secretion in humans." Eur J Clin Invest, 1998;28(10):826-30. PMID: 9792996.
- [pubmed] Blair AJ 3rd, et al. "Comparison of acid secretory responsiveness to gastrin heptadecapeptide and of gastrin heptadecapeptide pharmacokinetics in duodenal ulcer patients and normal subjects." J Clin Invest, 1986;78(3):779-83. PMID: 3745438.
- [pubmed] Blair AJ 3rd, et al. "Variable contribution of gastrin to gastric acid secretion after a meal in humans." Gastroenterology, 1987;92(4):944-9. PMID: 3557000.
- [clinical-trial] Zimmerhackl B, et al. "In man histamine and muscarinergic mechanisms are essential mediators of acid secretion in response to synthetic human gastrin (1-17)." Regul Pept, 1993;46(3):583-92. PMID: 8105512.
- [clinical-trial] Straathof JW, et al. "Effect of gastrin-17 on lower esophageal sphincter characteristics in man." Dig Dis Sci, 1997;42(12):2547-51. PMID: 9440634.
- [pubmed] Allescher HD, et al. "Effect of human gastrin-17 with and without acid suppression on human esophageal motility." Z Gastroenterol, 1995;33(7):385-91. PMID: 7571756.
- [clinical-trial] Verkijk M, et al. "Effect of gastrin on antroduodenal motility: role of intraluminal acidity." Am J Physiol, 1998;275(5):G1209-16. PMID: 9815053.
- [pubmed] Berna MJ, et al. "Serum gastrin in Zollinger-Ellison syndrome: I. Prospective study of fasting serum gastrin in 309 patients from the National Institutes of Health and comparison with 2229 cases from the literature." Medicine (Baltimore), 2006;85(6):295-330. PMID: 17108778.
- [pubmed] Berna MJ, et al. "Serum gastrin in Zollinger-Ellison syndrome: II. Prospective study of gastrin provocative testing in 293 patients from the National Institutes of Health and comparison with 537 cases from the literature. evaluation of diagnostic criteria, proposal of new criteria, and correlations with clinical and tumoral features." Medicine (Baltimore), 2006;85(6):331-364. PMID: 17108779.
- [review] Lundell L, et al. "Systematic review: the effects of long-term proton pump inhibitor use on serum gastrin levels and gastric histology." Aliment Pharmacol Ther, 2015;42(6):649-63. PMID: 26177572.
- [review] Rehfeld JF, et al. "Pitfalls in diagnostic gastrin measurements." Clin Chem, 2012;58(5):831-6. PMID: 22419747.
- [review] Rehfeld JF. "Gastrin and the Moderate Hypergastrinemias." Int J Mol Sci, 2021;22(13). PMID: 34209478.
- [review] Rehfeld JF, et al. "The biology of cholecystokinin and gastrin peptides." Curr Top Med Chem, 2007;7(12):1154-65. PMID: 17584137.
- [review] Koh TJ, et al. "Gastrin as a growth factor in the gastrointestinal tract." Regul Pept, 2000;93(1-3):37-44. PMID: 11033051.
- [review] Syrjänen K. "A Panel of Serum Biomarkers (GastroPanel®) in Non-invasive Diagnosis of Atrophic Gastritis. Systematic Review and Meta-analysis." Anticancer Res, 2016;36(10):5133-5144. PMID: 27798873.
- [other] UniProt P01350: GAST_HUMAN, gastrin; peptide 76-92 is gastrin (gastrin-17) with a pyroglutamate at its first residue, a C-terminal phenylalanine amide and a partly sulfated tyrosine; peptide 59-92 is big gastrin (gastrin-34). Read October 28, 2026. https://www.uniprot.org/uniprotkb/P01350/entry
Sources & Citations
Studies were read from their PubMed abstracts on October 28, 2026; the sequence is from UniProt P01350. Gastrin has no label. Searches on October 28, 2026 found no gastrin medicine in Drugs@FDA or the EMA list (0 records each), and the 20 ClinicalTrials.gov records for 'gastrin' were mostly gastrin-releasing peptide receptor tracers, not treatment trials of gastrin.
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.