GLP-1
The gut hormone behind every GLP-1 drug: what infusing the real thing showed about insulin, appetite and the stomach, and why it lasts only minutes
GLP-1 is released by the gut after meals and tells the pancreas to make more insulin, the stomach to slow down and the brain that you have eaten. The enzyme DPP-4 destroys it in about two minutes, so the medicines are long-lasting copies; the hormone itself has been given to people only in research.
Used in human trials: 0.4 then 1.2 pmol/kg/min GLP-1(7-36) amide, Continuous infusion, Intravenous (Study: mild type 2 diabetes and matched controls, under a glucose c...) Details ↓
Recommended Dosing
Used in human trials
No manufacturer dose exists for this use: these are amounts given in published trials, not recommendations.
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What is it?
GLP-1, short for glucagon-like peptide-1, is a hormone made by L-cells, endocrine cells scattered through the lining of the lower small intestine and the colon. They cut it from proglucagon, the same precursor the pancreas uses to make glucagon, and release it within minutes of a meal. In the human gut about 80% of it is GLP-1(7-36) amide and about 20% GLP-1(7-37); both are active. Fasting blood holds only a few picomoles per litre, rising several-fold after breakfast.
It was identified in 1987, when three groups showed that the shortened form of the peptide releases insulin. Holst's team purified it from pig intestine, Mojsov's showed that only the truncated 7-37 form works on a rat pancreas while the full-length 1-37 peptide does nothing, and the Hammersmith group infused it into volunteers and found it a stronger insulin signal than GIP, the other gut hormone of this kind. A hormone that the gut releases to boost insulin after a meal is called an incretin, and GLP-1 is the more powerful of the two.
Given to people as an infusion, GLP-1 does four things that matter. It raises insulin, but only while glucose is above normal, and stops doing so once glucose falls below about 4.3 mmol/L. It lowers glucagon at normal and high glucose but not when glucose is low, so the body can still defend itself against hypoglycaemia. It slows the stomach so strongly that, given with a meal, it can reduce the insulin response rather than increase it. And it makes people feel full and eat less: pooled data from 115 volunteers put the drop at about 12% of a meal. It also makes the kidney excrete more sodium.
The reason the hormone itself is not a medicine is speed. The enzyme DPP-4 cuts off its first two amino acids, turning it into the inactive GLP-1(9-36) amide, and much of that happens in the small blood vessels of the gut wall before the hormone even reaches the circulation. In people, intact GLP-1 has a half-life of about two minutes. A six-week pilot in which a pump fed it under the skin around the clock lowered HbA1c by 1.3 points and weight by about 2 kg, which showed the effect was worth having if it could be made to last.
That is the origin of the drug classes. Exenatide, liraglutide, dulaglutide and semaglutide are modified so that DPP-4 cannot switch them off quickly, and tirzepatide and retatrutide also act on other hormone receptors. DPP-4 inhibitors take the other route and protect the body's own GLP-1. All of those are different molecules with their own entries, and their trials are carded there, not here. Beinaglutide is the exception that sits closest: a recombinant copy of human GLP-1, already used to treat type 2 diabetes and tested for weight loss in Chinese adults, which also has its own entry.
A long-running question is whether people with type 2 diabetes make less GLP-1. Two careful studies in 2001 found smaller responses to a meal, especially later in the meal, but a 2013 meta-analysis of 22 trials found that, overall, total GLP-1 responses were no lower than in people without diabetes, and that poorer glucose control rather than diabetes itself went with lower secretion. The drugs work because the receptor still responds, not because the hormone is missing.
Infusions of native GLP-1 were also tried in heart disease. In small, unrandomised studies of people after a heart attack and with severe heart failure, ejection fraction improved by several points over three days to five weeks. A randomised, double-blind crossover in 20 people with stable heart failure found no change in heart function after 48 hours, a small rise in heart rate, and low blood sugar in eight patients, so the early signal did not hold up.
This entry covers the hormone itself: studies that infused native GLP-1, measured the body's own, or worked out how it is made, recognised and destroyed. Grey Peptides sells nothing and links to no seller.
Mechanism of Action
GLP-1 is a 30- or 31-amino-acid peptide released from L-cells of the lower gut after eating. It acts on the GLP-1 receptor in the pancreas, stomach, brain and kidney, and DPP-4 inactivates it within minutes.
Insulin, only when glucose is high
It amplifies glucose-triggered insulin release through its receptor on beta cells and stops adding insulin once glucose falls below about 4.3 mmol/L.
Glucagon
It lowers glucagon at normal and raised glucose; blocking its receptor raises glucagon, so the body's own GLP-1 holds glucagon down all the time. At low glucose the glucagon defence is left intact.
Stomach and appetite
It slows stomach emptying, part of the 'ileal brake', and increases fullness, cutting how much people eat at the next meal.
Kidney
It reduces sodium reabsorption in the first part of the kidney tubule, so more salt reaches the urine, without changing kidney blood flow in healthy men.
Switched off by DPP-4
DPP-4 removes its first two amino acids within minutes, much of it in the gut's own capillaries; the kidneys clear what remains.
Published Research
These studies gave native GLP-1 to people or animals, measured the body's own, or showed how it is made, recognised and broken down, read from their PubMed abstracts. Trials of GLP-1 drugs are on those drugs' entries.
Found in pig gut, and it releases insulin
Working with pig intestinal lining, Holst's group purified a peptide matching residues 78 to 107 of proglucagon, which is the truncated GLP-1 later called GLP-1(7-36) amide. Both the purified natural peptide and a synthetic copy raised insulin output from an isolated pig pancreas, more as the amount went up, and the authors proposed that the gut releases it to help control insulin.
Only the shortened form works
Mojsov and colleagues tested two synthetic forms of GLP-1 on an isolated rat pancreas kept at a moderately raised glucose. The 31-residue GLP-1(7-37) multiplied insulin release three- to tenfold at concentrations as low as 50 picomolar, while the full-length GLP-1(1-37) did nothing even at ten thousand times that amount. The cut at the front of the chain is what switches the hormone on.
First shown to be an incretin in people
The Hammersmith group found GLP-1(7-36) amide in human bowel and saw its blood level climb after oral glucose and after breakfast. Infused into seven fasting volunteers at a rate copying the level seen after meals, it raised insulin and lowered both glucose and glucagon; during an intravenous glucose load it boosted insulin release enough to cut peak glucose, and some volunteers dipped into low blood sugar once the infusion stopped. GIP infused to normal levels was the weaker insulin stimulus. Very high levels after meals in people with dumping syndrome after stomach surgery hinted that the hormone drives the low blood sugar seen in that condition.
Still works in type 2 diabetes, unlike GIP
Nine people with mild type 2 diabetes and nine matched controls were held at a raised glucose while receiving GIP, GLP-1(7-36) amide at 0.4 and then 1.2 pmol/kg/min, or placebo. Both hormones raised insulin and C-peptide in both groups, but with GIP the diabetic group's best response was 54% below the controls', while with GLP-1 they reached 71% of the controls' C-peptide rise, a gap that was not statistically significant. Only GLP-1 also lowered glucagon. This is the study that pointed drug developers at GLP-1 rather than GIP.
Fasting glucose brought to normal in four hours
Ten people with poorly controlled type 2 diabetes (average HbA1c 11.6%) on sulphonylureas received an intravenous infusion of GLP-1(7-36) amide at 1.2 pmol/kg/min or placebo while fasting. Starting from an average glucose of 13.1 mmol/L, every patient's insulin and C-peptide rose, glucagon fell, and glucose reached a normal 4.9 mmol/L within four hours, which placebo did not do. Once glucose was normal, insulin drifted back down and glucose stayed level even though the infusion continued, which is the glucose dependence that limits how low GLP-1 alone can push blood sugar.
Fuller, and 12% less eaten at lunch
Twenty healthy normal-weight young men took part in a blinded, randomised crossover study. GLP-1 infused at 50 pmol/kg per hour, starting with a fixed breakfast, made them feel more satisfied and full than saline did, and at a later free-choice lunch they ate 12% less energy. Insulin, glucagon and glucose all shifted with the infusion.
A dose-dependent drop in food intake
Sixteen healthy men received graded intravenous infusions of synthetic human GLP-1 (0, 0.375, 0.75 and 1.5 pmol/kg/min) in a double-blind placebo-controlled design. Food eaten fell in step with the dose, by up to 35%, and calories by 32%; they also drank 18% less. At the top dose they reported less hunger and earlier fullness before the meal, and the authors saw no obvious side effects. Intake fell even at blood levels in the normal range, which they took as evidence that the body's own GLP-1 helps end a meal.
Pooled: about 12% less eaten
Verdich and colleagues gathered individual data from 115 people across the published intravenous GLP-1(7-36) amide feeding studies and two unpublished ones. During the infusion people ate about 727 kJ less at a free meal, an 11.7% cut. Lean people dropped more energy in absolute terms than overweight people, but the percentage cut was similar (13.2% against 9.3%). The infusion rate was the only factor that predicted the size of the effect, stomach emptying was slower on GLP-1, and the infusion did not affect how well people felt.
Most of it is cut within minutes
Using assays that can tell the intact hormone from its shortened form, Deacon's group followed GLP-1(7-36) amide given under the skin or into a vein to eight healthy people and eight with type 2 diabetes. Both routes produced a breakdown product matching GLP-1(9-36) amide, which has lost its first two amino acids. Thirty minutes after an injection under the skin, that product made up 88.5% of the extra hormone in diabetic patients' blood and 78.4% in healthy people. Even during an intravenous infusion only about a fifth to a quarter of the extra peptide was still intact.
Slower stomach emptying wins over extra insulin
Nine healthy volunteers were infused with GLP-1(7-36) amide at 0.4, 0.8 or 1.2 pmol/kg/min, GLP-1(7-37) at 1.2, or placebo, before and during a 327-kcal liquid meal while a tube measured how much stayed in the stomach. Emptying slowed in step with the dose, and the 7-37 form behaved almost exactly like the 7-36 amide. Before the meal GLP-1 raised insulin, but after it the glucose and insulin rises were smaller, not larger, because food reached the intestine more slowly. Even the lowest, near-normal dose had a measurable effect, which casts GLP-1 as part of the 'ileal brake'.
Six weeks of continuous infusion
Twenty people with type 2 diabetes were alternately assigned to a pump giving GLP-1 under the skin around the clock, or saline, for six weeks. On GLP-1 fasting glucose fell by 4.3 mmol/L, the eight-hour average by 5.5 mmol/L and HbA1c by 1.3 percentage points; free fatty acids fell, stomach emptying slowed, appetite dropped and weight fell by 1.9 kg. Both insulin sensitivity and beta-cell function improved, and the team saw no important side effects. Because the native hormone only works while it is being infused, this pilot made the case for longer-lasting versions rather than for GLP-1 itself.
Blocking the receptor shows what the body's own GLP-1 does
Six healthy volunteers were each studied ten times under a raised glucose, receiving saline, GLP-1(7-36) amide (0.3 then 0.9 pmol/kg/min), the receptor blocker exendin(9-39) amide at three doses with or without GLP-1, or GIP. The blocker cut GLP-1's insulin effect in step with its own dose, fully cancelled GLP-1's suppression of glucagon, and left GIP's action alone. Given by itself it raised glucagon and, under high glucose, lowered insulin. The authors concluded that the body's own GLP-1 constantly holds glucagon down and, when glucose is high, keeps pushing insulin up.
Measuring the intact, active hormone
With new assays that count only the active, uncut hormone, Vilsboll's team followed twelve people with type 2 diabetes and twelve matched controls through a 566-kcal breakfast. In both groups only about half of the GLP-1 in blood was intact (48% and 51%). The patients' intact GLP-1 rose a little early on but its later phase, 75 to 150 minutes after eating, was clearly smaller, while GIP responses were barely changed.
Pooled: secretion is not generally reduced
This systematic review and meta-analysis pooled 22 trials with 29 glucose-drink or meal tests, covering 275 people with type 2 diabetes and 279 without. Total GLP-1 responses were similar in the two groups across every measure in the main analysis; liquid meals and a 50 g glucose drink even gave higher responses in the diabetic group, and only solid meals gave lower ones. Worse HbA1c and fasting glucose went with smaller responses. It revises the older idea, from single studies like Toft-Nielsen's, that GLP-1 deficiency is a general feature of type 2 diabetes.
Heart attack with a weak left ventricle
Ten patients with an acute heart attack and an ejection fraction under 40% after successful angioplasty received GLP-1 at 1.5 pmol/kg/min for 72 hours on top of usual care, compared with eleven patients on usual care alone. Ejection fraction rose from 29% to 39% on GLP-1, and global and regional wall-motion scores improved, regardless of where the infarct was or whether the patient had diabetes. The only side effects were brief stomach upsets. The comparison group was not randomised, so the result is a signal rather than proof.
No heart benefit in a randomised, blinded test
Twenty non-diabetic patients with stable heart failure from coronary disease (ejection fraction about 30%) received 48 hours of GLP-1 at 0.7 pmol/kg/min and 48 hours of placebo in random order, double-blind; fifteen finished. GLP-1 raised insulin and lowered glucose, and nudged heart rate up by about two beats a minute and diastolic pressure by about three mmHg, but ejection fraction, cardiac output, tissue Doppler measures, weight and BNP did not change. Eight patients had low blood sugar on GLP-1, so the authors urge caution in people with heart failure who do not have diabetes.
A half-life of about two minutes
Ten people with chronic kidney insufficiency and ten matched healthy controls had a glucose drink and, on other days, a 30-minute intravenous infusion of GLP-1 (0.5 pmol/kg/min) or GIP. Intact GLP-1 reached the same levels in both groups, but the cut-down form, GLP-1(9-36) amide, built up higher in the kidney patients. The plasma half-life of intact GLP-1 was 2.3 minutes in the controls and 3.4 minutes in the patients, while the metabolite lasted 3.3 against 5.3 minutes. DPP-4 does the first, fast step whatever the kidneys are doing; the kidneys handle the final removal.
Which forms the human gut and pancreas make
Orskov's group measured the different GLP-1 molecules in human tissue and blood. In the small intestine all of it was the active, shortened form: about 80% GLP-1(7-36) amide and 20% GLP-1(7-37). The pancreas held mostly a large proglucagon fragment and the longer, inactive 1-36 amide and 1-37 forms. In six people, fasting blood held about 7 pM of the amidated form, which rose to about 41 pM ninety minutes after breakfast, while the glycine-extended form rose only to about 10 pM. The amidated 7-36 form is the main one in human circulation.
It does not block the body's defence against low blood sugar
Nine healthy volunteers had their glucose stepped down from 4.3 to 2.3 mmol/L under an insulin clamp, once with GLP-1 at 1.2 pmol/kg/min and once with saline. GLP-1 lowered glucagon only at the normal-glucose step; once glucose fell to 3.7 mmol/L or below, glucagon rose just as much with GLP-1 as without. Cortisol, adrenaline, symptoms and the slowing of thinking at low glucose were the same, apart from a smaller growth hormone rise. GLP-1 also stopped driving insulin release once glucose was below 4.3 mmol/L. This glucose dependence is why native GLP-1 rarely causes hypoglycaemia on its own.
What makes the gut release it
Ten healthy volunteers were given nutrients by mouth, into a vein or straight into the duodenum. Fasting GLP-1 sat at about 0.4 to 1.4 pM and peaked at 10 to 12 pM after eating. Glucose by vein did nothing, but glucose by mouth produced a two-humped rise over 30 to 60 minutes; galactose and amino acids also triggered quick release, and fat gave a strong rise lasting more than two hours. A small glucose infusion into the upper intestine raised GLP-1 quickly even though GIP and insulin did not move. The authors propose that nerve signals and factors from the upper gut help trigger the L-cells further down, alongside nutrients that touch them directly.
More salt in the urine
Fifteen healthy men and sixteen obese men (average BMI 36) received a three-hour GLP-1 infusion or placebo after an intravenous salt load, in a double-blind crossover. In healthy men sodium excretion rose with the dose, from 74 to 143 mmol over three hours. In obese men it rose from 59 to 96 mmol, acid excretion fell, and glomerular filtration, which was abnormally high, came down by 6%. The pattern points to an action on the first part of the kidney tubule.
DPP-4 is the enzyme that switches it off
Mentlein's group showed that dipeptidyl peptidase-4 purified from human placenta snips the first two amino acids (histidine-alanine) off GLP-1(7-36) amide, and does the same to GIP and two related peptides. Human serum produced exactly the same fragments, and two DPP-4 blockers stopped it completely. Since this family of hormones needs an intact front end to work, the cut inactivates GLP-1, and the enzyme's measured affinity suggested it would act even at the tiny concentrations found in blood. This finding underlies the DPP-4 inhibitor drugs.
The receptor is cloned
Thorens screened a rat pancreatic islet library in cultured cells for anything that bound labelled GLP-1 and pulled out a receptor 463 amino acids long with seven membrane-spanning segments. It bound GLP-1 tightly and switched on cyclic AMP production, but did not bind glucagon, GIP, VIP or secretin. Its closest relatives were the receptors for secretin, calcitonin and parathyroid hormone. Every GLP-1 drug since acts on this receptor.
Cut before it even leaves the gut
In pig ileum, studied both as an isolated perfused segment and in anaesthetised pigs, almost 95% of the GLP-1 stored in the gut wall was intact, yet only about half of what came out of the perfused gut, and a third in living pigs, was still the active 7-36 amide. A DPP-4 blocker raised the intact share of released GLP-1 to nearly 100%. Staining showed DPP-4 in the walls of the small blood vessels lying right next to the L-cells, so the hormone is largely inactivated as it enters the gut's own capillaries.
The standard review of its physiology
Holst's review in Physiological Reviews covers how proglucagon is processed differently in gut L-cells, which nutrients and signals release GLP-1, and how fast DPP-4 inactivates it, often before it leaves the gut, which raises the possibility that some of its effects travel through sensory nerves in the gut wall and liver. It stresses that assays measuring only the intact hormone and assays measuring total secretion answer different questions. Its main jobs: raising insulin, lowering glucagon, slowing the gut as part of the ileal brake, and helping regulate appetite; too little may contribute to obesity, and too much may cause low blood sugar after meals.
Dosing Data
Native GLP-1 is not an approved medicine in the United States, and its effect ends within minutes of stopping it. These are intravenous infusion rates from published human research studies, as stated in their abstracts; none is a treatment dose.
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 GLP-1 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 GLP-1, 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 GLP-1 stays intact once mixed.
How it is taken
As it was given in human studies: Intravenous (Continuous infusion; Study: mild type 2 diabetes and matched controls, under a glucose clamp).
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 about 2.3 minutes for intact GLP-1 in healthy people and 3.4 minutes with chronic kidney insufficiency, after a 30-minute intravenous infusion (PMID 14988249). After about five half-lives almost none is left.
How long the doses were given: Study: mild type 2 diabetes and matched controls, under a glucose clamp: 1 hour at each rate; Study: poorly controlled type 2 diabetes, fasting: Single session; glucose was normal within 4 hours; Study: food intake in healthy men: Single session per rate.
When effects appear: unknown; no source on this page gives a time to effect for GLP-1. Results reported in the studies are under Published Research.
Source: half-life: PMID 14988249; 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: Low blood sugar: some volunteers dipped after an infusion ended, and 8 non-diabetic heart failure patients had hypoglycaemia during 48 hours of infusion (PMIDs 2890903, 20081109); Brief stomach upset during a 72-hour infusion after a heart attack (PMID 14981009); A small rise in heart rate, about two beats a minute, and in diastolic blood pressure (PMID 20081109); Stomach emptying slowed sharply, enough to blunt the rise in glucose and insulin after a meal (PMIDs 9374685, 8550773); In a six-week continuous infusion and in single-session feeding studies, the authors saw no important side effects (PMIDs 11897280, 9862830). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping GLP-1. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“Native GLP-1 has been given only in research, mostly for hours to days, so what is known comes from short studies”).
Interactions
Unknown: a PubMed search for human interaction studies of GLP-1 (reviewed 2026-11-04) 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 GLP-1 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 GLP-1's expected mass, 3,297.7 Da, from this entry's molecular data. Trust & Verification explains what independent testing can and cannot show.
Legal status
US: Research Chemical (Not approved as a drug: Drugs@FDA (openFDA) returns no application for glucagon-like peptide-1 itself (read November 4, 2026)). Sport: Unsettled (S0 may apply).
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
Native GLP-1 has been given only in research, mostly for hours to days, so what is known comes from short studies.
Contraindications & Cautions
Not a medicine. These cautions concern the hormone as a research substance.
Legal Status
The hormone itself is not an approved drug in the United States; several drugs built on it are, each with its own entry.
Frequently Asked Questions
?What is GLP-1?
A hormone the lower gut releases after you eat. It raises insulin when glucose is high, lowers glucagon, slows the stomach and makes you feel full.
?Is GLP-1 the same as semaglutide or Ozempic?
No. Semaglutide is a modified version built to last far longer; native GLP-1 lasts about two minutes in blood. They act on the same receptor, but they are different molecules with different evidence, and semaglutide has its own entry.
?Why can't the natural hormone be used as a drug?
DPP-4 cuts it within minutes. In a six-week study it worked when pumped in around the clock, but an injection is gone within two hours, so the medicines are resistant analogues instead.
?Does GLP-1 cause low blood sugar?
Rarely on its own, because it stops boosting insulin once glucose drops below about 4.3 mmol/L and leaves the glucagon response to low glucose intact. Lows have still been seen after infusions ended and in non-diabetic heart failure patients.
?Does GLP-1 reduce appetite?
Yes. Infusions made healthy people feel fuller and eat about 12% less at the next meal, with bigger doses having bigger effects; part of this comes from slowing the stomach.
?Do people with type 2 diabetes lack GLP-1?
Not generally. Some studies found lower meal responses, but a 2013 meta-analysis of 22 trials found similar overall secretion, with lower levels tied to worse glucose control.
?What is the difference between GLP-1(7-36) amide and GLP-1(7-37)?
They are the two active forms, differing by one glycine at the end. The amide is about 80% of what the human gut makes, and the two behaved almost identically on the stomach in a direct comparison.
?Can you buy GLP-1?
Native GLP-1 is not an approved medicine in the US. Products sold online as 'GLP-1' are usually one of the drugs, sold outside a pharmacy, and their contents are unverified.
References
- [other] UniProt P01275 (GLUC_HUMAN), pro-glucagon: GLP-1(7-37) is mature peptide 98-128 and GLP-1(7-36) amide is residues 98-127 with an amidated C-terminal arginine; read November 4, 2026. Formula and mass computed from the 30-residue amidated sequence. https://www.uniprot.org/uniprotkb/P01275/entry
- [other] FDA. Drugs@FDA (openFDA): no application for glucagon-like peptide-1 itself. Read November 4, 2026.
- [pubmed] Holst JJ, et al. "Truncated glucagon-like peptide I, an insulin-releasing hormone from the distal gut." FEBS Lett, 1987;211(2):169-74. PMID: 3542566.
- [pubmed] Mojsov S, et al. "Insulinotropin: glucagon-like peptide I (7-37) co-encoded in the glucagon gene is a potent stimulator of insulin release in the perfused rat pancreas." J Clin Invest, 1987;79(2):616-9. PMID: 3543057.
- [pubmed] Kreymann B, et al. "Glucagon-like peptide-1 7-36: a physiological incretin in man." Lancet, 1987;2(8571):1300-4. PMID: 2890903.
- [pubmed] Nauck MA, et al. "Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus." J Clin Invest, 1993;91(1):301-7. PMID: 8423228.
- [pubmed] Nauck MA, et al. "Normalization of fasting hyperglycaemia by exogenous glucagon-like peptide 1 (7-36 amide) in type 2 (non-insulin-dependent) diabetic patients." Diabetologia, 1993;36(8):741-4. PMID: 8405741.
- [pubmed] Flint A, et al. "Glucagon-like peptide 1 promotes satiety and suppresses energy intake in humans." J Clin Invest, 1998;101(3):515-20. PMID: 9449682.
- [pubmed] Gutzwiller JP, et al. "Glucagon-like peptide-1: a potent regulator of food intake in humans." Gut, 1999;44(1):81-6. PMID: 9862830.
- [pubmed] Verdich C, et al. "A meta-analysis of the effect of glucagon-like peptide-1 (7-36) amide on ad libitum energy intake in humans." J Clin Endocrinol Metab, 2001;86(9):4382-9. PMID: 11549680.
- [pubmed] Deacon CF, et al. "Both subcutaneously and intravenously administered glucagon-like peptide I are rapidly degraded from the NH2-terminus in type II diabetic patients and in healthy subjects." Diabetes, 1995;44(9):1126-31. PMID: 7657039.
- [pubmed] Nauck MA, et al. "Glucagon-like peptide 1 inhibition of gastric emptying outweighs its insulinotropic effects in healthy humans." Am J Physiol, 1997;273(5):E981-8. PMID: 9374685.
- [pubmed] Zander M, et al. "Effect of 6-week course of glucagon-like peptide 1 on glycaemic control, insulin sensitivity, and beta-cell function in type 2 diabetes: a parallel-group study." Lancet, 2002;359(9309):824-30. PMID: 11897280.
- [pubmed] Schirra J, et al. "Exendin(9-39)amide is an antagonist of glucagon-like peptide-1(7-36)amide in humans." J Clin Invest, 1998;101(7):1421-30. PMID: 9525985.
- [pubmed] Vilsbøll T, et al. "Reduced postprandial concentrations of intact biologically active glucagon-like peptide 1 in type 2 diabetic patients." Diabetes, 2001;50(3):609-13. PMID: 11246881.
- [pubmed] Calanna S, et al. "Secretion of glucagon-like peptide-1 in patients with type 2 diabetes mellitus: systematic review and meta-analyses of clinical studies." Diabetologia, 2013;56(5):965-72. PMID: 23377698.
- [pubmed] Nikolaidis LA, et al. "Effects of glucagon-like peptide-1 in patients with acute myocardial infarction and left ventricular dysfunction after successful reperfusion." Circulation, 2004;109(8):962-5. PMID: 14981009.
- [pubmed] Halbirk M, et al. "Cardiovascular and metabolic effects of 48-h glucagon-like peptide-1 infusion in compensated chronic patients with heart failure." Am J Physiol Heart Circ Physiol, 2010;298(3):H1096-102. PMID: 20081109.
- [pubmed] Meier JJ, et al. "Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects." Diabetes, 2004;53(3):654-62. PMID: 14988249.
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Sources & Citations
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