What Is GLP-1? The Hormone Behind Ozempic, Explained
GLP-1 stands for glucagon-like peptide-1, a gut hormone the body makes that regulates insulin secretion, carbohydrate metabolism and appetite. Drugs like Ozempic are GLP-1 receptor agonists that switch on the same receptor; incretins explain two-thirds or more of the insulin response to oral glucose in healthy people.
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GLP-1 stands for glucagon-like peptide-1, a hormone the gut releases that helps control insulin secretion, carbohydrate metabolism and appetite [1][3][5]. It is one of two hormones conventionally called “incretins” — gut hormones that stimulate insulin secretion at physiological concentrations [3]. Drugs like Ozempic are not the hormone itself; they are GLP-1 receptor agonists, molecules that switch on the same receptor the natural hormone targets [2][5]. The Ozempic label describes the drug exactly that way: “a glucagon-like peptide 1 (GLP-1) receptor agonist” [2].
When people say a drug “is GLP-1,” they mean the medicine imitates a hormone the body already makes on its own. What that hormone does — and why it exists — explains both the benefits and the side effects of the drug class.
What does GLP-1 stand for?
The abbreviation breaks down as glucagon-like peptide-1 [1][3]. The name came from what the gene sequences showed: glucagon and related GLP sequences are encoded within larger precursor proteins, and the mammalian precursor contains glucagon plus two glucagon-related peptides, designated GLP-1 and GLP-2 [1]. The active circulating form of the hormone is a truncated version known as GLP-1(7–36) [3], and laboratory studies of the receptor often use a labeled version called GLP-1(7–36)amide [7].
The “-1” distinguishes it from GLP-2, the second glucagon-related peptide encoded in the same precursor [1].
Is GLP-1 a hormone the body makes on its own?
Yes. GLP-1 is a gut hormone with roles in regulating insulin secretion, carbohydrate metabolism and appetite [5]. It is the second of the two incretin hormones; the first to be discovered was GIP, glucose-dependent insulinotropic polypeptide [1].
The body builds GLP-1 through a step-by-step process. Mammals make a large precursor protein called preproglucagon, which contains glucagon plus the two glucagon-related peptides, GLP-1 and GLP-2 [1]. Enzymes called prohormone convertases (PC1 and PC2) then cleave the precursor at pairs of basic amino acids to liberate the finished bioactive peptides [1]. Which peptides get released depends on the tissue: the pancreas and the intestine process the same precursor differently, producing different sets of peptides [1].
How was GLP-1 discovered?
Unlike GIP, which was isolated by classical peptide purification, GLP-1 was found through recombinant DNA technology [1]. In the early 1980s, the Habener lab worked out proglucagon sequences from anglerfish cDNAs and genes, followed shortly by rat proglucagon sequences [1]. Graeme Bell and others identified the corresponding hamster, bovine and human proglucagon sequences in the early 1980s as well [1].
The anglerfish turned out to have two different preproglucagon cDNAs, encoded by separate nonallelic genes, each carrying glucagon plus one glucagon-related peptide [1]. Mammals, by contrast, carry glucagon plus two related peptides — GLP-1 and GLP-2 — in a single precursor [1]. Notably, the GLP-1 amino acid sequence was identical across the four mammalian species examined, a hint that it did something important [1].
The story was reviewed by Daniel Drucker, Joel Habener and Jens Juul Holst in the Journal of Clinical Investigation in 2017 (volume 127, issue 12, pages 4217–4227), work recognized with the 2017 Harrington Award Prize for Innovation in Medicine [1].
What does GLP-1 actually do in the body?
GLP-1 itself is described as a hormone with essential roles in regulating insulin secretion, carbohydrate metabolism and appetite [5]. The more detailed action list comes from studies of the medicines built on it. A 2025 review in the American Journal of Medicine describes how GLP-1 receptor agonists affect the body:
- They enhance insulin secretion [8].
- They reduce glucagon release [8].
- They delay gastric emptying — the rate at which food leaves the stomach [8]. The Ozempic label notes this same effect, warning that delayed emptying may affect the absorption of oral medicines taken alongside the drug [2].
- They act on brain regions that control appetite, influencing neurotransmitter and peptide release, hunger and energy expenditure [8].
That same review lists peripheral effects of GLP-1 receptor agonists: lower triglycerides and LDL cholesterol, reduced inflammation in adipose tissue, and less ectopic fat deposition (fat accumulating in places it does not belong) [8].
What is the incretin effect?
The incretin effect is the observation that set the whole drug class in motion: glucose taken by mouth triggers a bigger insulin response than the same glucose level reached by IV, because the gut releases insulin-stimulating hormones when food arrives [1][3]. An incretin is defined as a gut hormone that stimulates insulin secretion at physiological concentrations [3].
The word has a long history. Belgian physiologist Jean La Barre coined the term “incrétine” in 1932 [3]. Two years earlier, in 1930, La Barre and Still had reported separating duodenal extracts into two fractions — one containing crude secretin that stimulated the exocrine pancreas, and another that lowered blood glucose without affecting exocrine pancreatic secretion [3].
Progress then stalled. Ivy and colleagues published three papers in 1939–1940 concluding that an incretin was unlikely to exist, and that skepticism held the field back for roughly 25 years [3]. The logjam broke in 1960, when Berson and Yalow invented the radioimmunoassay, first applied to insulin [3]. In 1964, McIntyre’s group in London and Elrick’s group in Denver independently demonstrated that oral glucose provokes a considerably larger insulin response than intravenous glucose at similar blood glucose concentrations [3].
How big is the effect? Perley and Kipnis showed that the incretin portion of the insulin response to oral glucose in humans is more than half, and later estimates put it at two-thirds or more of the insulin response in healthy people [3]. The incretin response is smaller with older age and with some gastrointestinal diseases [3].
One researcher, Jens Rehfeld, has argued the incretin concept may now be too narrow — other gut hormones likely contribute during normal mixed meals containing protein, fat and complex carbohydrates, not just pure glucose [3].
How is GLP-1 different from GIP and GLP-2?
Two hormones are conventionally called incretins: GIP and GLP-1 [3]. GIP was originally named “gastric inhibitory polypeptide” and was later renamed “glucose-dependent insulinotropic polypeptide” [3]. It was isolated by John Brown in the 1970s [1], and Dupre and Brown showed in 1973 that it augments glucose-dependent insulin secretion [1].
GLP-2 comes from the same proglucagon precursor as GLP-1 [1]. The two peptides have very different uses: GLP-1-based medicines are used for type 2 diabetes and obesity, while GLP-2 is used to treat short bowel syndrome, because it promotes growth of the intestinal mucosa [1].
Researchers studying gut hormones also frequently measure other peptides alongside these, such as PYY (peptide tyrosine-tyrosine) and ghrelin [3].
What is a GLP-1 receptor agonist?
A receptor agonist is a molecule that binds a receptor and activates it, the way the natural hormone would. The GLP-1 receptor is a class B G-protein-coupled receptor that signals mainly through the stimulatory G protein Gs [5].
In 2017, researchers reported the cryo-electron microscopy structure of the peptide-activated GLP-1 receptor–Gs complex at near-atomic resolution: 4.1 Å overall, and 3.9 Å for the most stable region, covering the GLP-1 peptide, the transmembrane domain and part of Gs [5]. The peptide sits clasped between the receptor’s N-terminal domain and its transmembrane core, stabilized by extracellular loops; a sharp kink forms in the middle of transmembrane helix 6, whose intracellular half pivots outward to make room for the G protein [5]. A separate structure, PDB entry 7KI0, captures semaglutide itself bound to the GLP-1 receptor in complex with Gs [12].
Binding studies rank the receptor’s partners clearly: GLP-1(7–36)amide and exendin-4 bind with equal potency, far ahead of GLP-2 and glucagon(1–29) [7]. Emerging dual and triple co-agonists target GLP-1 alongside the GIP and glucagon pathways [8].
Where are GLP-1 receptors found in the body?
A receptor-mapping study used autoradiography with a labeled GLP-1(7–36)amide ligand to examine 419 human tumors and 209 nonneoplastic human tissues [7]. In normal tissues, receptors turned up in generally low amounts in specific compartments of the pancreas, intestine, lung, kidney, breast and brain [7]. No receptors were identified in lymph nodes, spleen, liver or the adrenal gland [7].
In tumors, the study found high receptor amounts in pheochromocytomas, with receptors also present in brain tumors and embryonic tumors but absent in carcinomas and lymphomas [7]. Earlier work had shown the receptor is massively overexpressed in gut and lung neuroendocrine tumors, especially insulinomas [7]. The study also examined selected rodent tissues for comparison: rat lung (n=3), mouse lung (n=6), rat thyroid (n=12) and mouse thyroid (n=5) [7]. These are laboratory tissue findings, not clinical results in people.
What does the Ozempic label actually say?
Ozempic is a semaglutide injection given under the skin, first approved in the United States in 2017 and marketed by Novo Nordisk [2]. Its approved uses are to improve glycemic control in adults with type 2 diabetes, to reduce the risk of major adverse cardiovascular events in adults with type 2 diabetes and established cardiovascular disease, and to reduce the risk of sustained eGFR decline, end-stage kidney disease and cardiovascular death in adults with type 2 diabetes and chronic kidney disease [2].
The label lays out the following dosing steps:
| Label step | Dose | Label condition |
|---|---|---|
| Starting dose | 0.25 mg once weekly | First 4 weeks [2] |
| First increase | 0.5 mg once weekly | After 4 weeks [2] |
| Second increase | 1 mg once weekly | If additional glycemic control is needed, after at least 4 weeks on 0.5 mg [2] |
| Final increase | 2 mg once weekly | If additional glycemic control is needed, after at least 4 weeks on 1 mg [2] |
The 2 mg once weekly step is the highest dose listed in the label [2]. For the kidney indication, the label directs increasing the dosage to 1 mg once weekly after at least 4 weeks on the 0.5 mg dose [2]. If a dose is missed, the label says to administer it within 5 days [2]. The most common adverse reactions reported in 5% or more of patients are nausea, vomiting, diarrhea, abdominal pain and constipation [2].
The label also carries a boxed warning: semaglutide causes thyroid C-cell tumors in rodents, and it is unknown whether Ozempic causes such tumors, including medullary thyroid carcinoma, in humans [2]. The drug is contraindicated in people with a personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and in anyone with serious hypersensitivity to semaglutide [2]. Other warnings include acute pancreatitis, diabetic retinopathy complications, acute kidney injury from volume depletion, severe gastrointestinal reactions (the label states Ozempic is not recommended in patients with severe gastroparesis), gallbladder disease, and pulmonary aspiration during general anesthesia or deep sedation [2]. The risk of hypoglycemia, including severe hypoglycemia, rises when the drug is combined with an insulin secretagogue or insulin [2]. The label advises women to discontinue the drug at least 2 months before a planned pregnancy, because of semaglutide’s long washout period [2].
Why do these drugs cause nausea and fullness?
The prescribing label does not explain why these symptoms occur. It lists the stomach effects above as the most common adverse reactions and notes, as a drug-interaction point, that Ozempic delays gastric emptying [2]. Reviews of the class describe that same delayed emptying, along with effects on appetite-regulating brain regions, as part of how these medicines work [8].
Is Ozempic a hormone?
No — Ozempic is a medicine, not a hormone. It is a semaglutide injection, and semaglutide is classified on the label as a GLP-1 receptor agonist, a molecule that activates the receptor the natural hormone GLP-1 targets [2][5]. The hormone itself is something the body produces on its own, with roles in insulin secretion, carbohydrate metabolism and appetite [5].
Sources
- Journal of Clinical Investigation. Discovery, characterization, and clinical development of the glucagon-like peptides.
- National Library of Medicine DailyMed. OZEMPIC- semaglutide injection, solution.
- Frontiers in Endocrinology. The Origin and Understanding of the Incretin Concept. July 15, 2018.
- MDPI. Incretin-Based Therapies Through the Decades: Molecular Innovations and Clinical Impact.
- PubMed. Cryo-EM structure of the activated GLP-1 receptor in complex with a G protein.
- FEBS Letters. Tissue-specific expression of the human receptor for glucagon-like peptide-I: brain, heart and pancreatic forms have the same deduced amino acid sequences. January 30, 1995.
- Journal of Nuclear Medicine. GLP-1 Receptor Expression in Human Tumors and Human Normal Tissues: Potential for In Vivo Targeting. May 2007.
- The American Journal of Medicine. Mechanisms of GLP-1 Receptor Agonist-Induced Weight Loss: A Review of Central and Peripheral Pathways in Appetite and Energy Regulation. June 2025.
- PubMed Central. Therapeutic stimulation of GLP-1 and GIP protein with DPP-4 inhibitors for type-2 diabetes treatment.
- PubMed Central. The discovery and development of GLP-1 based drugs that have revolutionized the treatment of obesity.
- PubMed Central. Battle of GLP-1 delivery technologies.
- RCSB Protein Data Bank. 7KI0: Semaglutide-bound Glucagon-Like Peptide-1 (GLP-1) Receptor in Complex with Gs protein.
Frequently asked questions
What does GLP-1 stand for?
GLP-1 stands for glucagon-like peptide-1. The gene sequences showed that glucagon and related GLP sequences are encoded within a larger precursor protein, alongside a second glucagon-related peptide called GLP-2. The active circulating form is a truncated version, GLP-1(7–36).
Is GLP-1 a hormone the body makes on its own, or only a drug?
It is a hormone the body makes on its own. GLP-1 is a gut hormone with roles in regulating insulin secretion, carbohydrate metabolism and appetite. Drugs in this class are not the hormone itself — they are receptor agonists, molecules that activate the same receptor the natural hormone targets.
What is the difference between GLP-1 the hormone and a GLP-1 receptor agonist?
The hormone is what the body produces; a receptor agonist is a medicine built to bind and activate the hormone's receptor. The GLP-1 receptor is a class B G-protein-coupled receptor that signals mainly through the stimulatory G protein Gs. The Ozempic label identifies the drug as a GLP-1 receptor agonist.
What is the incretin effect, and how much of the insulin response does it explain?
The incretin effect is the finding that oral glucose triggers a larger insulin response than intravenous glucose at the same blood sugar level, because the gut releases insulin-stimulating hormones. Perley and Kipnis showed the incretin portion is more than half the insulin response to oral glucose; later estimates put it at two-thirds or more in healthy people.
How does GLP-1 differ from GIP?
Both are gut hormones conventionally called incretins. GIP was isolated first, by John Brown in the 1970s, and was originally named gastric inhibitory polypeptide before being renamed glucose-dependent insulinotropic polypeptide. GLP-1 was the second incretin discovered, identified through recombinant DNA work in the 1980s.
What is GLP-2, and what is it used to treat?
GLP-2 is a second glucagon-related peptide encoded in the same preproglucagon precursor as GLP-1. It promotes growth of the intestinal mucosa and is used to treat short bowel syndrome, whereas GLP-1-based medicines are used for type 2 diabetes and obesity.
Where are GLP-1 receptors found besides the pancreas?
A study of 209 nonneoplastic human tissues found GLP-1 receptors in generally low amounts in the pancreas, intestine, lung, kidney, breast and brain, with none identified in lymph nodes, spleen, liver or the adrenal gland. These were laboratory tissue-mapping findings, not clinical results.
Why do GLP-1 drugs cause nausea and fullness?
The Ozempic label lists nausea, vomiting, diarrhea, abdominal pain and constipation as the most common adverse reactions, each reported in 5% or more of patients, and notes that the drug delays gastric emptying. A review describes the class as also modulating brain regions that control appetite.
This article summarizes FDA labeling, published research and company information current as of September 14, 2026. It is not medical advice and does not replace a conversation with your own healthcare provider. How we research and verify.