Glucagon
Glucagon is the 29-aa counter-regulatory hormone from pancreatic alpha cells that stimulates hepatic glycogenolysis, gluconeogenesis, and lipolysis in response to hypoglycemia. Its receptor agonism is incorporated into retatrutide and other triple-agonist drug candidates.
Community Rating
No ratings yet
Compound Profile
Glucagon
Key Data
Research reference only
Research Focus
Preclinical data
⚠ Research & Educational Use Only. Glucagon is a research chemical documented here for scientific education. All information references peer-reviewed literature and preclinical/clinical study data. Not for human consumption. Not medical advice. Consult a licensed researcher or healthcare professional before any laboratory use.
- Emergency treatment of severe hypoglycemia — raises blood glucose within 10-15 minutes via hepatic glycogenolysis
- Stimulates hepatic gluconeogenesis — produces new glucose from amino acids and lactate
- Promotes lipolysis in adipocytes and increases fatty acid oxidation in liver
- Glucagon is not FDA-approved for human use. FDA-approved drug for hypoglycemia management. Available as GlucaGen (Novo Nordisk) and Baqsimi (nasal, Eli Lilly). Prescription required.
Research At a Glance
- Emergency treatment of severe hypoglycemia — raises blood glucose within 10-15 minutes via hepatic glycogenolysis
- Stimulates hepatic gluconeogenesis — produces new glucose from amino acids and lactate
- Promotes lipolysis in adipocytes and increases fatty acid oxidation in liver
- Increases energy expenditure via thermogenic effects on brown adipose tissue (GCGR)
In Plain English
Simple summaryGlucagon is a 29-amino acid peptide produced by pancreatic alpha cells -- the counter-regulatory hormone to insulin. When blood glucose falls too low, glucagon signals the liver to break down glycogen stores and release glucose into the blood. It also stimulates gluconeogenesis (making new glucose from amino acids and glycerol) and fatty acid oxidation. Pharmaceutical glucagon (GlucaGen, Baqsimi nasal powder) is a life-saving treatment for severe hypoglycemia in insulin-treated diabetics. Beyond emergency use, glucagon's receptor is now a key drug target: the glucagon receptor mediates energy expenditure and hepatic fat metabolism effects that researchers are trying to harness in combination with GLP-1 (as in retatrutide and cotadutide) to maximize weight loss while controlling the hyperglycemia that pure glucagon receptor activation would cause.
- Emergency treatment of severe hypoglycemia — raises blood glucose within 10-15 minutes via hepatic glycogenolysis
- Stimulates hepatic gluconeogenesis — produces new glucose from amino acids and lactate
- Promotes lipolysis in adipocytes and increases fatty acid oxidation in liver
The full scientific detail, mechanisms, citations, and dosing data, follows below.
What is Glucagon?
Tap any underlined term for an instant definition.
Glucagon is a 29-amino acid peptide hormone synthesized and secreted by alpha cells of the pancreatic islets of Langerhans. It is the primary counter-regulatory hormone to insulin, and its fundamental physiological role is to prevent and reverse hypoglycemia by mobilizing glucose from hepatic glycogen stores and stimulating gluconeogenesis.
Glucagon is encoded by the proglucagon gene — the same gene that encodes GLP-1, GLP-2, GIP-2, and oxyntomodulin, which are differentially produced by tissue-specific post-translational processing. In the pancreas, proglucagon is cleaved primarily to produce glucagon. In the intestinal L-cells, the same proglucagon precursor is cleaved to GLP-1 and GLP-2.
**Core mechanisms:** 1. **GCGR (glucagon receptor) activation in liver** → cAMP → PKA → phosphorylase kinase → glycogen phosphorylase activation → glycogenolysis 2. **GCGR in liver** → gluconeogenesis from lactate, alanine, glutamine 3. **GCGR in adipocytes** → lipolysis → free fatty acid release → hepatic ketogenesis 4. **GCGR in CNS/hypothalamus** → satiety signaling, thermogenesis
The relationship between glucagon and the GLP-1/GIP incretin system is complex and bidirectional. Normally, insulin/glucagon are secreted in inverse ratios to maintain euglycemia. GLP-1 receptor agonists suppress glucagon, while glucagon receptor agonism increases energy expenditure.
This creates an interesting therapeutic window: the energy expenditure benefits of glucagon receptor agonism can be harnessed if glucagon-induced hyperglycemia is simultaneously prevented by co-agonism at GLP-1R (insulinotropic). This is the rationale for dual (cotadutide) and triple (retatrutide) agonists that include GCGR agonism as a component.
Glucagon also has therapeutic applications beyond hypoglycemia: beta-blocker overdose (GCGR in the heart increases heart rate and contractility), bowel relaxation for radiology procedures, growth hormone stimulation testing, and diagnostic evaluation of glucagonomas.
By the Numbers
Key Research Benefits
Documented effects observed in preclinical and clinical studies on Glucagon. See all Metabolic & Weight peptides for comparison.
Side Effects & Risks
Adverse effects reported in the research literature. All data sourced from preclinical and clinical study reports. View all peptides' side effects →
Dosing Data from the Literature
Doses referenced below are sourced from published preclinical and clinical studies. Use the peptide dose calculator to convert these values to injection volume.
Glucagon (GlucaGen, Baqsimi) for hypoglycemia rescue:
Adult severe hypoglycemia: 1 mg IM, SC, or IN (nasal) Pediatric: 0.5 mg for body weight <25 kg; 1 mg for ≥25 kg
Research applications: - Clamp studies: IV infusion 1-2 ng/kg/min for glucagon counter-regulation research - Diagnostic: 1 mg IV for glucagonoma evaluation, GH stimulation testing - Drug development: GCGR agonism component studied via cotadutide (150-300 mcg SC) and retatrutide
Administration in Research Settings
Standard reconstitution and administration methodology for laboratory research use.
Emergency glucagon kits (GlucaGen) require reconstitution before injection. Nasal glucagon (Baqsimi) does not require reconstitution — one 3 mg nasal puff. For IV research use, dilute in 0.9% saline.
What the research doesn't show
Glucagon receptor agonism raises blood glucose, which is therapeutic in hypoglycemia but problematic in type 2 diabetes and metabolic disease. The entire challenge of glucagon receptor-targeting obesity drugs is co-activating GLP-1 (which lowers blood glucose) to offset the hyperglycemic effect of glucagon receptor stimulation. Getting this balance right is the active research challenge, and it's not fully solved.
Medical Expert Videos
Physicians, researchers, and pharmacologists explain Glucagon, covering mechanisms of action, clinical context, and study findings.
Videos sourced from YouTube search. KnowYourPeptide does not endorse any individual creator. For research education only.
The Bottom Line
Glucagon has a growing body of preclinical evidence and a well-characterised safety profile in research settings. The most-studied application is: emergency treatment of severe hypoglycemia — raises blood glucose within 10-15 minutes via hepatic glycogenolysis.
The most commonly reported side effect in research subjects is nausea and vomiting are common at therapeutic doses. It is a research chemical, not approved for human use.
Frequently Asked Questions
Explore Further
Quick Reference
How It Compares
Insulin is glucagon's direct counterpart -- insulin lowers glucose, glucagon raises it. GLP-1 suppresses glucagon release postprandially (part of why GLP-1 drugs improve glucose control). In the obesity drug context, the glucagon receptor provides energy expenditure benefits that GLP-1 alone doesn't -- which is why triple agonists like retatrutide that include glucagon receptor activity are showing the highest weight loss numbers.
Compare Glucagon side-by-sideResearch Use Only
This information is for educational research purposes only. This is not medical advice. Consult a qualified healthcare professional.