Adropin
The diet-sensitive hormone from the ENHO gene: what injecting it does in obese mice, and what its blood levels do and do not tell us in people
Adropin is a 43-residue peptide hormone made mainly in the liver and brain from the ENHO (energy homeostasis associated) gene. Found in mice in 2008, it rises and falls with what an animal eats. Injected into obese mice it lowered blood glucose, eased fatty liver and shifted the heart toward burning glucose. In people it has only been measured: meta-analyses find lower blood levels in type 2 diabetes, obesity and coronary disease, but the studies are observational and vary widely. No study has given adropin to a person.
No established human dose Details ↓
Recommended Dosing
No established human dose
Adropin has never been given to people. The treatment evidence comes from injections in mice and rats; the human evidence is blood measurements in observational studies and inside trials of diet, exercise and diabetes drugs, where adropin was the outcome, not the treatment.
What is it?
Adropin was reported in 2008 by researchers looking for liver genes whose activity tracks diet. The ENHO gene they found is expressed in liver and brain and codes for a small secreted peptide. In lean mice a high-fat diet quickly raised its expression and fasting lowered it, but after months of obesity-inducing feeding expression fell. In obese mice, either extra adropin from a transgene or adropin injections reduced fatty liver and insulin resistance without changing body fat or food intake.
Later mouse studies explored how. Three days of injections in obese mice restored the heart's ability to burn glucose by changing the acetylation of its fuel-handling enzymes. In fasted mice, adropin injections preserved insulin's ability to suppress fat burning in the heart, raised cardiac work and improved efficiency. In obese mice it lowered fasting blood glucose, mainly by reducing glucose output from the liver. Mice lacking the gene did worse on a high-fat diet. A review of rodent studies tried to pin down the most effective injected amount, a sign of how early this work still is. Expression of the gene follows the body clock, peaking at feeding times in mice and monkeys, and a high-cholesterol diet suppresses it.
In people, adropin has been measured, not given. The most consistent finding is lower blood levels in type 2 diabetes: a 2023 meta-analysis of 15 studies with 2,813 participants found a small average difference, with very high heterogeneity. Similar analyses found lower levels with overweight or obesity and with coronary artery disease, and higher levels in gestational diabetes, a reminder that the direction is not the same in every condition. A family with a variant in the ENHO gene had low adropin, fatty pancreas and diabetes.
Blood adropin also moves with diet and treatment. In controlled feeding studies, fructose raised it and glucose lowered it, and in women it tracked fat intake. In a weight-loss trial only the highest baseline levels fell. Twelve weeks of aerobic exercise raised it in obese adolescents along with blood-vessel function, and in a 2026 trial adropin rose similarly with two different diabetes drugs, which the authors read as a marker of better metabolic control rather than a drug-specific effect. In older adults, higher adropin went with more variable blood pressure.
Taken together, adropin looks like a signal that reflects the liver's handling of fat and sugar, and possibly a lever for treatment in rodents. Whether raising it would help people is untested: there is no adropin medicine, the human studies cannot separate cause from effect, and the levels reported differ widely from one study to the next. ClinicalTrials.gov lists studies that measure adropin, none that give it.
Mechanism of Action
Adropin is a diet- and clock-regulated hormone from the liver and brain that, in mice, shifts tissues from burning fat toward burning glucose and curbs the liver's glucose output; its receptor is not settled.
Liver glucose and fat
In obese mice it suppressed hepatic glucose production and lipogenic genes, easing fatty liver and insulin resistance (PMIDs 19041763, 31004398).
Heart fuel choice
In mice it moved the heart from fatty-acid toward glucose oxidation and improved efficiency (PMIDs 30822408, 31202835).
Clock and diet control
Clock proteins drive a daily rhythm in the gene; cholesterol suppresses it and fat or fructose intake raise blood levels in people (PMIDs 29331507, 26435060).
Published Research
These studies were read from their PubMed abstracts on October 29, 2026. The treatment studies used mice; the human studies measure adropin in blood, sometimes inside trials of diet, exercise or diabetes drugs. None gave adropin to a person.
Discovery: a diet-regulated liver hormone
The ENHO gene, expressed in liver and brain, rose with a high-fat diet and fell with fasting in lean mice but declined with long-term obesity. In obese mice, transgenic overexpression or adropin injections reduced fatty liver and insulin resistance without changing fat mass or food intake.
Lower blood glucose in obese mice
In obese mice, adropin treatment lowered fasting glucose and improved glucose tolerance; clamp studies showed it suppressed glucose output from the liver and improved the liver's insulin sensitivity.
The heart burns more glucose
In mice on a long-term high-fat diet, three days of adropin injections restored cardiac glucose oxidation and pyruvate dehydrogenase activity, through changes in the acetylation of fuel-metabolism enzymes rather than through Pdk4.
Better cardiac efficiency
Fasted mice given adropin injections had hearts that kept insulin's suppression of fat burning, did more work and were more efficient; adding adropin directly to isolated hearts also cut fatty-acid oxidation and raised glucose oxidation.
A family with an ENHO variant
In a three-generation family with type 2 diabetes and fatty pancreas, affected members shared an ENHO variant and patients had low serum adropin and fewer regulatory T cells; knockout mice lacking adropin developed fatty pancreas and diabetes on a high-fat diet.
What amount works in rodents
A systematic review found only six rodent studies that tested adropin doses, and proposed a best-supported injection schedule for mice and another for rats, calling for more work to define effective doses.
The body clock and cholesterol
In 750 adults, plasma adropin was inversely related to LDL cholesterol in men but not women. In mice the gene followed a daily rhythm set by clock proteins, monkeys showed peaks at feeding times, and cholesterol-rich diets suppressed it, but extra adropin did not prevent high cholesterol.
Lower in type 2 diabetes
A meta-analysis of 15 observational studies with 2,813 participants found lower serum adropin in type 2 diabetes than in controls (about 0.6 ng/mL), with extreme heterogeneity between studies (I2 99.5%).
Lower with overweight or obesity
Across five observational studies with 643 participants, circulating adropin was lower in overweight or obese people than in normal-weight people (about 1 ng/mL), most clearly in Asian participants and people with metabolic disorders.
Lower in coronary artery disease
Seven studies with 945 participants found lower serum adropin in coronary artery disease than in healthy controls, in heart attack, unstable and stable angina alike.
Higher in gestational diabetes
Pooling eight observations, maternal adropin was higher in women with gestational diabetes than in those without, the opposite direction to type 2 diabetes.
Fructose raises it, glucose lowers it
In controlled feeding studies, adropin fell slightly when glucose supplied a quarter of daily energy and rose when fructose did, with no change on high-fructose corn syrup; the rise with fructose was strongest in people with high triglycerides.
Tracks fat intake in women
In lean adults in a sleep-restriction study, sleep loss did not change plasma adropin, but in women fasting adropin correlated positively with chosen fat intake and negatively with carbohydrate intake.
Carbohydrate intake and weight loss
In a weight-loss trial, only people in the top quarter of baseline adropin saw it fall; across the normal range adropin was lower with higher habitual carbohydrate intake, and its distribution was skewed.
Exercise raises it in obese adolescents
Obese adolescents had lower adropin and poorer blood-vessel function than normal-weight peers; 12 weeks of aerobic exercise raised both, independent of weight change.
Rises with diabetes treatment
In a randomised trial in 100 adults with type 2 diabetes, serum adropin rose by a similar amount over 12 weeks whether empagliflozin or sitagliptin was added to metformin, which the authors read as a marker of improved metabolism rather than an effect of either drug.
Blood pressure variability in older adults
In 443 older adults followed for five years, higher plasma adropin was linked to greater visit-to-visit variability in systolic pressure, mainly in people taking blood-pressure medicines.
Tested as a pulmonary embolism marker
In 29 patients with pulmonary embolism and 28 controls, adropin was lower in embolism; a cutoff gave 82% sensitivity and 75% specificity in this small study.
From hepatokine to neurohormone
A review describes adropin as a stress-responsive peptide acting across tissues: it inhibits liver glucose output, stimulates the breakdown of glucose, opposes fibrosis and supports blood vessels, and is highly expressed in the brain, where recent data suggest protective actions.
No Established Human Dose
Adropin has never been given to people. The treatment evidence comes from injections in mice and rats; the human evidence is blood measurements in observational studies and inside trials of diet, exercise and diabetes drugs, where adropin was the outcome, not the treatment. There is no human dose, and the rodent amounts are not one.
What this rests on: PMID 19041763, PMID 31004398, PMID 37029398, PMID 42177445.
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 Adropin 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 Adropin 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 Adropin, 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 Adropin stays intact once mixed.
How it is taken
Unknown: with no established human dose, there is no established way of taking Adropin. 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 Adropin 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: The abstracts of the mouse treatment studies report metabolic outcomes, not adverse effects; Blood levels differ in direction between conditions (lower in type 2 diabetes, higher in gestational diabetes), so a level alone is hard to interpret (PMIDs 37029398, 34378485). Full list and cautions ↓
When to stop or get help: unknown; no label or trial on file sets rules for stopping Adropin. Treat a severe or unexpected reaction as a reason to stop and see a doctor.
Source: the Side Effects section below (“No human safety data exist, because no one has been given adropin in a study”).
Interactions
Unknown: a PubMed search for human interaction studies of Adropin (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 Adropin 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 Adropin's expected mass, 4,501.9 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: no approval and no human treatment trial 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
No human safety data exist, because no one has been given adropin in a study.
Contraindications & Cautions
Adropin is a research peptide, not a medicine.
Legal Status
Adropin is an endogenous hormone studied in research. It is not a medicine.
Frequently Asked Questions
?What is adropin?
A 43-amino-acid peptide hormone made mainly in the liver and brain from the ENHO gene, whose levels change with diet.
?Has adropin been tested as a treatment in people?
No. All the treatment studies used mice or rats. In people it has only been measured in blood.
?What did it do in mice?
In obese mice it lowered blood glucose, reduced fatty liver and insulin resistance, cut glucose output from the liver and made the heart burn more glucose.
?Is low adropin a sign of diabetes?
Meta-analyses find lower levels in type 2 diabetes, obesity and coronary disease on average, but the studies differ hugely, the levels overlap, and in gestational diabetes adropin is higher. It is not a diagnostic test.
?Can diet or exercise change adropin?
In studies, fructose raised it, glucose lowered it, women's levels tracked fat intake, and 12 weeks of aerobic exercise raised it in obese adolescents.
?Why is it called adropin?
The abstracts read do not explain the name; they describe it as the product of the energy homeostasis associated (ENHO) gene.
References
- [other] UniProt Q6UWT2: Adropin (human ENHO), chain 34-76. Read October 28, 2026. https://www.uniprot.org/uniprotkb/Q6UWT2/entry
- [pubmed] Kumar KG, et al. "Identification of adropin as a secreted factor linking dietary macronutrient intake with energy homeostasis and lipid metabolism." Cell Metab, 2008;8(6):468-81. PMID: 19041763.
- [pubmed] Thapa D, et al. "Adropin reduces blood glucose levels in mice by limiting hepatic glucose production." Physiol Rep, 2019;7(8):e14043. PMID: 31004398.
- [pubmed] Thapa D, et al. "Adropin treatment restores cardiac glucose oxidation in pre-diabetic obese mice." J Mol Cell Cardiol, 2019;129:174-178. PMID: 30822408.
- [pubmed] Altamimi TR, et al. "Adropin regulates cardiac energy metabolism and improves cardiac function and efficiency." Metabolism, 2019;98:37-48. PMID: 31202835.
- [pubmed] Chen S, et al. "Adropin deficiency worsens HFD-induced metabolic defects." Cell Death Dis, 2017;8(8):e3008. PMID: 28837146.
- [pubmed] Alzoughool F, et al. "Optimal therapeutic adropin dose intervention in mice and rat animal models: A systematic review." Vet World, 2021;14(6):1426-1429. PMID: 34316188.
- [pubmed] Ghoshal S, et al. "Adropin: An endocrine link between the biological clock and cholesterol homeostasis." Mol Metab, 2018;8:51-64. PMID: 29331507.
- [pubmed] Soltani S, et al. "Circulating levels of adropin and diabetes: a systematic review and meta-analysis of observational studies." BMC Endocr Disord, 2023;23(1):73. PMID: 37029398.
- [pubmed] Soltani S, et al. "Circulating levels of adropin and overweight/obesity: a systematic review and meta-analysis of observational studies." Hormones (Athens), 2022;21(1):15-22. PMID: 34897581.
- [pubmed] Zheng J, et al. "Association between serum adropin level and coronary artery disease: a systematic review and meta-analysis." Cardiovasc Diagn Ther, 2019;9(1):1-7. PMID: 30881871.
- [pubmed] Vivek K, et al. "Maternal adropin levels in patients with gestational diabetes mellitus: a systematic review and meta-analysis." Gynecol Endocrinol, 2022;38(2):105-109. PMID: 34378485.
- [pubmed] Butler AA, et al. "Differential Responses of Plasma Adropin Concentrations To Dietary Glucose or Fructose Consumption In Humans." Sci Rep, 2015;5:14691. PMID: 26435060.
- [pubmed] St-Onge MP, et al. "Fasting plasma adropin concentrations correlate with fat consumption in human females." Obesity (Silver Spring), 2014;22(4):1056-63. PMID: 24115373.
- [pubmed] Stevens JR, et al. "Inverse association between carbohydrate consumption and plasma adropin concentrations in humans." Obesity (Silver Spring), 2016;24(8):1731-40. PMID: 27460714.
- [pubmed] Zhang H, et al. "Aerobic exercise improves endothelial function and serum adropin levels in obese adolescents independent of body weight loss." Sci Rep, 2017;7(1):17717. PMID: 29255252.
- [pubmed] Taha OS, et al. "Beyond glycemic control: differential effects of empagliflozin and sitagliptin on insulin sensitivity and a shared increase in adropin in type 2 diabetes." BMC Endocr Disord, 2026;26(1). PMID: 42177445.
- [pubmed] Aggarwal G, et al. "High circulating adropin levels predict long-term blood pressure variability in old adults: evidence from the Multidomain Alzheimer Prevention Trial." Am J Physiol Heart Circ Physiol, 2025;329(6):H1684-H1692. PMID: 41252423.
- [pubmed] Orun S, et al. "Diagnostic accuracy of adropin as a preliminary test to exclude acute pulmonary embolism: a prospective study." BMC Pulm Med, 2022;22(1):351. PMID: 36115957.
- [pubmed] Butler AA, et al. "Adropin: A cardio-metabolic hormone in the periphery, a neurohormone in the brain?." Peptides, 2025;187:171391. PMID: 40097041.
Sources & Citations
Every study on this page was read from its PubMed record on October 29, 2026. The sequence is UniProt Q6UWT2's. Status comes from Drugs@FDA (openFDA), the EMA medicines list and ClinicalTrials.gov. 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.