Adropin
Adropin, the secreted product of the ENHO (energy homeostasis associated) gene
Written by Aaron CuhaReviewed Sep 2026
Also known as: ENHO gene product, Adropin34-76
A secreted peptide whose blood level falls with obesity and age in humans. Every human study is a measurement, not a treatment: no one has given adropin to a person, and the cognitive benefit that gets quoted was in aging mice.
Overview
Adropin is encoded by ENHO and circulates at low nanogram per millilitre concentrations. It came out of mouse work suggesting a peptide required for metabolic homeostasis and for preventing obesity-associated insulin resistance.
The human literature that followed is entirely observational. In a 2012 study of 130 volunteers, plasma adropin correlated negatively with body mass index (r = -0.335, p < 0.001) and with age (r = -0.263, p = 0.003), was higher in men than women, and was lower in overweight and obese participants, though that weight effect was seen in men only. In 19 women followed through Roux-en-Y gastric bypass, adropin rose after surgery and peaked at three months. Having two or more metabolic syndrome risk factors went with lower adropin regardless of sex.
The most quoted paper carries its own split inside the title. A 2021 study reported that adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice. The human half is correlation with post-mortem or imaging pathology. The mouse half is the intervention. Those two halves get merged in retail copy into a claim that adropin improves cognition, which no human study has tested.
Searching the trial registry returns adropin studies that are all observational: adropin levels in periodontal disease, in endometrioma, in chronic disease severity, in placenta accreta. Adropin is an outcome measure in all of them. Not one gives adropin to anybody.
Mechanism of action
A secreted peptide that in animal work influences fuel selection, favouring glucose over fatty acid oxidation in muscle, and improves insulin sensitivity and endothelial function. Receptor biology is unsettled: GPR19 has been proposed and is disputed, and a 2025 review frames adropin as a cardio-metabolic hormone in the periphery and a neurohormone in the brain, which is a way of saying the mechanism differs by tissue and is not pinned down in either.
Human evidence
Human data exists in reasonable quantity and is entirely observational. Adropin has never been administered to a human being in a registered trial.
- 130 volunteers: adropin falls with BMI and with age, is higher in men, and is lower in people with two or more metabolic syndrome risk factors.
- 19 women undergoing gastric bypass: adropin rose after surgery, peaking at 3 months, which is a response to weight loss rather than a treatment effect of adropin.
- A 2021 study reports correlation between adropin and ageing-related neuropathology in humans; the cognitive improvement in that paper is in mice.
- Registered human studies of adropin, including work in periodontitis, endometrioma and placenta accreta, all measure it as a biomarker.
What this does not tell you: A biomarker that falls with obesity and age describes the company it keeps, not a causal role. Low adropin in metabolic disease is equally consistent with adropin being a consequence of the metabolic state, which is what the gastric bypass data suggest: fix the obesity and adropin rises. Assay specificity for circulating peptides of this size is a known problem across the exerkine literature and has not been formally settled for adropin. Nothing here tells you what giving adropin to a human would do.
Reading the research record
Adropin belongs to the group of exerkines and metabolic peptides, alongside irisin and GDF-15, where the entire human record is correlation and the entire intervention record is rodent. That pattern is worth naming because the marketing does the opposite: it takes the mouse intervention and the human correlation and presents them as one body of evidence about people.
There is also no product. Unlike compounds that reach the research chemical market, adropin is not widely sold, which is why this page exists mainly to stop the mouse cognition result being cited as a human one.
The most useful thing to take from the human data is the direction of the gastric bypass finding. Adropin rose after surgical weight loss. If adropin were driving metabolic health, you would expect the causal story to be told the other way around. It is the same shape as the osteocalcin problem on the neighbouring page: the peptide tracks the state of the organism rather than obviously setting it.
The evidence, charted
Fig. 1 · evidence composition
1of 3 citations (33%) are in people
Counted from the citation list on this page. The Human count is the same number shown in the badge at the top. Both understate any literature larger than the sources we cite.
Fig. 2 · evidence over time
Evidence spans 3 distinct years, 2012 to 2025, counted from the citation list on this page.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Key studies & citations
- Human2012
Low circulating adropin concentrations with obesity and aging correlate with risk factors for metabolic disease and increase after gastric bypass surgery in humans
85 women and 45 men. Adropin correlated negatively with BMI (r = -0.335, p < 0.001) and age (r = -0.263, p = 0.003), was higher in men (4.1 ng/mL) than women (3.0 ng/mL, p = 0.001), and was lower in overweight (3.3 ng/mL) and obese (2.7 ng/mL) than healthy-weight participants (4.1 ng/mL), with the weight effect confined to men. In 19 women having gastric bypass, adropin rose and peaked 3 months after surgery. Observational throughout.
The Journal of Clinical Endocrinology and Metabolism - Animal2021
Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice
Read the title as two studies. The human component is a correlation between adropin and ageing-related neuropathology. The intervention, and the cognitive improvement, is in aging mice. Classified here as animal because that is where the treatment was given.
npj Aging and Mechanisms of Disease - Review2025
Adropin: A cardio-metabolic hormone in the periphery, a neurohormone in the brain?
Recent review of the field. The question mark in the title is the authors', and it reflects how unsettled the receptor biology and the tissue-specific actions remain.
Peptides
Frequently asked questions
Can I buy adropin?
It is not sold as an established product and has never been given to a human in a registered trial. Anything marketed under that name has no human pharmacokinetic or safety data behind it at all.
Does adropin improve memory?
In aging mice, yes, in the study that reported it. The human part of that same paper is a correlation between adropin levels and ageing-related neuropathology. No human has been treated with adropin for cognition or anything else.
Does exercise raise adropin?
Adropin is lower with obesity and age and rises after surgical weight loss, so it moves with metabolic state. Exercise studies measuring it exist but are small and inconsistent, and none of them shows that changing adropin changes an outcome.
Is a low adropin level something to treat?
There is nothing to treat it with, and no evidence that raising it would help. Low adropin travels with high BMI, older age and metabolic syndrome risk factors, all of which have treatments of their own with actual outcome data.