What Is Asprosin? Definition and What Research Reports
Asprosin is a small protein hormone released from white adipose tissue, formed when the C-terminal end of profibrillin-1 is cleaved by furin. It was first described in 2016 as a fasting-induced factor that acts on the liver to raise glucose output, and later work reported a central appetite-stimulating action and a receptor, OLFR734. Published research has since examined circulating asprosin in diabetes, kidney, liver and cardiac models. This glossary entry is definitional only and carries no guidance on use.
Definition
Asprosin is a 140-amino-acid protein hormone secreted mainly by white adipose tissue. It is not transcribed from its own gene: it corresponds to the C-terminal cleavage product of profibrillin-1, the precursor protein encoded by FBN1, and is released when furin cuts profibrillin. The 2016 paper that named it reported that asprosin was induced by fasting, circulated at nanomolar levels, and acted on the liver to drive hepatic glucose release into the circulation (PMID 27087445). Because of that origin and behaviour, asprosin is usually classed as an adipokine — a signalling protein made by fat tissue — and more specifically as a glucogenic adipokine.
This page is for educational purposes only and is not medical advice; consult a licensed physician for any question about health, diagnosis or treatment. Nothing here describes how any substance should be used.
Where the Term Comes From
The name entered the literature in 2016, when researchers investigating patients with neonatal progeroid syndrome — a condition linked to truncating mutations at the 3' end of FBN1 — traced the phenotype to loss of this cleavage fragment. The study reported that asprosin was secreted by white adipose tissue, that plasma levels rose with fasting, and that it was recruited to the liver where it stimulated glucose release through a cAMP-dependent pathway (PMID 27087445). That founding description — fat-derived, fasting-induced, liver-acting — is still the standard definition used in subsequent papers.
Molecular class at a glance
| Attribute | What the literature describes |
|---|---|
| Molecule type | Protein hormone / adipokine (proteolytic fragment, not a synthetic analogue) |
| Parent protein | Profibrillin-1, encoded by FBN1; released by furin cleavage (PMID 27087445) |
| Primary tissue source | White adipose tissue (PMID 27087445) |
| Stimulus described | Fasting (PMID 27087445) |
| Candidate receptor | OLFR734, an olfactory receptor family member on hepatocytes (PMID 31230984) |
How the Term Is Used in Peptide and Metabolic Research
In research writing, "asprosin" appears in three distinct senses, and the three are often conflated in non-technical summaries:
- As an endogenous hormone. Papers describe the body's own circulating asprosin and how its concentration changes with feeding state or disease.
- As a measured biomarker. Clinical and observational papers report serum asprosin concentrations across patient groups — for example, one 2021 study reported that serum asprosin was increased and correlated with diabetic nephropathy (PMID 33933135), and a 2025 report examined asprosin alongside TLR4 as candidate biomarkers in endometrial cancer (PMID 40871563).
- As a laboratory reagent. Recombinant asprosin is applied to cells or administered to animals in preclinical experiments so that researchers can observe downstream signalling. This is a research-only context; asprosin is not an approved medicine.
Asprosin is a protein rather than a short synthetic peptide, so it sits at the larger end of what is loosely grouped under "peptides" in popular writing. Its literature is almost entirely mechanistic and observational.
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Glucose regulation
The founding study reported that asprosin acted on hepatocytes via a cAMP-dependent pathway to increase glucose release, and that neutralising circulating asprosin in insulin-resistant mice lowered blood glucose and insulin (PMID 27087445). A 2019 study in Cell Metabolism identified OLFR734 as a hepatic receptor mediating asprosin's effect on glucose metabolism, reporting that loss of OLFR734 blunted the glucogenic response (PMID 31230984). A 2023 review in Archives of Physiology and Biochemistry summarised asprosin as a novel glucogenic adipokine and discussed its possible relevance to diabetes mellitus (PMID 33663304).
Appetite and central action
A 2017 Nature Medicine paper reported that asprosin crossed the blood-brain barrier and acted directly on hypothalamic AgRP neurons to stimulate appetite, describing it as a centrally acting orexigenic hormone; the study reported that antibody-mediated sequestration of asprosin reduced appetite and body weight in obese mice (PMID 29106398). This second, central role is why later reviews describe asprosin as having both peripheral (glucogenic) and central (orexigenic) actions.
Liver, lipid handling and other organ systems
More recent work has extended the picture to lipid metabolism. A 2025 study reported an asprosin–FABP5 interaction that modulated mitochondrial fatty acid oxidation through PPARα and contributed to metabolic dysfunction-associated steatotic liver disease (MASLD) in experimental models (PMID 40231957). A separate 2025 report in the Journal of Lipid Research examined asprosin as a regulator of hepatic lipogenesis and described its association with hepatic steatosis (PMID 41061856).
Findings outside the liver are mixed in direction, which is worth noting for anyone reading summaries of this molecule. Researchers reported that asprosin protected against ischemia/reperfusion-induced kidney injury in mice (PMID 40794335), and a 2025 study reported that asprosin attenuated diabetic cardiomyopathy in a model by inhibiting autophagy via the AMPK/mTOR/ULK1 pathway (PMID 40560772). A 2026 cell study reported that asprosin protected H9C2 cardiomyocytes from ferroptosis after hypoxia/reoxygenation by promoting mitophagy (PMID 42449477).
Reported Harms and Negative Associations: What Studies Report
No human safety trial of administered asprosin appears in the verified literature summarised here, so there is no clinical adverse-event profile to describe. What the published work does report are associations and mechanistic harms attributed to elevated endogenous asprosin in disease models. Researchers reported that serum asprosin was increased and correlated with diabetic nephropathy in a clinical cohort (PMID 33933135). A 2026 study reported that asprosin mediated diabetes-associated depressive behaviour in animals by provoking pyroptosis, neuroinflammation and kynurenine pathway disorder in the hippocampus (PMID 41338151). In the liver, elevated asprosin signalling was reported to contribute to MASLD development through the FABP5–PPARα axis (PMID 40231957). These are model and cohort findings, not statements about any product.
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Several points recur when the asprosin literature is read as a whole:
- Direction of effect depends on the model. Some studies reported protective effects in kidney and cardiac injury models (PMID 40794335), while others reported harmful contributions in metabolic and hippocampal models (PMID 41338151). Asprosin is not a single-direction "good" or "bad" hormone in the published record.
- Most data are preclinical. The mechanistic findings above came from rodents and cultured cells; human data are largely correlational serum measurements.
- Biomarker ≠ treatment. Reporting that a hormone tracks with a disease does not establish that altering it changes outcomes.
- It is a research molecule. Asprosin is not an approved drug in any indication.
This entry is definitional. It does not describe protocols, quantities or regimens, and it is not medical advice; questions about metabolic health belong with a licensed physician.
References
- Asprosin, a Fasting-Induced Glucogenic Protein Hormone (Cell, 2016)
- Asprosin is a centrally acting orexigenic hormone (Nature Medicine, 2017)
- OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin (Cell Metabolism, 2019)
- Increased serum asprosin is correlated with diabetic nephropathy (Diabetology & Metabolic Syndrome, 2021)
- Asprosin, a novel glucogenic adipokine: a potential therapeutic implication in diabetes mellitus (Archives of Physiology and Biochemistry, 2023)
- Asprosin-FABP5 Interaction Modulates Mitochondrial Fatty Acid Oxidation through PPARα Contributing to MASLD Development (Advanced Science, 2025)
- Asprosin as a regulator of hepatic lipogenesis and its association with hepatic steatosis (Journal of Lipid Research, 2025)
- Asprosin protects against ischemia/reperfusion-induced kidney injury in mice (Journal of Molecular Histology, 2025)
- Asprosin attenuates diabetic cardiomyopathy through inhibiting autophagy mediated by AMPK/mTOR/ULK1 pathway (American Journal of Physiology. Cell Physiology, 2025)
- Effects of Asprosin and Role of TLR4 as a Biomarker in Endometrial Cancer (Molecules, 2025)
- Asprosin mediates diabetes-associated depression via provoking the cascade of pyroptosis-neuroinflammation-kynurenine pathway disorder in the hippocampus (International Immunopharmacology, 2026)
- Asprosin Protects H9C2 Cells From Ferroptosis Following Hypoxia/Reoxygenation by Promoting Mitophagy (Cardiovascular Therapeutics, 2026)
Frequently asked questions
Is asprosin a peptide or a protein?▾
It is best described as a small protein hormone rather than a short synthetic peptide. Researchers reported that asprosin is a 140-amino-acid fragment released from the C-terminus of profibrillin-1 by furin cleavage, secreted by white adipose tissue (PMID 27087445). Popular writing often files it under "peptides," but its literature sits within adipokine and endocrine research.
Where does asprosin come from in the body?▾
The founding study reported that asprosin originates in white adipose tissue as the cleaved C-terminal product of profibrillin-1, the protein encoded by FBN1, and that its plasma levels rose during fasting (PMID 27087445). Because fat tissue secretes it and it signals to other organs, it is classified as an adipokine in the published literature.
What did researchers report asprosin does to blood glucose?▾
The 2016 study reported that asprosin acted on the liver through a cAMP-dependent pathway to increase hepatic glucose release, and that neutralising it lowered glucose and insulin in insulin-resistant mice (PMID 27087445). A later study identified OLFR734 as a hepatic receptor mediating this glucose effect (PMID 31230984). A 2023 review summarised asprosin as a glucogenic adipokine (PMID 33663304).
Does asprosin affect appetite?▾
A 2017 study in Nature Medicine reported that asprosin crossed the blood-brain barrier and acted on hypothalamic AgRP neurons, describing it as a centrally acting orexigenic hormone; the study reported that sequestering asprosin with an antibody reduced appetite and body weight in obese mice (PMID 29106398). These were animal findings, not human clinical results.
Is asprosin linked to liver disease in the literature?▾
Two 2025 papers examined this. Researchers reported an asprosin–FABP5 interaction that modulated mitochondrial fatty acid oxidation via PPARα and contributed to MASLD development (PMID 40231957). A separate report examined asprosin as a regulator of hepatic lipogenesis and described its association with hepatic steatosis (PMID 41061856). Both were mechanistic and preclinical in scope.
Why do some studies describe asprosin as protective?▾
Direction of effect varied by model. One 2025 study reported that asprosin protected against ischemia/reperfusion-induced kidney injury in mice (PMID 40794335), and another reported it attenuated diabetic cardiomyopathy by inhibiting autophagy via AMPK/mTOR/ULK1 (PMID 40560772). Other work reported harmful contributions, such as mediating diabetes-associated depressive behaviour in the hippocampus (PMID 41338151).
Is asprosin an approved medicine?▾
No. Asprosin is not an approved drug in any indication, and the published work summarised here is preclinical or observational — animal models, cell studies and serum biomarker cohorts such as one reporting increased serum asprosin correlated with diabetic nephropathy (PMID 33933135). This page is educational only and is not medical advice; consult a licensed physician with health questions.
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References
This page summarises published research for education — it is not medical advice, and nothing here is a recommendation to use, purchase, or dose any substance. Study parameters described are what researchers reported, not instructions. Consult a qualified clinician before any health decision.