Asprosin
Evidence: DNeuroendocrine / Appetite-Energy Balance Signaling
Evidence Snapshot
What this grade covers
Three independent human observational cohorts (Wang 2018, N=143 adult glucose-dysregulation; Wang 2019, pediatric obesity; Zhang 2019, adult T2DM) consistently show higher circulating asprosin associated with worse glucose/insulin parameters -- but this is a YOUNG field (discovery paper 2016) with zero human genetic population-association evidence (only 2 extreme monogenic discovery cases) and zero human administration/intervention evidence. Mishra 2022 (PTPRD receptor) and the 2023 Science Advances AgRP-neuron paper are MOUSE-only mechanism. The 2024 Prader-Willi study found NO significant correlation between asprosin and hyperphagic behavior or cardiometabolic risk and MUST be presented alongside the positive associations. FBN1-wide/Marfan-syndrome clinical literature is EXCLUDED entirely. Overall page grade: D.
Regulatory Context
Native Asprosin is an endogenous human hormone and is not itself an FDA-approved drug product.
In Plain English
A quick, research-focused overview. It does not replace, and cannot outrank, the detailed evidence below.
What is it?
A hormone discovered in 2016, the furin-cleaved C-terminal fragment of profibrillin-1 (the FBN1 gene's protein product).
Why are researchers interested in it?
Studied for its association with obesity, insulin resistance, and type 2 diabetes in several human cohorts.
What does the evidence look like?
Three independent human observational cohorts, no intervention studies, no population genetics -- only 2 extreme monogenic discovery cases.
Biggest things to know
Higher blood asprosin is associated with obesity, insulin resistance, and type 2 diabetes in several independent cohorts, but a 2024 study found no link between asprosin and hyperphagia in Prader-Willi Syndrome.
What don't we know yet?
Whether administering or blocking asprosin would change any human outcome -- no such study exists; the evidence base is still young and not one-directional.
Research Takeaway
Asprosin is the furin-cleaved C-terminal cleavage product of profibrillin-1 (FBN1 gene), identified via two neonatal progeroid syndrome patients with truncating FBN1 mutations who were insulin-sensitive despite lipodystrophy.
Evidence boundary: FBN1-wide/Marfan-syndrome literature beyond this discovery paper is EXCLUDED -- different clinical topic.
See all 5 evidence claims →Quick Summary
Asprosin is a hormone identified in 2016, released from a cleaved fragment of the FBN1 gene's protein product and involved in glucose regulation. Human research on asprosin remains at an early, observational stage.
Mechanism & Research Overview
Asprosin is a hormone identified in 2016, released from a cleaved fragment of the FBN1 gene's protein product and involved in glucose regulation. Human research on asprosin remains at an early, observational stage.
Evidence Claims
Individual scientific statements drawn from the sources cited below, each shown with the specific evidence boundary that statement does not establish.
Supported
Asprosin is the furin-cleaved C-terminal cleavage product of profibrillin-1 (FBN1 gene), identified via two neonatal progeroid syndrome patients with truncating FBN1 mutations who were insulin-sensitive despite lipodystrophy.
Does not establish
Evidence boundary: FBN1-wide/Marfan-syndrome literature beyond this discovery paper is EXCLUDED -- different clinical topic.
Sources: Asprosin, a Fasting-Induced Glucogenic Protein Hormone
Supported
In 143 adults across normal, impaired, and newly-diagnosed-diabetic glucose-regulation groups, plasma asprosin was positively correlated with fasting/postprandial glucose, HbA1c, triglycerides, and insulin resistance, and negatively correlated with beta-cell function.
Does not establish
Evidence boundary: Cross-sectional association only.
Supported
Serum asprosin is increased and associated with insulin resistance in children with obesity.
Does not establish
Evidence boundary: Cross-sectional association only; independent cohort.
Supported
Circulating asprosin is increased in adults with type 2 diabetes and independently associated with fasting glucose and triglycerides.
Does not establish
Evidence boundary: Cross-sectional association only; independent cohort.
Supported
In a cohort of Prader-Willi Syndrome patients, asprosin levels were higher in those with obesity, but showed NO significant correlation with hyperphagic behavior or cardiometabolic risk factors across the whole cohort.
Does not establish
Evidence boundary: Must be presented alongside, not omitted from, the positive association claims above.
Safety & Evidence Limitations
Considerations reported in the sources cited on this page — not a complete list of every possible risk, and not medical advice.
Safety Consideration
Asprosin shares a source gene (FBN1) with Marfan syndrome; Marfan-syndrome-specific clinical literature must never be cited as Asprosin evidence.Safety Consideration
A 2024 Prader-Willi-syndrome study found NO significant correlation between asprosin and hyperphagic behavior or cardiometabolic risk in that cohort -- this must be presented, not omitted, to avoid one-directional evidence selection.Safety Consideration
Asprosin was only discovered in 2016; all human evidence is cross-sectional observational, with zero intervention/administration studies and zero population genetic-association studies (only 2 extreme monogenic discovery cases).
Research Areas Being Studied
Research areas discussed on this page reflect the Neuroendocrine / Appetite-Energy Balance Signaling category and the sources cited below.
Findings Reported in Studies
Educational summary only — reported in cited studies, not a claim of proven benefit.
- Lack of correlation between asprosin serum levels and hyperphagic behavior in subjects with Prader-Willi Syndrome (2024):
- Circulating asprosin concentrations are increased in type 2 diabetes mellitus and independently associated with fasting glucose and triglyceride (2019):
- Serum asprosin concentrations are increased and associated with insulin resistance in children with obesity (2019):
- Plasma Asprosin Concentrations Are Increased in Individuals with Glucose Dysregulation and Correlated with Insulin Resistance and First-Phase Insulin Secretion (2018):
- Asprosin, a Fasting-Induced Glucogenic Protein Hormone (2016):
Study Tables by Evidence Type
Human Studies & Clinical Data
| Title | Year | Population / Model | Dose / Duration / Finding | Safety Notes | Source |
|---|---|---|---|---|---|
| Lack of correlation between asprosin serum levels and hyperphagic behavior in subjects with Prader-Willi Syndrome | 2024 | Prader-Willi Syndrome patients (children, adolescents, adults) | Asprosin levels were higher in PWS individuals with obesity than normal-weight individuals, but showed NO significant correlation with hyperphagic behavior or cardiometabolic risk factors across the whole cohort. | ||
| Circulating asprosin concentrations are increased in type 2 diabetes mellitus and independently associated with fasting glucose and triglyceride | 2019 | Adult type 2 diabetes mellitus cohort | Circulating asprosin increased in adults with T2DM, independently associated with fasting glucose and triglycerides (OR 3.278 for T2DM in top asprosin tertile, AUC 0.707). | ||
| Serum asprosin concentrations are increased and associated with insulin resistance in children with obesity | 2019 | Children with obesity (pediatric cohort) | Serum asprosin increased and associated with insulin resistance in children with obesity; independent cohort from the Wang 2018 adult study. | ||
| Plasma Asprosin Concentrations Are Increased in Individuals with Glucose Dysregulation and Correlated with Insulin Resistance and First-Phase Insulin Secretion | 2018 | 143 adults: normal glucose regulation (n=52), impaired glucose regulation (n=40), newly-diagnosed T2DM (n=51) | Plasma asprosin positively correlated with waist circumference, fasting/postprandial glucose, HbA1c, triglycerides, and insulin resistance; negatively correlated with beta-cell function and first-phase insulin secretion. | ||
| Asprosin, a Fasting-Induced Glucogenic Protein Hormone | 2016 | 2 neonatal progeroid syndrome patients with truncating FBN1 mutations; mouse mechanism follow-up | Asprosin is the furin-cleaved C-terminal cleavage product of profibrillin-1, identified via two neonatal progeroid syndrome patients with truncating FBN1 mutations who were insulin-sensitive despite lipodystrophy. |
Animal / Cell / Preclinical Data
| Title | Year | Population / Model | Dose / Duration / Finding | Safety Notes | Source |
|---|---|---|---|---|---|
| Asprosin promotes feeding through SK channel-dependent activation of AgRP neurons | 2023 | Mice; AgRP-ARH neurons | Asprosin activates AgRP neurons via an asprosin-Ptprd-SK3 channel mechanism, driving hyperphagia in mice. | ||
| Protein tyrosine phosphatase receptor delta serves as the orexigenic asprosin receptor | 2022 | Mice; hypothalamic AgRP neurons | Identifies protein tyrosine phosphatase receptor delta (Ptprd) as the orexigenic receptor for asprosin in hypothalamic AgRP neurons; genetic ablation of Ptprd causes loss of appetite and resistance to asprosin's orexigenic effect. |
Regulatory Documents & Official Trial Registries
No Regulatory Documents & Official Trial Registries Listed Yet
This section will be updated as sources are added.
Anecdotal Reported Patterns — Not Medical Advice
Anecdotal Reported Patterns — Not Medical Advice
Reported dosing patterns are included for educational context only. They are self-reported, unverified, not medical advice, and not instructions for human use. Community-submitted patterns are not yet available in this Phase 1 prototype; this section is a placeholder reserved for moderated, aggregated community data.
Lab Markers to Discuss With a Clinician
Educational topics only — not self-monitoring instructions.
FAQ
Disclaimer
This is an emerging area of research with observational human data only, including one study that found no link between asprosin and hyperphagia in Prader-Willi Syndrome.
Educational use only. This content is provided for informational and research-summary purposes only. It is not medical advice, not a treatment recommendation, not a dosing guide, and not a substitute for care from a licensed medical professional. Nothing here is intended to diagnose, treat, cure, prevent, or mitigate disease. Reported dosing patterns, when shown elsewhere on the site, must be labeled either as Study / Trial Dosing or Anecdotal Reported Patterns — Not Medical Advice. Community reports are self-reported, unverified, and not scientific proof.
Community-reported experiences, once enabled, must be displayed only as moderated, anonymized, or aggregated data. They are anecdotal, self-reported, unverified, and should never be presented as proof of safety, efficacy, or expected results.
Content status: Published. Last updated 2026-08-28.
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