Asprosin: The Fasting-Induced Hunger Hormone

The biology of hunger keeps getting more crowded. Leptin signals energy sufficiency, ghrelin signals hunger from the stomach, and amylin and GLP-1 signal fullness after meals. Asprosin, identified in the 2010s, added a newer character to this cast: a fat-derived hormone that rises during fasting to raise blood sugar and drive appetite. It is a good example of how the map of metabolic signaling is still being drawn.

What asprosin is

Asprosin is a protein hormone produced mainly by white adipose (fat) tissue. It is a fragment cleaved from a larger precursor protein called profibrillin — the product of the FBN1 gene, better known for its role in connective tissue. Asprosin was discovered through the study of a rare condition (neonatal progeroid syndrome) in which affected individuals have very low asprosin and are strikingly lean, which pointed researchers toward its role in metabolism.

Its defining feature is that it is a fasting-induced hormone: asprosin levels rise when the body goes without food and fall after eating. This timing is a clue to its function — it is part of the system that responds to energy scarcity.

What asprosin does

Asprosin appears to have two main actions, both fitting its role as a response to fasting.

• Raising blood glucose. Asprosin travels to the liver and stimulates the release of glucose, helping maintain blood sugar during fasting. This is a sensible adaptation when food is unavailable — the body mobilizes stored energy.
• Stimulating appetite. Asprosin crosses into the brain and acts on the hypothalamus, where it stimulates appetite-promoting neurons (AgRP neurons) and, in doing so, drives hunger. This makes asprosin an orexigenic (appetite-increasing) signal, in contrast to satiety hormones like leptin, amylin, and GLP-1.

Together, these actions make asprosin a coordinator of the fasting response: when energy is low, it both frees up glucose and encourages eating.

Asprosin in metabolic disease

Because asprosin raises glucose and stimulates appetite, it has attracted interest as a potential contributor to metabolic disease. Elevated asprosin levels have been associated with obesity, insulin resistance, and type 2 diabetes in various studies, raising the hypothesis that excess or dysregulated asprosin signaling could reinforce the very processes that drive these conditions — higher glucose and greater appetite.

This has made asprosin a target of research interest: in principle, blocking asprosin (for example, with antibodies that neutralize it) might reduce appetite and improve glucose control. Such approaches remain experimental and preclinical — asprosin is a research target, not a validated drug target with approved therapies, and much about its human biology is still being worked out. Claims that any supplement or peptide "controls asprosin" for weight loss are not supported by evidence.

How asprosin fits the bigger picture

Asprosin is best understood as one more thread in the complex web of energy-balance signaling. It complements the classic picture: where leptin reports long-term energy stores and satiety hormones report recent meals, asprosin reports and responds to the fasted state, working to keep glucose up and appetite active until food is found. That the body has multiple, redundant, and sometimes opposing hunger and satiety signals is a major reason obesity is biologically difficult to reverse — suppressing one pathway can leave others, like asprosin, still pushing in the opposite direction.

Established obesity drugs act elsewhere in this network: GLP-1 agonists like semaglutide engage satiety signaling, and the melanocortin-pathway agonist setmelanotide acts downstream in appetite circuits in specific genetic disorders. Asprosin-targeting therapies would represent a different, still-unproven angle on the same problem.

Key takeaways

• Asprosin is a fasting-induced hormone, cleaved from the fibrillin precursor and released mainly by fat tissue, discovered in the 2010s.
• It raises blood glucose by acting on the liver and stimulates appetite by activating hunger-promoting (AgRP) neurons in the hypothalamus.
• As an appetite-increasing signal, it contrasts with satiety hormones like leptin, amylin, and GLP-1, and helps coordinate the body's response to fasting.
• Elevated asprosin has been linked to obesity, insulin resistance, and type 2 diabetes, making it a research target — but asprosin-blocking approaches remain experimental and preclinical.
• Asprosin illustrates how the biology of hunger is still expanding, and why single-target strategies rarely fully control appetite.