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Body fat does more than store energy. It also releases hormones that communicate with the liver, brain, and other organs—and one of those hormones can increase hunger.
In this Metabolic Classroom lecture, Dr. Ben Bikman explores asprosin, a hormone that links two responses to fasting: releasing glucose into the blood and increasing the drive to eat.
The science offers a different way to think about body fat, appetite, and insulin resistance. It also comes with an important distinction: the clearest evidence for asprosin’s effects comes from animal experiments, while the human evidence is still developing.
What Is Asprosin?
Asprosin was identified in a 2016 study investigating a rare genetic condition. It is a small fragment cut from a larger protein made by the FBN1 gene—the same gene involved in producing the connective-tissue protein fibrillin-1.
Researchers initially identified white fat tissue as a major source. In early experiments, asprosin rose during fasting and fell when mice began eating. This pattern suggested that the hormone helps the body respond to a period without food.
The discovery illustrates a broader point: fat tissue is an endocrine organ. Its hormones carry information about energy availability to other parts of the body.
How Asprosin Signals the Liver to Release Glucose
Even when no food is coming in, some tissues still need glucose. The liver helps meet that need by breaking down stored glycogen and making new glucose.
In mice, giving asprosin raised blood glucose within minutes. Experiments in liver cells showed that asprosin stimulated glucose release through a signaling pathway similar to the one used by glucagon.
Insulin opposed that effect in the liver cells. This does not establish that insulin directly controls how much asprosin human fat tissue releases; it shows that insulin can counter the hormone’s action at the liver.
How Asprosin Increases Hunger in Mice
Asprosin also acts on appetite. A 2017 study found that circulating asprosin crossed the blood-brain barrier in mice and activated hunger-promoting nerve cells in the hypothalamus.
Those cells also quieted neurons that normally reduce eating. The result was greater food intake and, over time, increased body weight and body fat in the mice.
These two effects fit together during fasting: the liver makes glucose available while the brain encourages eating. Researchers have identified different receptors for asprosin in the liver and brain, although much of the brain research comes from one closely connected research network.
What the Human Evidence Can Tell Us
The human genetics offered an early clue. A small number of people with a rare FBN1-related disorder had very low asprosin, little fat under the skin, low insulin, and normal blood glucose. Later work also documented low appetite and extreme leanness.
These patients’ genetic condition affects more than asprosin alone, so their experience cannot fully isolate the hormone’s role. In mice engineered with similar mutations, giving asprosin back restored appetite and body weight, strengthening the experimental link.
Broader human studies often report higher asprosin in people with obesity, insulin resistance, or type 2 diabetes. However, results vary considerably, and commonly used measurement kits have produced widely differing values. These associations do not prove that asprosin causes metabolic disease, and the research does not yet support using an asprosin result to guide individual health decisions.
Asprosin, Ghrelin, Leptin, and GLP-1
Several hormones influence appetite, but they come from different tissues and carry different messages. Ghrelin is made mainly in the stomach and is associated with meal timing. Leptin comes from fat tissue and generally signals longer-term energy stores, helping reduce appetite.
GLP-1 is released mainly by the gut after a meal and helps lower appetite and regulate blood glucose. Asprosin’s fasting-related effects in animal studies move in the other direction: increasing hunger and liver glucose output.
Dr. Bikman’s point is that no single hormone deserves the entire label “the hunger hormone.” Appetite reflects communication among fat tissue, the gut, the pancreas, and the brain.
Could Blocking Asprosin Become a Treatment?
In a 2021 study, researchers tested three antibodies that neutralized asprosin in three mouse models of metabolic syndrome. The antibodies reduced appetite, body weight, and blood glucose. A separate experimental approach used a receptor fragment to capture asprosin before it reached its targets.
These are promising animal findings, but they do not establish safety or effectiveness in people. Independent replication and human intervention studies are needed before these approaches can inform treatment.
The lesson from this lecture is broader than any potential therapy: body fat actively communicates with other organs. Understanding those signals helps explain why hunger and blood sugar regulation involve much more than the amount of energy stored in fat.
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