Scientists have discovered how a natural hormone made by the liver may help reverse serious fatty liver disease.
The finding could support the development of a new generation of treatments for a condition that affects a large share of the world’s population.
The research was led by Dr. Matthew Potthoff and colleagues and was published in the journal Cell Metabolism in 2025. The study focused on fibroblast growth factor 21, better known as FGF21, a hormone that helps the body control energy use and other parts of metabolism.
Fatty liver disease is now commonly called metabolic dysfunction-associated steatotic liver disease, or MASLD. It develops when too much fat collects inside liver cells, often in people with obesity, type 2 diabetes or other metabolic health problems.
For many people, the condition remains relatively mild, but it can become much more serious. Some develop MASH, a form of the disease involving liver inflammation and damage that can lead to scar tissue, known as fibrosis.
Over time, severe scarring can interfere with the liver’s ability to work normally and may eventually lead to cirrhosis or liver failure. Because liver fibrosis is closely linked to serious outcomes, researchers are particularly interested in treatments that can reduce or reverse this damage.
The new research suggests FGF21 may have that ability, at least in mice. The scientists found that FGF21 reduced fat in the animals’ livers and helped reverse fibrosis even though the mice continued eating a high-fat diet that promoted liver disease.
One of the most interesting discoveries was where much of the hormone’s effect appeared to begin. Rather than acting only on the liver, FGF21 sent signals to the brain, which then changed nerve activity in ways that helped improve liver health.
This creates a communication system between the liver and the brain. The liver produces FGF21, the hormone carries information to the brain, and the brain responds by sending signals back through the nervous system that can influence what happens in the liver.
The researchers found another pathway as well. FGF21 could also produce effects that helped lower cholesterol, but the study suggested that signaling through the brain was responsible for much of the hormone’s ability to improve liver disease.
This brain connection has similarities with the way other hormones control metabolism. GLP-1, the hormone pathway targeted by medicines such as semaglutide, also communicates with the brain and helps regulate appetite, blood sugar and body weight.
FGF21-based medicines are already attracting attention as possible treatments for metabolic diseases. Several drug candidates designed to copy or extend the effects of FGF21 have been studied in people, including patients with serious fatty liver disease.
The new study is important because it provides more detail about how this hormone may produce its benefits. Understanding the brain-liver pathway could help researchers design treatments that target the most useful parts of FGF21 signaling.
However, the results should be interpreted carefully because much of this research was conducted in mice. A treatment that reverses liver scarring in laboratory animals may not necessarily produce the same result in people, so large human clinical trials are essential.
The findings nevertheless offer an encouraging direction for fatty liver research.
If scientists can successfully harness the signals that FGF21 sends between the liver and brain, future medicines may be able to tackle not only liver fat but also the dangerous scarring that can turn fatty liver disease into a life-threatening condition.
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