A hormone already known for reducing appetite and helping with weight loss may have another important job.
Researchers at McMaster University have discovered that GDF15 can help protect the liver from inflammation and scarring even when its effects on body weight are removed from the picture.
The finding could be important for people with a serious form of fatty liver disease called metabolic dysfunction-associated steatohepatitis, or MASH.
The disease can gradually damage the liver and, in advanced cases, lead to cirrhosis, liver cancer or liver failure.
The research was published on August 10, 2026, in the journal Cell Metabolism. The study was led by scientists including senior author Professor Gregory Steinberg and first and corresponding author Dongdong Wang at McMaster University.
MASH usually develops when excess fat builds up in the liver and is accompanied by ongoing inflammation and cell damage. Over time, the liver tries to repair itself, but repeated injury can cause scar tissue to accumulate.
This scarring is known as fibrosis. As fibrosis becomes more severe, healthy liver tissue can be replaced by scar tissue, making it increasingly difficult for the organ to perform essential jobs such as processing nutrients, removing waste and regulating metabolism.
Obesity and metabolic problems are major risk factors for fatty liver disease. New medicines that produce substantial weight loss can reduce liver fat and improve health for many patients, but losing weight does not always completely remove inflammation from the liver.
That gap led researchers to look more closely at GDF15. This hormone is produced by the body during certain types of stress and sends signals to the brain that can reduce appetite and food intake.
Scientists previously believed that many of GDF15’s metabolic benefits were mainly connected with eating less and losing weight. The new study shows that the hormone can also control liver inflammation through a separate route.
Using mice with a disease designed to closely resemble human MASH, the researchers studied what happened when GDF15 signaling was changed. They used several methods to examine genes, medicines, tissues and individual areas of the liver.
The team discovered a communication pathway running from the brain to the liver through the nervous system. GDF15 first sends a signal to the brain, which then helps trigger the release of steroid hormones called glucocorticoids.
Glucocorticoids are naturally produced by the body and are involved in the stress response, metabolism and control of the immune system. In this pathway, they helped reduce inflammatory activity inside the liver.
Importantly, this protective effect occurred separately from GDF15’s influence on appetite. The liver benefits remained even when researchers accounted for differences in food intake, body weight and the amount of fat stored in the liver.
The hormone also appeared to slow the development of fibrosis. This matters because liver scarring is one of the strongest signs that fatty liver disease is progressing toward more dangerous stages.
The researchers found that GDF15 changed the behavior of cells inside the liver. In particular, immune cells shifted toward a calmer, more protective state instead of continuing to drive damaging inflammation.
Steinberg said the results suggest GDF15 is part of a natural defense system against long-lasting liver injury. Rather than acting only as an appetite hormone, it may help the brain and liver communicate when the liver is under metabolic stress.
The discovery builds on earlier McMaster research published in 2023 showing that GDF15 can help the body maintain calorie burning during weight loss. The new work reveals a different role that may be useful even when weight loss itself is not the main goal.
The findings could eventually influence treatment for MASH. Current approaches often aim to reduce weight, improve metabolism and lower liver fat, while the new pathway raises the possibility of adding treatments designed specifically to calm inflammation and limit scarring.
However, this study was mainly based on animal models, so the results cannot yet show that targeting GDF15 will safely prevent liver damage in people. Human studies will need to determine whether the same brain-to-liver pathway is strong enough to produce meaningful benefits in patients.
There is also a challenge in turning a natural hormone pathway into a medicine. Researchers would need to find a way to capture the helpful anti-inflammatory effects without causing unwanted effects from prolonged changes in stress hormones or other parts of the nervous system.
Even with those questions, the study changes the picture of how GDF15 works. It suggests that future MASH treatment may be most effective when doctors tackle several problems at once, reducing weight and liver fat while also directly controlling the inflammation that drives lasting liver damage.
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Source: McMaster University.
