Researchers at McMaster University have discovered that the satiety hormone GDF15 can switch liver immune cells into a protective mode, slowing the progression of cirrhosis. This process is independent of calorie counting or fat loss, as reported by infohub.kz.
The findings, published in the journal Cell Metabolism, show that GDF15 can suppress liver inflammation and slow the progression of organ scarring, regardless of weight loss.
"We found that GDF15 activates a natural signaling pathway from the brain to the liver that helps suppress liver inflammation and reduce fibrosis. This changes our understanding of the hormone and suggests it may be part of the body's own defense system against chronic liver damage," says Gregory Steinberg, co-director of the Center for Metabolism, Obesity, and Diabetes Research (MODR) and senior author of the study.
In experiments on laboratory mice with severe liver disease (MASH), which mimics the human condition, the researchers found that the GDF15 protein sends a signal to the brain, which through the nervous system activates the production of protective glucocorticoids.
"Glucocorticoids helped suppress inflammation in the liver, and these protective effects occurred independently of changes in food intake, body weight, or liver fat content. It was also found that GDF15 helps limit the progression of liver fibrosis—the accumulation of scar tissue associated with advanced stages of the disease," the study authors noted.
A previous study published in 2023 showed that GDF15 supports calorie burning during weight loss, but this new work reveals a different role for the hormone: protecting the liver through a previously unknown anti-inflammatory mechanism.
According to the researchers, these findings could aid in the development of future treatments aimed at combating liver inflammation—a major driver of disease progression that has been difficult to treat.