Fatty liver disease is a growing health problem that can quietly damage the liver for years before serious symptoms appear.
Scientists at Georgetown University have tested an experimental drug that prevented severe fatty liver disease in mice and even reversed existing liver damage.
The results offer an early clue to a possible new way of treating advanced liver disease.
The condition was traditionally called nonalcoholic fatty liver disease, or NAFLD, and its more serious form was known as nonalcoholic steatohepatitis, or NASH.
Medical terminology has since changed, with these conditions now commonly called metabolic dysfunction-associated steatotic liver disease, or MASLD, and metabolic dysfunction-associated steatohepatitis, or MASH. They are closely linked to obesity, type 2 diabetes, and other metabolic problems.
The disease begins when too much fat collects inside liver cells in people whose condition is not mainly caused by heavy alcohol use. Some people remain in this early stage for years without major liver damage. In others, however, the liver becomes inflamed and injured, which can eventually lead to permanent scarring.
Advanced scarring can make it difficult for the liver to perform its many essential jobs, including processing nutrients, removing harmful substances from the blood, and producing important proteins. Severe disease can eventually lead to cirrhosis, liver failure, or liver cancer. This makes finding ways to stop or reverse liver damage an important research goal.
In the study, Georgetown University researchers investigated a small experimental molecule called CTPI-2. The drug targets a protein produced by a gene called Slc25a1, which is involved in how cells use and move citrate, a substance connected with energy production and fat metabolism. The researchers suspected that changing this pathway could reduce the processes that drive fatty liver disease.
They tested CTPI-2 in mice fed a high-fat diet that promoted obesity and serious liver disease. Some animals received the treatment early, allowing the scientists to see whether it could prevent disease. Other mice received the drug after significant liver injury had already developed.
The results were striking. In mice treated early, CTPI-2 largely prevented the development of severe fatty liver disease and obesity compared with untreated animals. This suggested that interfering with the targeted pathway could protect the liver even while the animals were exposed to a diet that normally causes metabolic problems.
The researchers also reported benefits when treatment began after the disease was established. CTPI-2 helped reverse signs of liver damage, reduced body weight, and improved the animals’ ability to handle glucose. Better glucose control is particularly relevant because fatty liver disease and type 2 diabetes often occur together and can worsen each other.
Additional experiments suggested that the drug reduced inflammation, an important driver of continuing liver injury. Research in genetically modified mice also pointed to possible effects related to cancer development. These findings raise the possibility that the pathway targeted by CTPI-2 may influence several processes involved in chronic liver disease.
However, the research is still at an early stage. A treatment that works well in mice may not have the same benefits in people, and scientists must determine whether CTPI-2 is safe before it can become a human treatment. Laboratory findings normally need to be followed by extensive safety testing and several stages of clinical trials.
For people with fatty liver disease, lifestyle and medical care remain important. Losing excess weight when appropriate, exercising regularly, eating a healthy diet, and managing conditions such as diabetes, high cholesterol, and high blood pressure can reduce liver risks. People concerned about their liver health should discuss testing and treatment options with a healthcare professional.
The Georgetown University research was published in the journal Cell Death & Differentiation. Although CTPI-2 is far from being an approved treatment, the study provides researchers with a promising biological target and another possible route toward therapies that could one day help repair damage caused by severe fatty liver disease.
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