Fatty liver disease, also known as metabolic-associated fatty liver disease (MASLD), has become very common in recent years.
Around one in three people worldwide may have this condition. It often develops silently, without clear symptoms, but can slowly damage the liver over time.
This disease is closely linked to modern health problems such as obesity and type 2 diabetes. When too much fat builds up in the liver, it can lead to inflammation and scarring. In serious cases, it may progress to liver failure or cancer. Despite its growing impact, there are still no widely effective drugs that directly treat the condition.
A new study has now provided important insight into how MASLD develops. The research was led by scientists at UNIST, along with teams from Pusan National University and Ulsan University Hospital. Their findings were published in Metabolism: Clinical and Experimental.
The researchers discovered that a small molecule called microRNA-93 plays a key role in the disease. MicroRNAs are tiny regulators inside cells that control gene activity. Although they are very small, they can have powerful effects on how the body functions.
In this study, the scientists found that people with fatty liver disease had much higher levels of miR-93 in their liver cells. The same pattern was seen in animal models. This suggested that miR-93 may be driving the disease process.
The team then explored how miR-93 affects the liver. They found that it blocks a gene called SIRT1, which is important for managing fat metabolism. When SIRT1 is active, the liver can process and remove fat efficiently. However, when miR-93 suppresses this gene, fat begins to accumulate.
To test this further, the researchers used genetic tools to reduce miR-93 levels in mice. The results were very clear. The mice had healthier livers, less fat buildup, and better metabolic function. In contrast, increasing miR-93 made liver damage worse.
After identifying this mechanism, the researchers searched for ways to control miR-93 using existing treatments. They tested many approved drugs and found that niacin, or vitamin B3, was especially effective.
Niacin reduced miR-93 levels and restored the activity of SIRT1. This helped the liver return to a more normal state and improved how fats were processed. Because niacin is already widely used and well understood, it may offer a fast path toward new treatments.
This is an exciting finding because it suggests that a simple vitamin could help manage a complex disease. However, the researchers caution that more studies are needed. The current results are based on animal experiments, and clinical trials in humans will be necessary.
From a critical perspective, the study is valuable because it identifies a clear biological target and provides experimental evidence to support it. The use of drug screening adds practical relevance.
However, the lack of human data means that the findings should be interpreted carefully. Future research will need to confirm safety and effectiveness in patients.
In summary, this study offers new hope for treating fatty liver disease. It shows that understanding small genetic regulators can lead to simple and accessible solutions.
If you care about liver health, please read studies about a diet that can treat fatty liver disease and obesity, and coffee drinkers may halve their risk of liver cancer.
For more information about liver health, please see recent studies that anti-inflammatory diet could help prevent fatty liver disease, and results showing vitamin D could help prevent non-alcoholic fatty liver disease.
Source: UNIST.
