Fatty liver disease has become one of the world’s most common liver problems.
The condition, now often called metabolic dysfunction-associated steatotic liver disease, or MASLD, may affect about one in three people worldwide.
Many people do not know they have it because it can develop for years without obvious symptoms.
MASLD happens when too much fat collects inside liver cells. It is strongly linked with obesity, type 2 diabetes, high blood sugar and other problems involving the way the body uses and stores energy. Over time, some people develop liver inflammation and scarring, which can eventually lead to severe liver disease, liver failure or liver cancer.
Lifestyle changes such as losing excess weight, exercising regularly and improving diet remain important parts of treatment. However, researchers are still searching for better ways to directly target the biological processes that cause fat to build up in the liver. A new study may have identified one such target.
Scientists from UNIST, Pusan National University and Ulsan University Hospital investigated a tiny molecule called microRNA-93, also known as miR-93. Their findings were published in the journal Metabolism: Clinical and Experimental. The research suggests that miR-93 may help drive the development of fatty liver disease.
MicroRNAs are very small pieces of genetic material that help control how genes behave inside cells. They do not build proteins themselves, but they can turn down the activity of genes that control important processes. Changes in these tiny regulators have been linked with many diseases.
The researchers found unusually high levels of miR-93 in liver cells from people with fatty liver disease. They also saw the same pattern in laboratory animals with the condition. This led the team to investigate whether higher miR-93 levels were simply associated with the disease or were actually helping cause it.
Their experiments pointed to an important connection with a gene called SIRT1. This gene helps the body control energy use and the processing of fats. When SIRT1 works normally, it supports healthy metabolism and helps prevent too much fat from collecting in the liver.
The study found that miR-93 can reduce SIRT1 activity. As miR-93 levels rise, this protective pathway becomes weaker, making it easier for fat to accumulate in liver cells. The researchers therefore suspected that reducing miR-93 might help restore healthier liver function.
They tested this idea in mice by using genetic methods to lower miR-93. The animals developed less fat buildup in their livers and showed improvements in measures of metabolic health. Increasing miR-93, on the other hand, made liver problems worse.
The researchers then looked for existing medicines or compounds that might reduce miR-93. Their screening identified niacin, a form of vitamin B3, as a promising candidate. Niacin lowered miR-93 and increased SIRT1 activity in the experiments, helping the liver process fat more normally.
Niacin is already familiar to medicine and has previously been used in much higher doses than ordinary dietary vitamin intake to change cholesterol and other blood fat levels.
That makes the finding especially interesting because an existing treatment can sometimes be studied for a new purpose more quickly than an entirely new drug. However, this does not mean people with fatty liver disease should begin taking high-dose niacin themselves.
Large doses of niacin can cause side effects and may not be suitable for everyone. More importantly, much of the evidence in this study came from laboratory and animal experiments. Human clinical trials would be needed to determine whether targeting miR-93 with niacin can safely improve fatty liver disease in patients.
The study provides scientists with a clearer picture of one pathway that may contribute to liver fat buildup. It also shows how a tiny regulator inside cells can have much larger effects on metabolism. If future human studies confirm the results, the miR-93 and SIRT1 pathway could become a useful target for new treatments.
For now, the research should be viewed as an encouraging early step rather than proof that vitamin B3 can treat fatty liver disease. Still, it offers a promising direction for a condition that is becoming increasingly common worldwide. Better understanding of these hidden biological changes may eventually lead to more effective and practical ways to protect the liver.
If you care about liver health, please read studies that refined fiber is link to liver cancer, and the best and worst foods for liver health.
For more health information, please see recent studies about how to boost your liver naturally, and simple ways to detox your liver.
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