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A popular vitamin turned out to be a cure for fatty liver disease

A popular vitamin turned out to be a cure for fatty liver disease

Metabolic dysfunction-associated fatty liver disease (FLD) affects approximately 30% of the global population — and still lacks effective targeted therapy. However, an international team of researchers has managed to uncover a key molecular mechanism of the disease and propose an unexpected solution: the long-known vitamin B3. The results of the study have been published in the journal Metabolism.

The scientists found that patients with fatty liver disease, as well as experimental models of the condition, exhibit sharply elevated levels of a specific molecule — microRNA-93. It suppresses the activity of the SIRT1 gene, which is responsible for regulating fat metabolism in liver cells. As a result, fat accumulation, inflammation, and fibrosis progressively build up in the organ.

A series of experiments in mice demonstrated impressive results: blocking microRNA-93 led to a notable reduction in fatty infiltration of the liver, improved insulin sensitivity, and overall organ recovery. At the same time, artificially increasing levels of this molecule, on the contrary, only worsened metabolic disturbances.

In the next phase, the researchers conducted a large-scale screening of more than 150 already approved drugs — and discovered a clear frontrunner. Niacin, also known as vitamin B3, was the most effective at reducing microRNA-93 levels. In animals receiving this substance, SIRT1 gene activity was restored and fat metabolism in the liver returned to normal.

The authors highlight an important advantage: niacin has long been widely used to correct lipid metabolism disorders, and its safety profile is well established. This makes vitamin B3 a promising candidate for a new strategy in combating FLD, including as part of combination therapeutic approaches.

According to the researchers, their work paves the way for a fundamentally different treatment — one targeting not the symptoms but the molecular roots of the disease. However, clinical trials involving human participants are still needed to confirm the effectiveness of this approach.