Metabolic-associated fatty liver disease (MAFLD) affects about 30% of the global population and, for a long time, lacked effective targeted treatments. Recent studies have identified a key genetic factor influencing the development of this condition and have shown that it can be targeted using an already approved and widely available agent—vitamin B3 (niacin).

Genetic Mechanism of MAFLD Development

An international team of researchers has identified the microRNA molecule miR-93 as a central regulator in MAFLD. It was found that miR-93 levels are significantly elevated in people and animals with fatty liver disease. This small RNA molecule, found in liver cells, regulates the activity of certain genes. Analysis revealed that miR-93 promotes fat accumulation, inflammation, and liver fibrosis by suppressing the SIRT1 gene, which plays a crucial role in regulating fat metabolism in liver cells.

Experimental Data

To study the role of miR-93, researchers used gene editing to stop its production in mice. These animals showed a significant reduction in liver fat accumulation, improved insulin sensitivity, and overall better liver function. In contrast, mice with excessive miR-93 production exhibited more pronounced metabolic disturbances in the liver.

Searching for an Effective Treatment

During the experiments, 150 FDA-approved drugs were tested to determine their effect on miR-93 levels. Niacin (vitamin B3) proved to be the most effective. In mice treated with niacin, miR-93 levels dropped sharply, while SIRT1 activity increased. This helped restore normal fat processing pathways in the liver and improved overall lipid balance.

Application Prospects

Niacin is a well-studied and safe agent for treating hyperlipidemia and may be considered a promising candidate for combination therapy targeting microRNA pathways in MAFLD.

The study results were published in the journal Metabolism: Clinical and Experimental.