Vitamin B3 Shows Promise as Treatment for Fatty Liver Disease by Targeting Key Genetic Factor

Researchers have discovered that vitamin B3 (niacin) can effectively target microRNA-93, a key genetic driver of fatty liver disease. The study shows niacin reduces miR-93 levels and increases SIRT1 activity, restoring normal fat-processing pathways in the liver. This finding suggests a widely available vitamin could become a new treatment for metabolic-associated fatty liver disease affecting 30% of people globally.

Researchers have identified microRNA-93 as a key genetic driver of fatty liver disease and discovered that vitamin B3 can effectively shut it down. This finding suggests a safe, widely available vitamin could become a powerful new treatment for metabolic-associated fatty liver disease (MASLD), which impacts roughly 30% of people globally and has long lacked effective, targeted therapies.

An international research team has identified microRNA-93 (miR-93) as a central regulator in MASLD. This marks the first time this molecule has been clearly linked to how the disease develops and progresses. The researchers discovered that levels of miR-93 are unusually high in both people with fatty liver disease and in animal models. Their analysis showed that miR-93 drives fat buildup, inflammation, and scarring in the liver by suppressing SIRT1, a gene that plays a key role in managing fat metabolism inside liver cells.

To better understand its role, the team used gene editing to stop the production of miR-93 in mice. These animals showed significantly less fat accumulation in the liver, along with improved insulin sensitivity and better overall liver function. In contrast, mice engineered to produce excess miR-93 experienced more severe metabolic problems in the liver.

The researchers then screened 150 FDA-approved drugs to see if any could reduce miR-93 levels. Niacin (vitamin B3) stood out as the most effective option. 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.

The research team explained, "This study precisely elucidates the molecular origin of MASLD and demonstrates the potential for repurposing an already approved vitamin compound to modulate this pathway, which has high translational clinical relevance." They added, "Given that niacin is a well-established and safe medication used to treat hyperlipidemia, it holds promise as a candidate for combination therapies targeting miRNA pathways in MASLD."

The findings were published online in Metabolism: Clinical and Experimental. This work was supported by several organizations, including the National Research Foundation of Korea (NRF) and the Korea Research Institute of Bioscience and Biotechnology (KRIBB).

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