Fatty liver breakthrough: A common vitamin shows promise

An international research team led by Professor Jang Hyun Choi at UNIST, working with Professor Hwayoung Yun at Pusan National University (PNU) and Professor Neung Hwa Park at Ulsan University Hospital (UUH), 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.

How miR-93 Disrupts Liver Function

MiR-93 is a small RNA molecule found in liver cells that controls the activity of certain genes. 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.

Vitamin B3 Emerges as a Potential Treatment

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."

Study Support and Publication Details

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). The findings were published online in Metabolism: Clinical and Experimental. Key contributors include Dr. Yo Han Lee and Kieun Park from UNIST, along with Professor Joonho Jeong from Ulsan University Hospital and Jinyoung Lee from Pusan National University, who served as co-first authors.