Fatty Liver Disease Breakthrough: Vitamin B3 Shows Promise in New Research
Metabolic-associated fatty liver disease (MASLD), affecting roughly 30% of the global population, has long presented a challenge for targeted therapies. However, recent research has identified a key genetic factor contributing to the condition and suggests a surprisingly accessible potential treatment: vitamin B3.
Uncovering the Role of miR-93
An international research team, led by Professor Jang Hyun Choi at UNIST, in collaboration with researchers at Pusan National University (PNU) and Ulsan University Hospital (UUH), has pinpointed microRNA-93 (miR-93) as a central regulator in the development and progression of MASLD. This marks the first time this molecule has been clearly linked to the disease process.
How miR-93 Disrupts Liver Function
MiR-93, a small RNA molecule found in liver cells, controls the activity of specific genes. Researchers discovered that individuals with fatty liver disease, as well as animal models, exhibit unusually high levels of miR-93. Their analysis revealed that miR-93 promotes fat buildup, inflammation, and scarring in the liver by suppressing SIRT1, a gene crucial for managing fat metabolism within liver cells.
Experiments involving gene editing to halt miR-93 production in mice demonstrated significantly reduced fat accumulation in the liver, alongside improved insulin sensitivity and overall liver function. Conversely, mice engineered to overproduce miR-93 experienced more severe metabolic issues in the liver.
Vitamin B3 as a Potential Therapeutic Agent
The research team screened 150 FDA-approved drugs to identify potential miR-93 level reducers. Niacin, or vitamin B3, emerged as the most effective option. In mice treated with niacin, miR-93 levels decreased substantially, while SIRT1 activity increased, restoring normal fat-processing pathways and improving lipid balance.
“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,” the research team explained. They further noted, “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 Details and Publication
This research was supported by 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 included Dr. Yo Han Lee and Kieun Park from UNIST, Professor Joonho Jeong from Ulsan University Hospital, and Jinyoung Lee from Pusan National University, who served as co-first authors.
Key Takeaways
- Researchers have identified microRNA-93 (miR-93) as a key genetic driver of fatty liver disease (MASLD).
- Vitamin B3 (niacin) has shown promise in reducing miR-93 levels and improving liver function in preclinical studies.
- This research suggests a potential new therapeutic avenue for MASLD, utilizing a safe and widely available vitamin.
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