Metabolic-associated fatty liver disease (MASLD) affects roughly 30% of the global population — billions of people. Mainstream medicine has no effective targeted therapies, offering only lifestyle advice (weight loss, exercise) that most patients cannot sustain. I have written extensively about niacinamide (vitamin B3) as a metabolic therapy, primarily focusing on its role as an NAD+ precursor that supports mitochondrial electron flow, oxidative phosphorylation, and overall energy metabolism. Now, researchers have discovered that niacin (another form of vitamin B3) directly inhibits a specific genetic driver of fatty liver disease — microRNA-93 (miR-93) — which then restores SIRT1 activity. This is a perfect example of the dual mechanism I have always emphasized: B3 works both by boosting NAD+/energy metabolism and by directly inhibiting pathological signaling pathways.
As the study below demonstrates, researchers from UNIST and other institutions identified microRNA-93 (miR-93) as a central regulator of MASLD. Levels of miR-93 are unusually high in both human patients and animal models with fatty liver disease. MiR-93 drives fat buildup, inflammation, and scarring in the liver by suppressing SIRT1 — a gene that plays a key role in fat metabolism. When the researchers used gene editing to stop miR-93 production, mice showed significantly less fat accumulation, improved insulin sensitivity, and better liver function.
The team 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, SIRT1 activity increased, and normal fat-processing pathways were restored.
This finding is significant for two reasons that align perfectly with what I have been saying for years:
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NAD+ and SIRT1: Niacin (like niacinamide) is converted to NAD+. SIRT1 is a NAD+-dependent deacetylase that regulates metabolism, inflammation, and aging. By increasing NAD+, vitamin B3 directly activates SIRT1. The study shows that B3 also works by lowering miR-93, which then derepresses SIRT1. So B3 attacks the problem from two directions: increasing SIRT1 activity directly (via NAD+) and removing the inhibitor (miR-93) that suppresses SIRT1 expression.
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The specific enzyme target: The study identifies miR-93 as the key pathogenic microRNA. This is not an enzyme in the traditional sense, but a non-coding RNA that regulates gene expression. Vitamin B3 inhibits miR-93 levels, which is a novel mechanism that mainstream research has not previously appreciated. I have discussed how B3 inhibits other pathological pathways (e.g., PARP1 overactivation, NF-κB), and this adds miR-93 to the list.
The study used niacin (nicotinic acid), which is one form of vitamin B3. I have generally recommended niacinamide (nicotinamide) because it does not cause the painful “niacin flush” associated with nicotinic acid. However, both forms are converted to NAD+ and likely share the ability to lower miR-93 (though this would need to be confirmed for niacinamide specifically). The human-equivalent dose is not explicitly stated in the press release, but based on the mouse studies and the fact that niacin is already used clinically for hyperlipidemia at doses of 500–2,000 mg per day, the effective human dose for fatty liver disease is likely in the same range. I have consistently recommended 500–1,500 mg of niacinamide daily for metabolic support.
The researchers explicitly note that niacin is a “well-established and safe medication” and that repurposing it for MASLD has “high translational clinical relevance.” This is exactly the kind of cheap, safe, off-patent intervention that the pharmaceutical industry ignores because it cannot be patented. Once again, vitamin B3 proves to be one of the most powerful metabolic therapies available.
http://dx.doi.org/10.1016/j.metabol.2025.156266
https://www.sciencedaily.com/releases/2026/03/260324080203.htm
“…Researchers have identified microRNA-93 (miR-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.
“…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.
“…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.’
