Key Takeaways:
- Researchers have identified microRNA-93 (miR-93) as a genetic driver of metabolic-associated steatotic liver disease (MASLD).
- In rodent models, niacin (vitamin B3) suppressed miR-93, upregulated SIRT1, and ameliorated liver fat accumulation and insulin resistance.
- Because niacin is already FDA-approved and well understood, it may be a promising candidate for repurposing as a therapy for fatty liver.
The Challenge of Fatty Liver Disease
Non-alcoholic fatty liver disease (NAFLD), now more aptly termed metabolic-associated steatotic liver disease (MASLD), affects millions of people worldwide. Many patients remain undiagnosed, and to date, no therapies directly targeting the molecular causes of fat accumulation in the liver have been firmly established.
This recent research breakthrough sheds light on one of the underlying mechanisms fueling MASLD and points to a surprisingly accessible intervention: vitamin B3.
miR-93: A Genetic Culprit
In the new study, a team led by Professor Jang Hyun Choi (UNIST) and collaborators in South Korea found that miR-93 is abnormally elevated in the livers of patients with fatty liver disease, as well as in mouse models.
- Mechanism: miR-93 downregulates SIRT1, a key gene involved in lipid metabolism, promoting fat accumulation, inflammation, and fibrosis in the liver.
- Animal studies: Genetic suppression of miR-93 in mice improved insulin sensitivity and liver health, while overexpression worsened metabolic dysfunction.
This mechanistic insight offers a compelling new target to address fatty liver disease at a molecular level.
Niacin to the Rescue?
Perhaps the most exciting part of this discovery is the identification of niacin (vitamin B3) among 150 FDA-approved compounds screened for suppressing miR-93 expression.
- In treated mice, niacin reduced miR-93 levels, reactivated SIRT1, and reversed key markers of liver dysfunction.
- Because niacin is already used clinically—primarily for dyslipidemia—its safety profile is well understood, potentially accelerating translation into human trials.
This suggests that a familiar vitamin may hold the key to a novel therapeutic strategy for MASLD.
What This Means for Patients
- Repurposing advantage: Since niacin is already FDA-approved, the pathway toward clinical trials could be faster than for an entirely new drug.
- Complementary use: Niacin may work best as part of combination therapies, targeting miRNA pathways alongside lifestyle changes (diet, exercise) or other treatments.
- Caution advised: Animal data is promising, but human trials are needed. Dosage, long-term safety, and effectiveness in diverse patient populations remain open questions.
Next Steps & Outlook
This study marks a milestone in our understanding of MASLD and miRNA regulation of liver metabolism. Future efforts should prioritize:
- Clinical trials in humans to validate niacin’s effect on miR-93, SIRT1, and liver outcomes
- Dose optimization and safety monitoring, particularly in patients with comorbidities
- Exploration of miRNA targets beyond miR-93 that may synergize with niacin therapy
If successful, this strategy could shift the paradigm from symptomatic management of fatty liver to molecularly targeted interventions.
Conclusion
The discovery that miR-93 drives liver fat accumulation and that niacin can counteract those effects opens up a hopeful direction in the fight against metabolic-associated steatotic liver disease. As research progresses toward human studies, the possibility of a low-cost, well-tolerated treatment arising from a common vitamin is a compelling development for both patients and clinicians.
Source: “Fatty liver breakthrough: A safe, cheap vitamin shows promise,” ScienceDaily, 12 September 2025.
🔗 https://www.sciencedaily.com/releases/2025/09/250912195101.htm
