Could a simple vitamin reveal the most common liver disease in the world?

MIR-93 promotes fatty liver disease, but vitamin B3 can counter its effects. This discovery suggests a new processing approach.

About 30% of people around the world are affected by a fatty liver disease associated with the metabolic (MASLD), a condition that until recently lacked targeted therapies. In an important breakthrough, scientists have identified a genetic factor that worsens the disease, and in particular the compound approved by the FDA which has proven to be the most effective against this factor B3.

A world premiere was produced by a collaborative research group led by Professor Jang Hyun Choi of the Unist Department of Life Sciences, with Professor Hwayoung Yun of the College of Pharmacy and Research Institute for Drug Development of Pusan ​​National University (UNDP) and Professor Neung Hwa Park of the University of Ulsan (UUH). Their work revealed the critical role of Microrna-93 (MIR-93), a molecule expressed in the liver, as a genetic regulator influencing the appearance and progression of Masld.

Role of MIR-93 in liver function

MIR-93 is a type of RNA Found in hepatocytes that remove the activity of specific target genes. Researchers have detected unusual levels of MIR-93 in human patients with fatty liver disease and in experimental animal models. Molecular studies have shown that the MIR-93 leads to an accumulation of lipids, inflammation and fibrosis by blocking the expression of SIRT1, an essential gene for regulating lipid metabolism in liver cells.

When scientists used gene editing techniques to block the production of mir-93 in mice, they observed major reductions in the accumulation of liver fats, as well as improvement insulin Helpatic sensitivity and markers. On the other hand, the mice designed to overexpress the MIR-93 displayed more serious deficiencies of the metabolism of the liver.

Vitamin B3 as therapeutic candidate

In addition, screening for 150 drugs approved by the FDA revealed that niacin (vitamin B3) most effectively remove MIR-93. Mouses treated with niacin have shown a significant decrease in the liver levels of MIR-93 and a significant increase in SIRT1 activity. The activated SIRT1 restored the lipid metabolism pathways, thus normalizing lipid homeostasis of the liver.

The research team explained: “This study accurately elucidated the molecular origin of Masld and demonstrates the potential for reuse of a vitamin compound already approved to modulate this path, which has a clinical relevance of high translation.”

They added: “Since niacin is a well -established and safe medicine used to treat hyperlipidemia, it is promising as a candidate for combined therapies targeting Miarn’s tracks in Masld.”

Reference: “Hepatical Mir-93 promotes the pathogenesis of the steatotic liver associated with metabolic dysfunction by removing Sirt1” by Yo Han Lee, Jinyoung Lee, Joonho Jeong, Kien Park, Bukyung Baik, Yuseong Kwon, Kimyeong Kim, Keon Woo Khim, Haneul Ji, Kimyeong, Kimyghe Kim, Ji won Kim, Tam Dao, Misung Kim, Tae Young Lee, Yong Ryoul Yang, Haejin Yoon, Dongryeol Ryu, Seonghwan Hwang, Haeseung Lee and Jang Hyun Choi, April 12, 2025, Metabolism.
DOI: 10.1016 / J.Metabol.2025.156266

This research was supported by various, including the National Research Foundation of Korea (NRF) and the Korea Research Institute of Bioscience and Biotechnology (Kribb).

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