Betical liver penetration: a safe and cheap vitamin shows a promise

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About 30 % of the world’s population is affected by metabolic -related fatty liver disease (MALD), a condition that previously lacks targeted treatments. In the discovery of a pioneer, the researchers have identified a genetic factor that is exacerbated by the disease, significantly, the drug adopted from the Food and Drug Administration (FDA), which targets this factor more effectively vitamin B3.

Cooperative research team led by Professor Yang Hyun Choi from the Department of Life Sciences at UNIST, in partnership with Professor Hyung Yun from the Institute of College of Pharmacy and Research to develop medicines at Busan National University (PNU), and Professor Nyong Hua Park from Ulsan University (UUH), for the first time, at the protein level). Expressible in the liver, as a major genetic organizer in the development and development of Masld.

Mir-93 is a specialized RNA molecule in liver cells that suppress the expression of specific targeted genes. The team noted abnormal high levels of Mir-93 in both patients with fatty liver disease and animal models. Through molecular analysis, they showed that the Mir-93 enhances the accumulation of fat, inflammation and fibrosis by inhibiting the expression of Sirt1, a gene involved in fat metabolism inside the liver cells.

In experiments that use genetic liberalization techniques to get rid of Mir-93 production in mice, the researchers noticed a noticeable decrease in hepatitis accumulation, as well as significant improvements in insulin sensitivity and liver function indicators. On the contrary, mice with excessive Mir-93 showed the exacerbation of hepatic metabolism.

Moreover, the examination of 150 approved drugs from the FDA (FDA) was revealed that niacin (vitamin B3) is more effective MIR-93. The mice that were treated with niacin showed a significant decrease in the Mir-93 hepatic levels and a noticeable increase in Sirt1 activity. The fat metabolism paths that were restored Sirt1 stimulating, thus normalizing the fat balance in the liver.

The research team explained: “This study shows the accuracy of the molecular origin of Masld and explains the possibility of re -use of a vitamin compound already approved to adjust this path, which is of high clinical importance.”

They added: “Given that niacin is a firm and secure drug used to treat hyperhidaries, it carries a promise as a candidate for compound treatments targeting MASLD paths in Masld.”

This research has been supported by the various National Research Corporation in Korea (NRF) and the Korea Institute for Research on Biological Science and Biological Technology (KRIBB). The results were published online in the prestigious vital medical magazine, Metabolism. Among the participants are Dr. Yu Han Lee and Keon Park from UIST, along with Professor Junho Jeong of Ulsan University Hospital and Jenyon Lee from Busan National University, as participating authors.

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