Scientists discover new mechanisms to successfully reverse fatty liver

Researchers have identified mechanisms that cause liver fat accumulation in one-fifth of the UK and can be reversed in mouse models.

People who do not have alcoholic fatty liver disease (NAFLD) will find excess fat in the liver even if they drink less or do not drink alcohol. The condition can range from simple fatty liver to fibrosis and cirrhosis, and eventually to liver cancer.

A group of international researchers published today in the journal Nature Communications reported that aging or old cells in the liver store too much fat because mitochondria (cell cells) are damaged and cannot effectively use fat as a fuel source. Causes its storage.

Reversal process

Researchers at the University of Newcastle's Institute on Ageing in the United Kingdom collaborated with researchers at the Mayo Clinic in the United States and the Erasmus Medical Center in the Netherlands to “kill” aging cells from mice using pharmacological and genetic methods to reduce accumulation in the liver. Unwanted fat restores normal liver function.

Dr. Diana Jurk from the University of Newcastle's Institute on Ageing led a research team. He said: "This is our first effective treatment for fatty liver disease. Our findings show that by using this new method that can kill aging cells. May have a major impact on dealing with this very common life-threatening disease.

“Although our approach works in laboratory mice, we hope to test these human interventions in the near future and may have a positive impact on people's lives.”

method

The team used two different methods to eliminate senescent cells; first by using genetically engineered mice, where aging old cells can be "killed", followed by drugs - dasatinib and quercetin ( The combination of D + Q) is treated, especially to kill senescent cells.

Both methods have also successfully reduced the accumulation of fat in the liver or the aging of mice caused by a high-fat diet.

Dr. Mikolaj Ogrodnik, Ph.D. student of the Institute of Ageing, and the lead author of the paper said: "We have witnessed a very exciting moment in the study of aging. Scientists have realized that aging cells are the cause of many diseases, and now we have a way to defeat them."

Dr. Jurk added: "As we age, we accumulate cell damage. We have shown that these older cells store excess fat due to their inefficient mitochondria. The exciting thing is that we have been able to remove these Old, worn cells open a potential treatment door."

This work was funded by the BBSRC and the Newcastle University Institute on Ageing.

The team is now planning to further study by studying how to develop the technology as a potential clinical treatment.