How to treat fatty liver? Here comes a new target

       How is fatty liver treated? Here comes a new target

　　Nonalcoholic fatty liver disease (nalfd) is the most common chronic liver disease, affecting at least a quarter of the world's adults.

　　It is associated with obesity and diabetes, and may lead to more serious liver damage, such as non-alcoholic steatohepatitis (nash), liver cirrhosis and liver cancer.

　　In order to understand the complexity of fatty liver disease progression, a research team explored the molecular mechanism of experimental nafld and nash, and determined a targeted therapeutic gene sh3bp5. also known as SAB.

　　The study was recently published in the Journal of Hepatology.

　　Medical Doctor of Gastroenterology and Hepatology Research of Medical Center said that SAB is the outer membrane protein of mitochondria and is called the power source of cells.

　　SAB is a key protein in acetaminophen (also known as paracetamol) induced liver injury model and tumor necrosis factor (TNF) induced acute liver failure model, and its level determines the severity of liver injury.

　　SAB is the target of stress activated kinase (JNK), which will lead to damage of mitochondrial function and increase of toxic reactive oxygen species.

　　The activation of SAB gene and the increase of protein level are related to the progress of mouse liver disease and human fatty liver.

　　It is known that a long-term high fat and high sugar diet will lead to obesity, diabetes and fatty liver.

　　In this design experiment, adult mice were fed a large amount of high-fat food supplemented with sucrose and fructose.

　　However, the Medical Research Center conducts medical research, that is, if the mice are fed a high fat and high sugar diet for one year, they will suffer from various inflammatory and fibrotic diseases in their liver. If we introduce this antisense gene targeting liver cells, we can reverse the whole process, normalize insulin resistance, significantly and effectively reduce the fat accumulation in the liver and inflammation and fibrosis of the liver.

　　We do not need to completely remove SAB protein.

　　Taking drugs that can maintain the normal level of SAB can prevent or reverse the development of the disease.

　　The partners of pharmaceutical companies designed and synthesized antisense oligonucleotides (ASO), and were optimistic about SAB targeted DNA therapy.

　　The study showed that giving antisense therapy to mice in the first six months actually helped them "lose weight".

　　Moderate changes can avoid liver damage caused by dietary choices.

　　However, researchers warn that research on mice may not be applicable to humans.

　　But the data show that sab protein is a potential target for the treatment of fatty liver.

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