Nogo-B protein complex: "non-alcoholic fatty liver" pathogenesis research progress.

"Non-alcoholic fatty liver" refers to the excessive accumulation of triglycerides and fatty acids in the liver caused by factors unrelated to alcohol consumption and hepatitis virus, and has a incidence rate of more than 20% among the general population in China.
recently, the research team of the School of Biological and Medical Engineering made research results at the cellular and molecular levels, which probed the pathogenesis of "non-alcoholic fatty liver" and discovered a new gene that regulates liver fatification.
The results were published in The Journal of Hepatology, an internationally renowned journal in the field of liver research, on the topic "Nogo-B protein digestion promotes liver lipid production by increasing the nuclear transport of liver X-like protein alpha dependence through adenosine-active protein alpha dependence" (Hepatology 2016 Nov; 64 (5): 1559-1576).
"non-alcoholic fatty liver" in obesity, diabetes and other insulin resistance population as high as 75%, and can be developed from simple liver fat degeneration and fatty hepatitis to liver fibrosis and hardening and even liver cancer, seriously threatening the health of the Chinese people.
The cause of its complexity, the current clinically considered obesity, diabetes, long-term use of hormones, inappropriate diet and lifestyle and inadequate exercise are the causes of the disease, but the specific mechanism of its pathogenesis is still lack of understanding, the corresponding treatment means are very limited. Han Zhihong, a special professor of Changjiang Scholars at the
School of Biological and Medical Engineering, in collaboration with the University of Wisconsin School of Medicine in the United States, has discovered a new gene Nogo-B protein subject that regulates liver fatization, which is expected to provide a new drug target for the treatment of "non-alcoholic fatty liver".
Nogo-B protein complex, also known as NgBR.
study found a direct link between lower levels of NgBR protein in the liver and fatty liver disease.
experiments, mice that knocked out the NgBR gene accumulated large amounts of triglycerides and free fatty acids in their livers.
studies confirm that this accumulation of fat is due to a decrease in NgBR levels leading to the nuclear transfer and activation of the central molecule liver X-receiving alpha, which regulates the synthesis of fatty acids in the liver, and is closely related to the inactivation of the adenosine activation protein kinase alpha, which enhances the function of energy metabolism sensors in the body.
, the current clinical use of cholesterol-lowering statins also have a certain anti-"non-alcoholic fatty liver" function, but because the mechanism has not yet been identified, affecting its practical application.
results show that regulating NgBR levels is one of the effective means to prevent and treat non-alcoholic fatty liver disease, and statins can inhibit the occurrence and development of NgBR levels in the liver by stimulating them.
results have obvious clinical significance for the prevention and treatment of related diseases.
.