Chinese scientists discover the pathogenesis of nonalcoholic fatty liver disease

Chinese scientists discover the pathogenesis of nonalcoholic fatty liver disease

December 22, 2016 Source: Chinese Journal of Science

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Recently, the research team of Hefei University of Technology has obtained a research result at the cellular and molecular level, and has explored the pathogenesis of nonalcoholic fatty liver disease and discovered a new regulation of liver fatification genes. The results were published in "Liver Science."

The causes of nonalcoholic fatty liver disease are complex and the corresponding treatments are very limited. Han Jihong, a special professor of Changjiang Scholars at Hefei University of Technology, has cooperated with the Wisconsin Medical College in the United States to discover a new Nogo-B protein receptor that regulates liver fatification. It is expected to provide new drugs for the treatment of nonalcoholic fatty liver disease. Target.

The Nogo-B protein receptor is also known as NgBR. The study found that a decrease in the level of NgBR protein in the liver is directly related to the onset of fatty liver disease. In related experiments, a large amount of triglycerides and free fatty acids accumulated in the liver of mice knocked out of the NgBR gene. Studies have confirmed that this accumulation of fat is due to the decrease in NgBR levels leading to nuclear transfer and activation of the central molecule of the liver X receptor alpha, which regulates fatty acid synthesis in the liver, and the loss of adenylate-activated protein kinase alpha with enhanced energy metabolism sensor function in vivo. Live is closely related.

According to reports, the current clinical use of cholesterol-lowering statins also have certain anti-alcoholic fatty liver function, but because the mechanism has not been proven, affecting its practical application. Related studies have shown that the regulation of NgBR levels is one of the effective means to prevent non-alcoholic fatty liver disease, and statins can inhibit the occurrence and development of NgBR by stimulating the liver. This result has obvious clinical guiding significance for prevention and treatment of related diseases.

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