Stop the Argonaut
Diabetes and liver obesity cured by protein blocking
Svetlana Maslova, Hi-tech+
Experiments on mice offer science a new and relatively simple way to cope with type 2 diabetes and diseases caused by obesity. The secret lies in maintaining the energy balance in the body due to the blocking of liver protein. The research is still at an early stage, but has solid prospects for potential treatment of people.
Scientists from the USA have proved that blocking the synthesis of Argonaute 2 protein in the liver, which is part of a protein complex that suppresses gene expression by the mechanism of RNA interference, can stop the development of type 2 diabetes mellitus, as well as fatty liver disease. Experiments on mice have already proven the effectiveness of therapy, according to the website of the Children's Hospital Medical Center in Cincinnati (Scientists Block RNA Silencing Protein in Liver to Prevent Obesity and Diabetes in Mice).
According to the results of the study, the Argonaute 2 protein (Ago2) controls the suppression of RNA in cells, affecting the overall energy metabolism in the body. As a result, it slows down the metabolism and the ability of the liver to process food with a high fat content.
To confirm the conclusion, the team removed Ago2 from the liver of mice, which stabilized energy metabolism. As a result, it was possible to stop obesity and the development of type 2 diabetes mellitus.
"The discovery of the role of Ago2 in this process connects previously disparate information about protein synthesis in the liver, as well as energy production and consumption in the body," says researcher Takahisa Nakamura.
The authors emphasize that these results need additional study and verification on laboratory models and the development of a therapeutic method for inhibiting Ago2 in clinical settings for patients. But the data obtained provides a solid basis for further work.
Article by Zhang et al. Hepatic Ago2-mediated RNA silencing controls energy metabolism linked to AMPK activation and obesity-associated pathophysiology published in the journal Nature Communications – VM.
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