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Micro-RNA blocks the effect of insulin in obesity
Date:3/31/2011

gical Research and scientific coordinator of the Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases at the University of Cologne assume, therefore, that micro-RNAs may also play a role in type 2 diabetes. These short ribonucleic acid molecules can regulate the activity of genes and thus control protein production.

The research group in Cologne has now discovered a new mechanism that leads to insulin resistance of the cells. Accordingly, obese mice form excess miRNA-143 in their livers. This RNA molecule silences genes that are responsible for the activation of the enzyme AKT and therefore inhibits insulin from activating AKT. "AKT is important for glucose transport in the cell and for the inhibition of glucose synthesis in the liver. When the enzyme is inhibited, insulin fails to take effect and the blood sugar remains elevated," explains Jens Brning.

For their research study, the researchers compared normal weight mice with obese mice with type 2 diabetes. They discovered that the diseased animals produce more than twice as much miRNA-143 in their livers than the normal ones. Moreover, the researchers found only a low concentration of the protein ORP8 in the obese mice which formed large quantities of miRNA-143. ORP8 stimulates insulin to activate AKT and therefore reduces the sugar content of the blood. If ORP8 is lacking, insulin is unable to take effect and the AKT remains inactive.

The researchers do not yet know why obese mice form more miRNA-143 than their normal weight counterparts. "If we succeed in explaining the signalling paths in the cell that lead to the production of miRNA-143, we will have a starting point for the development of new drugs for the treatment of type 2 diabetes," explains Jens Brning in reference to future research plans.


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Contact: Dr. Cornelia Weigelt
weigelt@nf.mpg.de
49-221-472-6301
Max-Planck-Gesellschaft
Source:Eurekalert

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