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

This release is available in German.

Body weight influences the risk of developing diabetes: between 80 and 90 percent of patients with type 2 diabetes are overweight or obese. According to scientists at the Max Planck Institute for Neurological Research in Cologne and the Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases (CECAD), short ribonucleic acid molecules, known as micro-RNAs, appear to play an important role in this mechanism. The researchers discovered that the obese mice form increased levels of the regulatory RNA molecule miRNA-143. miRNA-143 inhibits the insulin-stimulated activation of the enzyme AKT. Without active AKT, insulin cannot unfold its blood-sugar-reducing effect and the blood sugar level is thrown out of kilter. This newly discovered mechanism could provide the starting point for the development of new drugs for the treatment of diabetes.

The hormone insulin plays a key role in the regulation of blood sugar levels. If there is too much glucose in the blood, insulin opens the glucose transport channels in the cell membrane of muscles and fat cells. Glucose then reaches the body's cells and the blood's sugar content sinks. Additionally, the insulin inhibits the production of new sugar in the liver. Type 2 diabetics are able to produce sufficient volumes of insulin; however, their cells are resistant to it - and the hormone is unable to fulfil its task. If untreated, this disease damages the blood vessels due to the raised blood sugar levels, which can lead to a heart attack or stroke.

The molecular processes in the body's cells responsible for the connection between body weight and diabetes are largely unknown. However, in all tissues that respond to insulin, Micro-RNAs can be found. The Cologne-based scientists working with Jens Brning, Director at the Max Planck Institute for Neurolo
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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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