Nano-particles in RNA Render Insulin Ineffective in Obese Mice

A research team at the Max Planck in Cologne has developed a technique that enhances the insulin resistance of blood cells.

In clinical tests, obese mice were discovered to develop excess miRNA-143 in the liver. The RNA molecule eliminates genes that activate the enzyme AKT and prevents activating of AKT by the insulin. AKT is essential to deliver glucose in the cell and prevent liver glucose synthesis. Controlling the enzyme makes the insulin ineffective and maintaining high levels of blood sugar, according to Jens Brüning, director, Max Planck Institute for Neurological Research and scientific coordinator of the Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases at the University of Cologne.

The team compared normal mice with obese ones suffering from type 2 diabetes. The miRNA-143 in the livers of the sick mice exceeded than in normal ones. Only a low count of the protein ORP8 existed in the obese animals to create excessive miRNA-143. ORP8 forces insulin to activate AKT and so reduces sugar content. Insulin becomes ineffective if the ORP8 is insufficient, rendering the AKT inactive.