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Anti-MicroRNAs Are Possible New Therapeutic Target For Type 2 Diabetes

Researchers from Sweden and the Netherlands have shown that targeted silencing a tiny molecule called microRNA-132, which is over-expressed in type 2 diabetes, can result in improved insulin secretion and reduced blood glucose in mice and increased insulin secretion in isolated human islet cells.

“MicroRNAs are small non-coding RNAs that can fine-tune the expression of protein-coding genes,” Dr. Lena Eliasson, a professor at Lund University Diabetes Center tells dLife. “Proteins can be seen as ‘workers’ of the cell. MicroRNAs are one of the players adjusting how many of each ‘worker’ there are in a cell during a certain condition.”

She says the pattern of microRNAs differs between different cell type and tissues, which is why researchers talk more specifically about islet microRNAs, which are microRNAs expressed in the pancreatic islets of Langerhans.

How Was The Study Conducted?

Eliasson says it has been known that diabetes is associated with increased levels of certain microRNAs in the islet beta-cells.

“Increased level of microRNAs would lead to reduced expression of certain proteins,” she says, “Thus, a certain type of ‘workers’ for the cell will be missing leading to, in the case of the islet beta-cells, to reduced secretion of insulin and increased blood glucose.”

The increase in blood glucose will lead to diabetes, she says. That’s why a potential treatment would be to inhibit the expression of the specific microRNA to re-establish the beta-cell to secrete enough insulin to keep blood glucose low. “Our present work is the first attempt to do this,” she indicates.

The researchers treated mice and mouse and human islets with an agonist designed to block the expression of microRNA-132, called antagomir-132.

Earlier work has shown that the specific microRNA, miR-132, is overexpressed in pancreatic islets in a diabetic animal model.

“In our present work,” Eliasson says, we show that we can reduce the expression of this microRNA in islets through injection of an inhibitor of miR-132 (called antagomir-132) into the blood of mice.”

Moreover, she says this lowers blood glucose levels and increase insulin secretion.  

“Thus, our data provide the first proof-of-principle demonstration that in vivosilencing of microRNA-132 with antagomirs could be used as a therapeutic intervention for diabetes, improving insulin secretion and decreasing blood glucose,” she says.

The authors encourage additional studies of this new treatment approach in additional animal models of type 2 diabetes.

The new study and promising findings are reported in Nucleic Acid Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc. publishers.

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