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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 of 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.

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

The researchers reported that blood glucose levels remained low in treated mice for three days following the injection of antogamiR-132.

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

“This paper provides the first proof-of-principle demonstration that in vivo silencing of microRNA-132 with antagomirs could be used as a therapeutic intervention for diabetes, improving insulin secretion and decreasing blood glucose,” commented Dr. Graham C. Parker, from Wayne State University School of Medicine, Children’s Hospital of Michigan, Detroit, MI.

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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