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Home NEWS Science News Biology

Anti-microRNAs are possible new therapeutic target for type 2 diabetes

Bioengineer by Bioengineer
February 7, 2019
in Biology
Reading Time: 3 mins read
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Credit: Mary Ann Liebert, Inc., publishers


New Rochelle, NY, February 7, 2019–Researchers 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 new study and promising findings are reported in Nucleic Acid Therapeutics, a peer-reviewed journal from Mary Ann Liebert, Inc. publishers. Click here to read the full-text article free on the Nucleic Acid Therapeutics website through March 7, 2019.

“In Vivo Silencing of MicroRNA-132 Reduces Blood Glucose and Improves Insulin Secretion” is the title of the article coauthored by Roel Bijkerk, Johanne Ellenbroek, Yu Wah Au, Maaike Hanegraaf, Eelco de Koning, and Anton Jan van Zonneveld, Leiden University Medical Center, The Netherlands and Jonathan Esguerra and Lena Eliasson, Lund University and SIS Malmö, Malmö, Sweden.

The researchers treated mice systemically, and mouse and human islets with an agonist designed to block the expression of microRNA-132, called antagomir-132. They 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 therapeutic intervention for diabetes, improving insulin secretion and decreasing blood glucose,” says Executive Editor Graham C. Parker, PhD, The Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine, Children’s Hospital of Michigan, Detroit, MI.

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About the Journal

Nucleic Acid Therapeutics is an authoritative peer-reviewed journal published bimonthly in print and online that focuses on cutting-edge basic research, therapeutic applications, and drug development using nucleic acids or related compounds to alter gene expression. The Journal is under the editorial leadership of Co-Editors-in-Chief Bruce A. Sullenger, PhD, Duke Translational Research Institute, Duke University Medical Center and Annemieke Aartsma-Rus, PhD, Leiden University Medical Center, and Executive Editor Graham C. Parker, PhD. Nucleic Acid Therapeutics is the official journal of the Oligonucleotide Therapeutics Society. Complete tables of content and a sample issue may be viewed on the Nucleic Acid Therapeutics website.

About the Society

The Oligonucleotide Therapeutics Society is an open, non-profit forum to foster academia- and industry-based research and development of oligonucleotide therapeutics. The society brings together the expertise from different angles of oligonucleotide research to create synergies and to bring the field of oligonucleotides to its full therapeutic potential.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Human Gene Therapy, ASSAY and Drug Development Technologies, Applied In Vitro Toxicology, and DNA and Cell Biology. Its biotechnology trade magazine, GEN (Genetic Engineering & Biotechnology News), was the first in its field and is today the industry’s most widely read publication worldwide. A complete list of the firm’s 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

Media Contact
Kathryn Ryan
[email protected]
914-740-2250

Original Source

https://home.liebertpub.com/news/anti-micrornas-are-possible-new-therapeutic-target-for-type-2-diabetes/3504

Related Journal Article

http://dx.doi.org/10.1089/nat.2018.0763

Tags: BiologyCell BiologyDiabetesMedicine/HealthMetabolism/Metabolic Diseases
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