A Partnership to Save Beta Cells

What would it be like for those who may be prone to the development of Type 1 diabetes to encounter a solution that stops beta cells from being destroyed? A newly announced partnership hopes to answer that question.

A Partnership to Save Beta Cells: What would it be like for those who may be prone to the development of Type 1 diabetes to encounter a solution that stops beta cells from being destroyed? A newly announced partnership hopes to answer that question.

According to PRNewswire.com, “The Juvenile Diabetes Research Foundation, a leader in setting the agenda for diabetes research worldwide, said that it will begin working with The Johnson & Johnson Corporate Office of Science and Technology, and its affiliates, to speed the development of drug targets and pathways to promote the survival and function of insulin-producing cells in people who have diabetes. The program will look to fund research at academic centers around the world that could eventually lead to novel drug targets and industry collaborations for the treatment of type 1 diabetes.”

It may not be possible to completely stop the development of type 1 diabetes, but the long-term consequences could be diminished if insulin-producing cells can be spared from damage following an initial attack, “The joint program will solicit grant proposals from academia and medical research foundations for one- or two-year research projects. The research will focus on agents and compounds that safely promote survival and function of beta cells – the cells within the pancreas that produce insulin, and that are lost in the immune attack that causes type 1 diabetes. Preserving or maintaining beta cell mass and activity in people with type 1 diabetes can reduce insulin requirements, make controlling the disease easier and more effective, and lower the risk of both short- and long-term complications of the disease,” according to the PRNewswire report.

The release further quotes Alan J. Lewis, Ph.D., President and Chief Executive Officer of the Juvenile Diabetes Research Foundation, “This program will clearly help accelerate the translation of basic research into therapies useful in the treatment of diabetes. By creating this novel incubator program to support early stage research with a company known for first-class research and significant experience in the commercialization of products, we believe we can increase the number of viable drug targets identified and fundamentally change the pace of diabetes research.”

In type 1 diabetes the problem always originals with damaged cells that effectively destroy the ability of the pancreas to produce needed insulin. If therapies can be developed that result in salvaging remaining cells this would be a huge plus to type 1 diabetics. It could also be argued that if this partnership is successful it may be possible to develop therapies that not only preserve remaining cells, but also prevent damage before it starts.

Martin Fitchet, M.D., Therapeutic Area Head, Cardiovascular and Metabolism for Johnson & Johnson Pharmaceutical Research and Development, L.L.C was also quoted in the PRNewswire release, “Beta cell survival is a critical research focus to advance the understanding of the natural history of diabetes, and importantly, where to intervene to slow or arrest the progression of this disease. Establishing this alliance with The Juvenile Diabetes Research Foundation is a part of our commitment to access external innovation to drive discovery and development of new therapies for the patients who most need them.”

The partnership is designed to fast track ideas and initiatives that can accelerate the dynamics of diabetes research in a critical area that attempt to get at the root of the most prevalent problem in type 1 diabetes and provide substantial assistance in an arena that has previously been closed to medical intervention.

Author: Staff Writers

Content published on Diabetic Live is produced by our staff writers and edited/published by Christopher Berry. Christopher is a type 1 diabetic and was diagnosed in 1977 at the age of 3.