New innovative treatment prevents diabetes

New innovative treatment prevents diabetes

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Diabetes is a chronic condition characterized by high levels of sugar (glucose) in the blood. It is caused by a problem with the hormone insulin, which regulates the amount of glucose in the body. There are two main types of diabetes: type 1, in which the body does not produce enough insulin, and type 2, in which the body does not properly use the insulin it does produce.

Researchers at the Liston Laboratory in Babraham Institute recently published a study on preventive therapy for diabetes in mice. They were able to prevent diabetes in mice by modifying signaling pathways in pancreatic cells to prevent stress-induced cell death. The therapy targets a pathway that is common to both types of diabetes, making it a promising treatment option with enormous therapeutic potential when translated into a clinical setting.

Dr. Kailsah Singh, a former research associate in the Liston lab, describes their findings: “Our results show that MANF can prevent beta cell damage by preventing inflammation in the islets that is a hallmark of type 1 diabetes.”

For more than 35 years, there have been unsuccessful attempts to prevent the development of type 1 diabetes. Previous approaches sought to target the autoimmune nature of the disease, but Dr. Adrian Liston, senior group leader in the Immunology Research Program, wanted to investigate whether there is more to causing the deterioration in the later stages than just the immune response.

The Liston lab sought to understand the role of cell death in the development of diabetes and therefore approaches this problem by identifying the pathways that decide whether pancreatic stress-producing cells live or die and therefore determine the development of the disease.

Their hope was to find a way to stop this stress-related death, preventing the descent into diabetes, without having to focus solely on the immune system. First, the researchers needed to know which pathways would affect the life-or-death decision for the beta cell. In previous research, they were able to identify Manf as a protective protein against stress-induced cell death and Glis3, which determines the level of Manf in cells. While type 1 and type 2 diabetes in patients usually have different causes and different genetics, the GLIS3-MANF pathway is a common feature of both conditions and is therefore an attractive target for treatment.

To manipulate the Manf pathway, the researchers developed a gene delivery system based on a modified virus known as the AAV gene delivery system. AAV targets beta cells and allows those cells to produce more of the pro-survival protein Manf, tipping the life-or-death decision in favor of continued survival. To test their treatment, the researchers treated mice prone to spontaneously developing autoimmune diabetes. Treating mice in a prediabetic state resulted in a lower rate of developing diabetes from 58% to 18%. This mouse research is a key first step in developing treatments for humans.

“A key advantage of targeting this particular pathway is the high likelihood that it will work in both type 1 and type 2 diabetes,” explains Dr Adrian Liston. “In type 2 diabetes, while the initial problem is insulin insensitivity in the liver, most of the severe complications occur in patients where the beta cells of the pancreas are chronically stressed by having to produce more and more insulin. By treating early type 2 diabetes with this or a similar approach, we have the potential to block progression to major adverse events in late-stage type 2 diabetes.”

Reference: “Manf gene delivery to pancreatic islet beta cells protects NOD mice from developing type 1 diabetes” by Kailash Singh, Orian Bricard, Jason Haughton, Mikaela Bjorkqvist, Moa Thorstensson, Zhengkang Luo, Loriana Mascali, Emanuela Pasciuto , Chantal Mathieu, James Dooley and Adrian Liston, November 16, Biomolecules.
DOI: 10.3390/biom12101493

The study was funded by the Biotechnology and Biological Sciences Research Council, Vlaams Institutut voor Biotechnologie and The Research Foundation – Flanders.

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