Type 1 childhood diabetes could be reversed through a gene therapy that can rectify two defects in the gene which leads to the early onset disease.
Type 1 diabetes is caused by a certain condition in which body’s own cells start out to attack and destroy insulin producing beta cells in the pancreas.
Hence type 1 diabetes is called an auto immune disease. Once the beta cells in pancreas get destroyed the body loses its ability to produce insulin hormone that is essential for the processing of glucose.
Type 1 diabetes is a disease that affects about one in every 400 to 600 children and adolescents, reports indicate.
As of now there is no known cure to prevent the disease. External insulin is supplied through injections on a day-to-day basis to aid glucose metabolism.
In the experimental cure developed for Type 1 diabetes, researchers injected original gene along with the gene for interleukin-10, an important regulator of the immune system.
The interleukin-10 gene us used as a protective gene to shields the newly formed beta cells from autoimmune attack.
Interleukin-10 has been shown effective in preventing diabetes development in mice studies. Interleukin-10 can only prevent but cannot reverse type 1 diabetes once it has developed.
Interleukin-10 gene was also used in combination because earlier studies showed that the immune system destroys the newly formed beta cells in pancreas stimulated by the gene.
The researchers were able to successfully stimulate new formation of beta cells in the pancreas and restore insulin production and normal blood sugar levels in more than 100 mice with chemically induced diabetes.
In nonobese diabetic mice, however, the treatment failed to reverse type 1 diabetes because the mouse’s immune system killed the newly formed beta cells.
But when combined the gene therapy with interleukin-10 into a single intravenous injection, the treatment showed a complete reversal of diabetes in half of the mice during more than 20 months’ follow-up.
Researchers used nonobese diabetic mice, which spontaneously develop diabetes.
Although the combined gene therapy did not reverse autoimmunity throughout the body, it protected the new beta cells from the local destructive effect of autoimmunity.
“A single treatment cured about 50 percent of the diabetic mice, restoring their blood sugar to normal so that they no longer need insulin injections,” stated study co-author Lawrence Chan, MD, DSc, chief of diabetes, endocrinology and metabolism division, Baylor College of Medicine in Houston.
Chan and his colleagues are now in the process of developin other strategies to try to fortify the newly formed beta cells in order to increase the treatment’s cure rate.
They are also trying to identify why the gene therapy did not work in all the mice even though the animals lived a little longer than untreated mice.
The results of the research, which was funded by the National Institute of Diabetes, Kidney and Digestive Diseases, were presented at The Endocrine Society’s 92nd Annual Meeting in San Diego.