Article appeared in 2005.
Juvenile (type 1) diabetes occurs when the immune system mistakenly attacks and destroys the beta cells, which are the cells in the pancreas that produce insulin. The destruction of beta cells doesn’t take place overnight—rather, it happens over a period of time. Experts believe that a key to preventing type 1 diabetes is to detect it and treat it before the majority of beta cells are destroyed, leaving those diagnosed with the disease in need of insulin by injection or pump for the rest of their lives. Scientists involved in type 1 diabetes research believe that it may be possible to accomplish this by blocking this so-called auto-immune response—that’s why it’s one of the Juvenile Diabetes Research Foundation’s (JDRF) main scientific goals.
In a major new finding, a JDRF-funded human clinical trial provides enormous hope that scientists can control the autoimmune attack and, in doing so, change the clinical course of type 1 diabetes. The results of this study were reported in the June 23 issue of The New England Journal of Medicine. This trial, conducted in four centers in Europe, showed that a six-day course of a drug called an anti-CD3 antibody given to people who were diagnosed with type 1 diabetes recently, helped them keep producing insulin from their own beta cells for the 18 months of the study. This anti-CD3 drug, which is not yet approved anywhere in the world, blocks the destruction of beta cells. It stops this destructive process while leaving the immune system free to do its usual work defending the body against diseases. This finding represents an important step toward finding ways to both delay and prevent type 1 diabetes.
STUDY DETAILS
Eighty people with newly diagnosed type 1 diabetes were involved. Dr. Lucienne Chatenoud, M.D., Ph.D., from the Necker Hospital in Paris led the study team. There were two groups of people with type 1 diabetes studied—a group that was given the anti-CD3 antibody for six days and a group that didn’t receive the drug at all. The researchers found that the people in the study continued to produce their own insulin and needed less insulin by injection to keep their blood glucose levels in control. This was not true for those who didn’t receive the drug. The benefits of the six days of the anti-CD3 antibody therapy were still apparent more than 18 months after the treatment. According to the researchers, this suggests that its protective effect is lasting. Another important detail of this study is that the treatment's side effects were minor and lasted only a short time.
STUDY IMPACT
The results from this European study build on the results of a JDRF-funded study that used a similar therapy in 2002 by Kevan Herold, M.D., at Columbia University, and Jeffrey Bluestone, Ph.D., at the University of California, San Francisco/University of Minnesota. These researchers showed the promise of this treatment with 24 people with newly diagnosed type 1 diabetes. The European study takes the previous results—and anti-CD3 drug research verall—several steps further. This study involved a much larger group of people and tracked how well their beta cells were working before the study began. The researchers found that the anti-CD3 drug therapy worked even better in people who had more beta cells that were still functioning at the beginning of the study. More healthy beta cells can mean better blood glucose control, less need for insulin injections and fewer problems that can arise from many years of living with type 1 diabetes.
THE NEXT STEPS
JDRF’s goal is to move this treatment as quickly as possible through the remaining steps of the drug testing and approval process. JDRF also is launching a new research center under Dr. Bluestone’s direction, to expand Dr. Chatenoud’s findings. “There is no other current treatment that can actually change the course of type 1 diabetes once the disease has begun,” JDRF Executive Vice President for Research Richard Insel, M.D., said. “This study shows the research is on the right track. It opens the door for researchers to use this treatment in people who would receive the most benefit.”
The Summer 2005 “Research Update” reported on the increasing use of the insulin pump and its advantages for children with type 1 diabetes. The article indicated that the pump imitates a normal pancreas by delivering a precisely measured, continuous stream of insulin throughout the day, while also delivering smaller doses of insulin as needed, an advantage that allows people to give insulin in response to food. However, the article misstated how a pump works. A pump cannot sense when more insulin is needed and then deliver it. Rather, it must be programmed. As the article stated, pumps are still basically an insulin delivery system and dosages must be adjusted to cover food intake.
JDRF is actively pursuing the development of a medical device that, one day, will in fact combine glucose sensing with insulin delivery through a “closed loop” system that would mimic the human pancreas by registering blood glucose levels and, in response, delivering the necessary amount of insulin.
