The experimental method of therapy allows the symptoms of type 1 diabetes to be reversed in some laboratory mice, according to scientists from the University of Utah Health and several other universities in the journal Proceedings of the National Academy of Sciences. Their method of injecting an appropriate set of antibodies into the pancreas causes the cells that normally control glucose production to start producing insulin and the mouse heals.
Two hormones important for glucose management are produced in the cells of the pancreas called islets of Langerhans: glucagon and insulin. Type 1 diabetes mellitus is a disease associated with autoimmune destruction of insulin-producing beta cells in the pancreas. The loss of the ability to produce this hormone makes it impossible to control the proper metabolism of carbohydrates, fats and proteins. Researchers report that the injection of a single dose of human antibodies that block the action of glucagon, the hormone that controls glucose production and produced in the alpha cells of the pancreatic islets, leads to significant changes in the function of this organ. In experiments, the weight of insulin-producing cells increased up to seven times, and in animals the diabetic symptoms regressed.
The therapy stopped the animals that needed regular insulin injections from any therapy. Long after the injection is given, their body is able to maintain the correct glucose level on its own – explains prof. William L. Holland of U of U Health. For the millions of people suffering from type 1 diabetes, this means a chance to restore the body’s ability to produce insulin, regain normal glucose management, and make progress in recovery – he adds.
The authors of the study, researchers from U of U Health, Vanderbilt University Medical Center, Baylor College of Medicine, Lilly Research Laboratories, University of Texas Southwestern Medical Center, Veteran’s Administration in Dallas, and the Juvenile Diabetes Research Foundation (JDRF) note that There is still a long way to go to create real therapy. The results are promising, but this is the first of many steps that must lead to confirmation that it will work in type 1 diabetic patients – emphasizes Holland.
By the time patients are diagnosed with type 1 diabetes, they have probably lost around 90 percent of their cancer lives. insulin-producing cells. For them to be able to re-control their glucose levels efficiently and independently, something must cause their bodies to increase the number of these cells – explains prof. E. Danielle Dean of Vanderbilt University Medical Center. To find out if this was possible, Holland, Dean and their colleagues induced diabetes in mice by destroying beta cells. Then they gave them the human monoclonal antibody Ab-4, which blocks the binding of glucagon in the liver. They found that the mice’s blood sugar was returning to normal as some of the glucagon-producing cells were starting to produce insulin.
This experiment was carried out in mice whose bodies were able to regenerate insulin-producing cells when the immune system was not disturbing them. In subsequent experiments, an even more serious problem was addressed. Mice, whose immune systems spontaneously attack beta cells, have been studied. Their condition best simulates type 1 diabetes in humans. Again, the administration of Ab-4 antibodies was able to restore insulin-producing cells. It is very interesting that our therapy helps not only rebuild, but also protect beta cells, even if the immune system tends to attack them Holland says. It seems that the cells of the immune system are no longer able to destroy beta cells – he adds.
But this is not the end. There were already therapies that worked on the beta cells of mice, but they didn’t help people. To test this, human beta cells were transplanted into diabetic mice and the mice were destroyed. Therapy with Ab-4 antibodies increased the amount of human insulin in their blood and improved glucose control. Clearly experimental therapy does no harm to human alpha cells. The beneficial effects were maintained for at least 40 days after the treatment.
Now is the time to explain the exact mechanism behind the antibody therapy that makes the glucagon-producing cells start to produce insulin and cannot be destroyed. When scientists answer this question as well, the path to treating type 1 diabetes will be significantly shortened.
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