A larger study is needed to determine efficacy, but the small study has proven the safety profile of immunotherapy and its promising future as a therapy for treating type I diabetes.
In a small but rigorous clinical trial, British investigators gave patients recently diagnosed with the metabolic disorder a truncated version of the chemical that gives rise to insulin.
There is an ongoing race between scientists trying to restore insulin secretion within the human body in diabetes patients, by artificially created insulin-producing cells. "We wanted to see if we could protect these remaining cells by retraining the immune system to stop attacking them", said lead researcher Mark Peakman and King's College London professor in a university statement.
All 19 participants receiving the immunotherapy-in both arms-continued to produce their own insulin.
Experts believe it may be possible to "retrain" immune systems to safely slow the advance of type 1 diabetes, following a new trial.
The researchers reported their findings in the most recent (August 9th) edition of the journal Science Translational Medicine.
Speaking on the topic, Dr. Peakman said, "Type 1 diabetes comes about when the immune system inadvertently and irreparably damages beta cells that make insulin ..." In diabetes, it destroys a function that's essential to the body's ability to extract fuel from food and to keep freely circulating blood sugar from damaging organs and blood vessels.
Karen Addington, chief executive of type 1 diabetes charity JDRF, added: "Exciting immunotherapy research like this increases the likelihood that one day insulin-producing cells can be protected and preserved".
Here, researchers used a proinsulin peptide fragment-a snippet of the precursor form of insulin. However, the therapy has not been proven safe for type I diabetes, which is also an autoimmune disease, until now. The patients' glycemic control and insulin use was monitored for six months. The study's recruits were all at a stage of the disorder when the pancreas' insulin-producing cells were still at least partly intact and capable of producing the hormone in response to food intake.