Scientists have found a way to prevent type I diabetes in a mouse model, an
advance that may lead to treatments that slow progression of the disease in
Type I diabetes is a chronic autoimmune disease that occurs when the body's immune system destroys insulin producing pancreatic beta cells.
Current treatments for type I diabetes focus on controlling blood sugar with insulin therapy and must continue throughout a person's life.
"None of the animals on the treatment developed diabetes even when we started treatment after significant beta cell damage had already occurred. We believe this type of treatment would slow the progression of type I diabetes in people or potentially even eliminate the need for insulin therapy," said Thomas Burris, chair of pharmacological and physiological science at Saint Louis University.
In this study, researchers found that two nuclear receptors play critical roles in the development of TH17 cells, and that by targeting these receptors, they were able to stop autoimmunity from developing in several mouse models, sparing beta cells.
They blocked the receptors with SR1001, significantly reducing diabetes in mice that were treated with it.
These results confirmed that TH17 cells likely play a key role in the development of type I diabetes and suggest that the use of drugs that target this cell type may offer a new treatment for the illness.
The research was published in the journal Endocrinology.