In a recently published study in Endocrinology, Dr. Thomas Barris of St. Louis University reported a new method to prevent type 1 diabetes in a mouse model.
Type 1 diabetes is a chronic autoimmune disease. Your immune system destroys insulin-secreting β cells, making it unable to secrete insulin normally, resulting in insulin deficiency and high blood sugar. At present, the main treatment for type 1 diabetes is to control blood sugar through insulin therapy, which is often closely related to the life of the patient.
Burris and his research team focused on blocking the autoimmune process that destroys β cells. The goal is to develop treatments to prevent the development of the disease, not to treat it after the onset. "In our study, no mouse developed diabetic beta cells after receiving treatment after severe damage. This treatment slowed the onset of type 1 diabetes. We believe it may even reduce insulin. It needs to be known that there are at least two types of diabetes. T lymphocytes are involved in the development of type 1 diabetes, but another type of helper T. The role of cells (Thelpercell17, Th17) is currently unknown.
In this study, the researchers discovered that two nuclear receptors (nucleareceptors) play an important role in the development of Th17 cells. They found: ROR-α and OR-γt. They used Burris to invent a selective inverse agonist SR1001, which targets these two receptors and blocks autoimmunity in a mouse model. We have successfully protected β cells.
These results confirm that Th17 cells may play an important role in the development of type 1 diabetes and target this cell type. This shows that the use of drugs can become a new strategy for the treatment of diabetes.