A mechanism of type 1 diabetes can be directed with simple natural molecules, such as tauroursodeoxicolic biliary acid, to help prevent the disease, according to research directed by the Harvard Public Health School, in Boston (Massachusetts, United States)and published in the digital edition of Science Translational Medicine.
The work highlights a previously not recognized molecular route that contributes to the malfunction of the Beta Pancreatic Beta Cells Producing of Insulin in type 1 diabetes in human patients and in mice, and shows that a chemical intervention can help a correct function of thebeta cells and their survival.
Currently, there is no preventive regime or a cure for DM1, being injection or bomb insulin therapy the only treatment .In type 1 diabetes, beta cells are erroneously attacked by the body's own immune system, so, until now, research has focused on ways of preventing this autoimmune response.
According to the main author of this study, Gökhan S. Hotamisligil, president of the Department of Genetics and Complex Diseases and Professor of Genetics and Metabolism in HSPH, this work opens new paths by focusing on the increase in performance of beta cells, showing that itsPreservation is possible, even before the immune attack.
Using human pancreatic samples and mouse models, HSPH researchers and colleagues at Harvard Medical School, the Broad de Harvard Institute, the Massachusetts Institute of Technology, and the Brussels Free University, in Belgium, tried to separate the mechanismsfor those who fail beta cells in type 1 diabetes.
They focused on the function of the endoplasmic reticulum, a "mini -rgan" within the cells where proteins and lipids are processed and packagedA fundamental role in supporting the work of beta cells.
The researchers found that, in animal models and humans with type 1 diabetes, the function of ER is compromised by the immune attack.This decrease in the function of the endoplasmic reticulum produces stress in ER itself and contributes to the death of beta cells and insulin insufficiency characteristic of type 1 diabetes.
In previous studies, scientists in the Hotamisligil laboratory showed that ER stress in other tissues plays a key role in obesity and type 2 diabetes and can be corrected with the so -called "chemical chaperones", such as tauroursodeoxicolic acid (Tudca), a biliary acid.From that previous research, experts applied TUDCA to type 1 diabetes mouse models.
The authors of the work found that the function of the ER improved both in mice with diabetes and in people with prediabetes.Specifically, an improvement was seen in the function of beta cells, which were less likely to die, and the treated mice recorded a dramatic reduction in the incidence of type 1 diabetes, in addition to identifying the specific molecular mechanism through thewhich Tudca influences the function of ER.
