Funding outcome

Glucocorticoids are potent anti-inflammatory medications used from pregnancy to adulthood for a wide range of diseases, such as managing preterm birth risks in women, chemotherapy, asthma, and inflammatory bowel disease. Unfortunately, the long-term use of glucocorticoids is associated with the development of diabetes, which is a disease characterized by elevated sugar levels in the bloodstream. It is crucial to note that insulin produced by pancreatic beta cells is the sole hormone responsible for reducing sugar levels in our bloodstream. Our current understanding of how glucocorticoids contribute to the failure and demise of these cells in children is insufficient. This lack of knowledge is hindering the development of effective treatments to prevent the risk of diabetes development in children taking this medication. In our research endeavours, we have pinpointed a detrimental pathway that is amplified by glucocorticoids, leading to the deterioration of pancreatic beta-cell function. When activated, this pathway, known as ferroptosis, weakens the cell structure and induces swelling. Remarkably, by blocking ferroptosis, we have observed improvements in the capacity of pancreatic beta cells to produce insulin. Our ultimate goal is to utilize our findings to delve deeper into this pathway to comprehend better how glucocorticoids damage pancreatic beta cells in juvenile mice. We also aim to screen for drugs to inhibit the harmful effects of ferroptosis that can be combined with glucocorticoids to prevent their diabetogenic effect in children.