In “Paradigm-Shifting Approach,” Investigators Describe Changes to Pancreatic Beta Cell at Onset of Type 1 Diabetes

Therapeutic targeting of mechanistic pathway has potential to slow disease progression in mice and humans.       

Approximately eight million people live with Type 1 diabetes (T1D) worldwide, a chronic autoimmune condition in which the body attacks and destroys its own insulin-producing β-cells in the pancreas, leading to a lack of insulin and inability to regulate blood sugar. It’s not known why the body suddenly perceives its own β-cells as the enemy; some lines of evidence suggest environmental factors such as viral infections may trigger the onset of T1D, others suggest genetics may also play some role. Ground-breaking research by investigators at Joslin Diabetes Center sheds new light on the specific changes β-cells go through at the onset of T1D. Their findings—published February 26, 2024 in Nature Cell Biology—offer new avenues for targeted interventions for the chronic autoimmune condition. The article Is titled “Redox Regulation of m6A methyltransferase METTL3 in β-cells Controls the Innate Immune Response in Type 1 Diabetes.”

Login Or Register To Read Full Story