Type 2 diabetes develops gradually and is closely linked to inflammation in the pancreas, but the early events that trigger this process locally are not well understood. This project studies how sugar molecules attached to proteins — a process called glycosylation — help control communication between different pancreatic cell types and regulate inflammation. I have data suggesting that a high-fat diet alters these sugar structures in the pancreas: in digestive enzyme–producing cells, this causes enzymes to leak into insulin-producing regions, triggering inflammation. At the same time, insulin-producing cells lose protective sugar signals that normally keep inflammation down. Together, these changes promote inflammation and damage insulin-producing cells. Using advanced imaging techniques, this project will track how these changes develop over time and test if restoring protective sugar signals can reduce inflammation as a strategy to prevent or slow the development of type 2 diabetes.