Research in the Linnemann lab is focused on diabetes; specifically the study of the insulin producing pancreatic beta-cells under conditions of inflammatory stress. The beta-cells must adapt rapidly to changing conditions in the body in order to maintain blood glucose within a normal range. When pancreatic islets are exposed to additional stress and demand due to factors such as inflammation or obesity, some beta-cells are better able to adapt and respond in such a way that allows them to survive. An inability to adapt contributes significantly to the development of diabetes. Thus, we are particularly interested in how higher level metabolic signals contribute to molecular crosstalk within the islet and influence beta-cell adaptation to stress. In an effort to develop therapies that prevent beta-cell failure in type 1 and type 2 diabetes, projects in the lab are focused on 3 major areas:

1. Identifying mechanisms of adaptive stress response in the pancreatic islet that enable beta-cell survival.
2. Studying paracrine signaling in the islet under conditions of stress and increased demand.
3. Understanding the regulation of core mediators of autophagy and how this process contributes to beta-cell homeostasis and survivial.