The long-term goal of our laboratory is to understand the molecular mechanisms governing the regulation of beta-cell mass as a platform to develop novel strategies for the treatment of type 1 and 2 diabetes.
One of the major areas of study in our laboratory is the role of growth factor and nutrient
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more signaling in modulation of beta-cell mass in vivo. These studies identified the importance of Akt as a critical component in the regulation of beta-cell mass and function. More specifically, this work has explored the components that link proximal events in the insulin signaling pathway to basic cell cycle machinery and beta-cell replication. In these pursuits, our laboratory also identified Tuberous Sclerosis Complex 2 and the rapamycin sensitive mTORC1 complex as a critical downstream component responsible for the changes in beta-cell mass and proliferation. We are currently expanding this work to understand the importance of these signaling molecules in beta-cell programming and pancreas development. These results are quite important because of their clinical relevance both in current immunosuppresive therapies and in further development of diabetes-specific treatments that address beta-cell insulin resistance.
Finally, our recent work has unraveled some of the molecular mechanisms of cellular plasticity and programming, demonstrating for the first time that activation of Akt signaling regulates the fate of differentiated pancreatic cells in vivo. These studies suggest that modulation of this pathway could be used to drive reprogramming to beta-cells as alternative therapy for diabetes.
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