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Dr. Polonsky’s laboratory focuses on the role of abnormal insulin secretion in the pathogenesis of type 2 diabetes. His research utilizes mouse models of diabetes to investigate mechanisms underlying pancreatic β-cell dysfunction. A central area of interest is pancreatic β-cell death, which significantly contributes to the reduction in insulin secretion seen in diabetes. Through the use of the Pdx1 deficiency experimental model, Dr. Polonsky’s lab has shown that major forms of programmed cell death—such as autophagy, apoptosis, and programmed necrosis—contribute to the loss of β-cell mass. Current efforts are directed towards identifying novel strategies to interrupt these cell death pathways. In particular, the lab has focused on BH3-only proteins Puma and Bim, which mediate β-cell apoptosis. Studies have demonstrated that reducing the expression of Puma and Bim decreases pancreatic β-cell apoptosis in models of diabetes, resulting in improved insulin secretion, increased β-cell mass, and reduced blood glucose levels. Dr. Polonsky’s work aims to uncover mechanisms to preserve β-cell function and mass, offering potential therapeutic strategies for the treatment of type 2 diabetes.
Department of Philosophy