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overview
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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 the mechanisms underlying pancreatic ß-cell dysfunction. A central area of interest is pancreatic ß-cell death, which significantly contributes to the reduction in insulin secretion seen in diabetes.
Using Pdx1 deficiency as an experimental model, Dr. Polonsky’s lab has shown that all three major forms of programmed cell death—autophagy, apoptosis, and programmed necrosis—contribute to the loss of ß-cell mass. Current efforts are directed toward identifying novel strategies to interrupt these cell death pathways. In particular, the lab has focused on the BH3-only proteins Puma and Bim, which mediate ß-cell apoptosis. Their studies have demonstrated that reducing the expression of Puma and Bim decreases pancreatic ß-cell apoptosis in various models of diabetes, resulting in improved insulin secretion, increased ß-cell mass, and reduced blood glucose levels.
Dr. Polonsky’s work aims to uncover mechanisms that can be targeted to preserve ß-cell function and mass, offering potential therapeutic strategies for the treatment of type 2 diabetes.
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