Dr. Kahn’s research focuses on the role of the islet β-cell in diseases associated with disturbed glucose metabolism.
His basic science research revolves around the role of islet amyloid formation in the loss of β-cells and development of β-cell secretory dysfunction. As part of this work, he and his group have identified a number of islet proteins that have detrimental effects on the β-cell, including most recently the cholesterol transport protein Steroidogenic Acute Regulatory Protein (StAR). They have also observed that the innate immune system is activated by amyloid formation and are examining the role of necroptosis, an immune form of cell death, in the loss of β-cells. Their work also aims to find novel approaches to prevent islet amyloidogenesis, including the tissue plasminogen activator/plasmin system and synthetic peptides that interfere with amyloid formation.
His clinical research focuses on physiological studies of the mechanisms by which the β-cell adapts to changes in secretory demand, the importance of propeptide processing in the development of hyperglycemia, the role of central adiposity as a determinant of metabolic disease and the mechanisms responsible for hypoglycemia in patients with cystic fibrosis. In addition, he participates in and holds leadership positions in a number of major clinical trials related to type 2 diabetes including the Diabetes Prevention Program and its follow up the Diabetes Prevention Program Outcomes Study (DPP/DPPOS), Look AHEAD, Restoring Insulin Secretion Study (RISE) and Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness Study (GRADE).