Barbara Kahn is the George Minot Professor of Medicine at Harvard Medical School and Vice-Chair for Research Strategy in the Medicine Department at Beth Israel Deaconess Medical Center (BIDMC). Dr. Kahn’s pioneering research established a critical role for the GLUT4 glucose transporter in adipocytes in regulating systemic insulin sensitivity and Type 2 diabetes risk. She performed early investigations of GLUT4 regulation in humans with obesity and diabetes. These, with observations in novel genetic mouse models created in her lab, led to her discovery that GLUT4 down-regulation in adipocytes can cause Type 2 diabetes. Dr. Kahn identified the underlying molecular mechanisms including co-discovering a novel class of mammalian lipids with anti-diabetic and anti-inflammatory effects. She also discovered that AMP-activated-protein-kinase regulates systemic energy balance. Dr. Kahn received her MD from Stanford University and an MS in Health Sciences from University of California Berkeley. She did a General Medicine Fellowship at University of California Davis and an Endocrine Fellowship at NIH. She was Chief of the Diabetes Unit and Chief of the Division of Endocrinology, Diabetes, and Metabolism at BIDMC. She received the Banting Medal from the American Diabetes Association and the Gerald Aurbach Award from the Endocrine Society. She is a member of the National Academy of Sciences and the National Academy of Medicine.

Research Interests

My lab investigates the cellular and molecular mechanisms for insulin resistance in obesity and Type 2 diabetes. Our work established the critical role of the GLUT4 glucose transporter in adipocytes in regulating systemic insulin sensitivity, energy balance and inflammation. We showed that down-regulation of GLUT4 in adipocytes markedly increases the risk for Type 2 diabetes and GLUT4 overexpression in adipocytes enhances glucose tolerance. We use genomic, metabolomics and lipidomic approaches in human tissues and genetically-engineered mouse models to discover novel adipocyte-associated molecules. This has revealed important biomarkers and mechanisms for insulin resistance and diabetes. For example, we demonstrated that retinol-binding-protein-4 levels are elevated in insulin-resistant people and this causes insulin resistance by activating both innate and adaptive immune responses in adipose tissue. We also showed that de novo lipogenesis in adipocytes has a major role in regulating systemic insulin sensitivity. With Alan Saghatelian, we used global lipidomics to discover a novel class of lipids made in mammalian tissues, which correlate highly with insulin sensitivity in humans and have anti-diabetic and anti-inflammatory effects. We are investigating the receptors/signaling pathways by which these lipids enhance insulin secretion and insulin action, and determining the biosynthetic and degradative enzymes that regulate these lipids. A major goal is to discover new approaches to prevent and treat diabetes.

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Primary Section

Section 42: Medical Physiology and Metabolism

Secondary Section

Section 23: Physiology and Pharmacology