Dr. Steven Kahn received his medical degree in 1978 from the University of Cape Town, South Africa. He came to the University of Washington in 1986 to undertake his training in endocrinology and metabolism and subsequently was appointed to the faculty where he has pursued both basic and clinical studies of the pathophysiology, prevention and treatment of type 2 diabetes.

Dr. Kahn was appointed to the faculty in 1988 and is now a Professor in the Department of Medicine and an Adjunct Professor in Pathology. He is also a Staff Physician at VA Puget Sound Health Care System. He plays a number of leadership roles at the University of Washington, including directing the NIDDK-funded Diabetes Research Center and NIDDK-funded Diabetes, Obesity and Metabolism Training Program.

Since he was appointed to the faculty, Dr. Kahn has had a very active and successful research program that has been continuously funded by investigator-initiated awards from NIH, the Department of Veterans Affairs and the American Diabetes Association. Aside from his successful research career, he has a stellar track record in training postdoctoral fellows and medical students. Most of his postdoctoral trainees hold faculty and leadership positions at institutions around the world, including the University of Washington.

Dr. Kahn chairs a seven center NIH study that is examining the pathophysiology of type 2 diabetes in youth and adults. He is currently an associate editor of two major diabetes journals, Diabetes Care and Diabetologia, and previously served as deputy editor of The Journal of Clinical Endocrinology and Metabolism. He has served on numerous grant review panels and on advisory panels for a number of research centers and research initiatives focused on diabetes.

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).

Dr. Kahn has received numerous awards for his research, some of which include The Endocrine Society Clinical Investigator Award, Department of Veterans Affairs John B. Barnwell Award, European Association for the Study of Diabetes Albert Renold Award, and American Diabetes Association Outstanding Achievement in Clinical Diabetes Research Award.

The loss of islet β-cell function and mass is the critical component responsible for the development of hyperglycemia in individuals with type 2 diabetes and those at high risk of developing the disease. Advancing our understanding of the mechanisms responsible for these defects is critical for the development of new approaches to prevent and treat type 2 diabetes in order to reduce the excess morbidity and premature mortality associated with the disease.

Funding
Our work is, or has been, funded by the Department of Veterans Affairs, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institute of Aging (NIA), American Diabetes Association, Juvenile Diabetes Research Foundation, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, Novartis and Pfizer.