C. Ronald Kahn, M.D., Chief Academic Officer at Joslin Diabetes Center, Honored by Washington University in St. Louis
BOSTON – May 9, 2012 – Washington University in St. Louis will bestow a Doctor of Science (Honoris Causa) on C. Ronald Kahn, MD, of Newton, MA, Chief Academic Officer at Joslin Diabetes Center. He will receive this high honor at the 151st Commencement ceremony on May 18, 2012, along with six other recipients.
Dr. Kahn is being recognized for his 30 years of diabetes and obesity research, in particular his significant work in insulin signal transduction and the mechanisms of altered insulin signaling in disease, as well as his leadership of the diabetes effort worldwide.
In addition to his role as Chief Academic Officer at Joslin Diabetes Center, Dr. Kahn is co-head of Joslin’s Integrative Physiology and Metabolism section and the Mary K. Iacocca Professor of Medicine at Harvard, where he has been a member of the faculty since 1981.
From 2000-07, Dr. Kahn was president of Joslin Diabetes Center, after serving as its director of research for two decades. Under his leadership, Joslin’s research grew more than 20-fold, clinical and educational activity tripled. He was named the center’s first chief academic officer in January 2012. In his new role, Kahn oversees faculty recruitment, appointments and promotions at the center, which trains about 150 doctors and doctoral fellows a year.
Dr. Kahn is a renowned investigator of insulin signal transduction and the mechanisms of altered signaling in disease. His laboratory discovered the insulin receptor kinase, its two primary substrates and the molecular components of the insulin-signaling network.
In addition, he was the first to define alterations in the signaling network in type 2 diabetes, including the important role of insulin action in the brain, both in physiologic regulation and control of brain cholesterol metabolism.
His lab has made significant contributions to the understanding of obesity by showing that fat cells, called adipocytes, have different developmental origins and cellular functions that lead to risk of metabolic disease.