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  4th Annual Stefan S. Fajans Lecture in Diabetes

c ronald kahn md

C. Ronald Kahn, M.D.

stefan s. fajans, m.d.
Stefan S. Fajans, M.D.


Friday, April 12, 2013
3:00–4:00 p.m.
(reception following)

Oliphant-Marshall Auditorium
Kellogg Eye Center
Brehm Tower, ground floor
1000 Wall Street, Ann Arbor 48105

Map and directions


“Gene-Environment Interaction in the Pathogenesis of Type 2 Diabetes: Potential Role of the Gut Microbiome"

C. Ronald Kahn, M.D.

Mary K. Iacocca Professor, Harvard Medical School
Chief Academic Officer, Joslin Diabetes Center

This annual lecture in honor of Dr. Stefan S. Fajans, sponsored by the University of Michigan Division of Metabolism, Endocrinology & Diabetes, recognizes a renowned diabetes investigator and/or physician who has made significant contributions to the field. The 2013 Stefan S. Fajans Lecture in Diabetes will be given by C. Ronald Kahn, M.D., Mary K. Iacocca Professor at the Harvard Medical School, Chief Academic Officer of the Joslin Diabetes Center, and co-head of the Joslin Section on Integrative Physiology and Metabolism.

Dr. Kahn is an internationally recognized researcher. Educated at University of Louisville, he trained at Washington University and served as the Section Head of Cellular and Molecular Physiology of the Diabetes Branch of NIH. In 1981, he became Research Director of Joslin, and in 1984, Professor of Medicine at Harvard. In 1986 he was awarded the Iacocca Professorship. From 2000 to 2007, Dr. Kahn served as Joslin's President and Director.

Dr. Kahn has received the highest scientific awards of the American Diabetes Association, U.S. Endocrine Society, the British Diabetes and Endocrine Societies, Juvenile Diabetes Research Foundation, International Diabetes Federation, and American Federation for Clinical Research, as well as many other honors, including election to the National Academy of Sciences and the Institute of Medicine. He chaired the congressionally established Diabetes Research Working Group and holds honorary doctorates from the Universities of Paris, Louisville, and Geneva, as well as an honorary professorship from Peking University.

Over three decades, C. Ronald Kahn, M.D., and colleagues have literally defined the field of insulin signal transduction and mechanisms of altered signaling in disease. His laboratory discovered the insulin receptor tyrosine kinase, identified its first two major substrates and showed how these were linked in other intracellular molecules, especially phosphatidylinositol (PI) 3-kinase, to create a complex signaling network through which insulin exerts multiple effects on metabolism and growth. His laboratory demonstrated how this network is altered in insulin-resistant states, such as type 2 diabetes and obesity, and the impact of genetics and environment on these signaling functions.

In an elegant series of studies using genetically engineered mice, Kahn’s laboratory defined the role of the insulin receptor and various downstream molecules in insulin action and insulin resistance. This work includes creation and characterization of single-gene knockouts, compound knockouts (which mimic the polygenic nature of diabetes), multiple tissue-specific knockouts and the use of RNA interference in both cells and intact animals. These studies demonstrate the specific roles of each tissue in control of glucose and lipid metabolism and illustrate how the various signal molecules act to produce a complex integrated network where different substrates and molecules serve unique, complementary roles. Kahn’s laboratory showed that insulin receptors in tissues such as the brain, beta cells and endothelial cells also play important roles in normal and disease states, including obesity, hyperlipidemia, gallstone formation and Alzheimer’s disease.

Additionally, Dr. Kahn’s laboratory defined the roles of insulin and IGF-1 signaling on adipocyte development and function. Using both gene expression and fat transplantation, Kahn’s lab identified differences between white fat in different areas of the body, which may account for why people with abdominal obesity are more prone to developing diabetes than people with peripheral obesity. The fundamental genes controlling developmental patterning may play a role in determining the amount and function of fat in different depots.

Dr. Kahn leads a large consortium of investigators at multiple institutions using gene and protein expression studies to define obesity, diabetes and other insulin-resistant states (the Diabetes Genome Anatomy Project). These studies have defined the role of genes and the environment in the development of type 2 diabetes. Several new pathways in the pathogenesis of type 2 diabetes have been elucidated, including the role of the genes of mitochondrial oxidative phosphorylation, the role of developmental genes in fat distribution and obesity, and the role of the altered gene expression in pancreatic beta cells in islet function. This research also provides insight about new targets for the treatment or prevention of this disease. 

Questions: Annette Murphy, (734) 763-3056 or

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Stefan S. Fajans, M.D., Active Professor Emeritus of the Department of Internal Medicine, Division of Metabolism, Endocrinology & Diabetes, became a member of the University of Michigan Medical School faculty in 1949.  He served as Chief of the Division of Endocrinology & Metabolism from 1973 to 1987 and as the Director of the University of Michigan Diabetes Research and Training Center from 1977 to 1986.  Dr. Fajans devoted a large portion of his scientific career to the study of diabetes and made important contributions to the understanding of its etiology, diagnosis, and treatment.  For more on his work and career, please see this bio of Dr. Stefan S. Fajans [PDF].