Ronald Cohen, MD

A skilled endocrinologist, Dr. Cohen specializes in the diagnosis and management of thyroid diseases with a particular focus on thyroid cancer. He also has a clinical interest in diabetes, obesity and metabolic disorders.

Dr. Cohen’s research explores the relationship between diabetes and adipocyte — a complex endocrine cell that regulates feeding behavior and insulin sensitivity. Through his research findings, Dr. Cohen is working to develop novel therapies for the treatment of obesity and type 2 diabetes.

Dr. Cohen has authored several book chapters on the medical management of thyroid diseases, and frequently is invited to present his work at local and national conferences. A dedicated educator and mentor, Dr. Cohen is the co-director of the University of Chicago’s Endocrinology Research Seminar Series. He was awarded the University of Chicago “Quantrell Award for Excellence” in undergraduate education.

Dr. Cohen also serves on the editorial boards of Journal of Biological Chemistry and Frontiers in Pituitary Endocrinology and is actively involved in the American Thyroid Association.

A deeper look into his research

Dr. Cohen’s lab studies the function of corepressors in the adipocyte. The adipocyte is a complex endocrine cell that regulates feeding behavior and insulin sensitivity, and aberrant function of the adipocyte in obesity leads to insulin resistance and potentially to Type 2 diabetes. However, the relationship between adiposity and diabetes is complex; thiazolidinedione (TZD) medications increase fat mass, yet improve insulin sensitivity. Although TZDs serve as agonists for the peroxisome proliferator-activated receptor γ (PPARγ), the exact role of PPARγ and its corepressors in the regulation of insulin action remains unclear.

The two main nuclear receptor corepressors are the nuclear receptor corepressor protein (NCoR) and the silencing mediator of retinoid and thyroid hormone receptors (SMRT). Dr. Cohen and his lab have shown that SMRT and NCoR repress PPARγ transcriptional activity in 3T3-L1 cells, an in vitro model system to study adipocyte differentiation and function. SMRT, in particular, is recruited to PPARγ via specific residues in its C-terminal interacting domain. His lab data suggests that SMRT and NCoR decrease the expression of key adipocyte-specific proteins during adipogenesis, and that endogenous levels of corepressors dictate the ability of cells to respond to TZDs.

Dr. Cohen and his team are using in vitro analysis of adipocyte cell lines and isolated murine adipocytes to evaluate corepressor effects on adipogenesis and adipocyte function. In addition, they are developing novel mouse models of corepressor deficiency to dissect the molecular mechanisms underlying the physiology of SMRT and NCoR action in the adipocyte and on insulin sensitivity in vivo. Understanding the roles of corepressors in adipocyte biology is crucial if we are to design novel approaches to the treatment of obesity and type 2 diabetes.

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