Scott Soleimanpour, M.D. is an Associate Professor of Internal Medicine and Molecular and Integrative Physiology, Director of the Michigan Diabetes Research Center (as of 12/1/2023) and Director for T1D Basic Research and Islet Biology Programs in the University of Michigan Caswell Diabetes Institute. He was formerly Director of the Islet Core of the Michigan Diabetes Research Center, Director of the Michigan Diabetes Transition Program, Director of Pilot and Feasibility Programs for the MDRC, and Co-director of the JDRF Center of Excellence at the University of Michigan. Diagnosed with type 1 diabetes (T1D) in 1986, Dr. Soleimanpour is deeply invested in basic research focused on the genetic causes of T1D. Dr. Soleimanpour attended Kent State University and the Northeast Ohio Medical University as part of a combined B.S./M.D. program. During his pre-doctoral and post-doctoral research training, Dr. Soleimanpour completed diabetes research fellowships in the Vanderbilt University/NIDDK medical scholars program, the Howard Hughes Medical Institute-National Institutes of Health (HHMI-NIH) Research Scholars program, and in the William Osler Society of Fellows at the University of Pennsylvania. Among Dr. Soleimanpour’s key research contributions include studies focused on islet cell transplantation, mitochondrial quality control, and include recent seminal studies focused on control of pancreatic beta cell and immune cell function by mitophagy. His clinical research efforts are focused on improvement of clinical care outcomes for diabetes patients in the transition from pediatric to adult endocrine care. He has received awards and honors from the Juvenile Diabetes Research Foundation, American Diabetes Association, the American Society of Clinical Investigation, the Central Society for Clinical and Translational Research, the Alpha Omega Alpha National Medical Honors Society, and The Endocrine Society. The Soleimanpour Lab has pioneered the study of mitochondrial quality control in diabetes pathophysiology, and his lab continues to focus on how defects in the diabetes gene Clec16a lead to beta cell dysfunction and affects mitochondrial health.

1. Understanding the role of the mitochondrial quality control in the development, function, and post-natal maintenance of beta cells
2. Investigating the primary role of pancreatic beta cells in the pathogenesis of T1D
3. Clarifying mitochondrial-ER crosstalk mechanisms in the pathogenesis of beta cell failure
4. Elucidating the role of the diabetes gene Clec16a in the regulation of mitochondrial quality control