Skip to main content

Scott Soleimanpour MD

Scott Soleimanpour, M.D. is an Assistant Professor of Internal Medicine, Investigator in the Brehm Diabetes Research Center, and Director of the Diabetes Transition Program at the University of Michigan Medical School. Diagnosed with type 1 diabetes (T1D) in 1986, Dr. Soleimanpour is deeply invested in basic research focused on the genetic causes of T1D while also directing a thriving clinical program that empowers diabetic young adults during their transition to self-care. 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, beta cell failure after islet cell transplantation, and include recent seminal studies in understanding the genetic causes of pancreatic beta cell failure in T1D. 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. He has also been featured on the NBC Nightly News, the Philadelphia Inquirer, Medicine at Michigan, Reader’s Digest, and the PBS medical series Second Opinion. The Soleimanpour Lab has pioneered the study of mitochondrial health and quality control in pancreatic beta cells and T1D pathophysiology, and he continues to focus on how defects in T1D genes lead patients to develop diabetes.


The Soleimanpour Lab focuses on the molecular and genetic regulation of the mitochondrial life cycle, with a focus on mitophagy, a pathway to dispose of unhealthy or damaged mitochondria. Our studies also concentrate on novel genetic targets affecting the mitophagy pathway, which are also associated with diabetes in humans, through studies in cellular and mouse genetic model systems, as well as isolated human islets. Our goal is to discover how the dysregulation of mitochondrial respiration and mitophagy leads to diabetes pathogenesis, along with determining strategies to improve mitophagy to prevent or treat diabetes.