ABOUT US
“My overarching research goal is to free people with insulin-dependent diabetes from daily insulin injections to control glucose”
Ernesto Bernal-Mizrachi, M.D.
Interim Scientific Director
Professor of Medicine
Chief of the Division of Endocrinology, Diabetes, and Metabolism
Diabetes Research Institute,
University of Miami, Miller School of Medicine
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DRI Affinity Group: Beta cell robustness and augmentation
Dr. Ernesto Bernal-Mizrachi is a nationally recognized physician-scientist and academic leader in endocrinology whose work has advanced understanding of β-cell biology, insulin signaling, and the mechanisms that drive type 1 and type 2 diabetes progression. His program spans basic discovery through translational studies and has been supported by competitive peer-reviewed funding. Beyond his own scholarship, he has built collaborative, multidisciplinary teams and clinical research infrastructure that accelerate innovation and trial readiness. A committed mentor and educator, he has trained multiple fellows and junior faculty who have gone on to independent careers, and he is an active reviewer for leading journals and grant panels. He also contributes to institutional strategy recruitment, program development, and curriculum helping to grow vibrant academic communities around diabetes and metabolism. Together, these accomplishments underscore his stature and impact in the field.
In addition to his role as a prominent academic figure, Dr Ernesto Bernal-Mizrachi holds the position of Vice Chair of Research in the Department of Medicine, Deputy Director for Signal Transduction at the Diabetes Research Institute, and research director of the Geriatric Research, Education, and Clinical Center at the Miami Veterans Administration Hospital.
He joined the University of Miami in 2015, bringing a wealth of experience from his previous appointment as the Larry D Soderquist Professor at the University of Michigan. Dr Bernal-Mizrachi initiated his research career as a junior faculty member at Washington University. Dr Bernal-Mizrachi has secured substantial grant funding, including multiple R01 grants from the National Institutes of Health, a VA MERIT award, and support from the Juvenile Diabetes Research Foundation. His contributions to the field have earned him accolades, including Junior Faculty and Career Development Awards and Mentor Advisory Group from the American Diabetes Association and the 2023 Department of Medicine Andrew Schally Research Award. Dr. Bernal-Mizrachi’s has actively participated in scientific study sections at esteemed funding agencies such as the NIH, Veterans Administration study section, Juvenile Diabetes Research Foundation, and American Diabetes Association. His standing in the medical community is further underscored by his election to the American Society for Clinical Investigation (ASCI).
Research Focus: As a distinguished physician-scientist, his research centers on unraveling the intricacies of the pancreatic beta cell (insulin-producing cell) particularly in the context of T1D. These contributions extend beyond basic science. Dr Bernal-Mizrachi has reshaped our understanding of beta and alpha-cell biology with significant translational implications for diabetes prevention and treatment. It is longstanding dogma in the diabetes field that pancreatic beta cells cannot regenerate or replicate. Work from the Bernal-Mizrachi lab has clearly demonstrated that this is not the case: pancreatic beta cells absolutely can and do replicate, and this is the major means of maintaining adult beta cell mass. This research has major implications in the designing therapies for type 1 and 2 diabetes. Through over 100 peer-reviewed publications, active involvement in the scientific community, and mentoring, Dr. Bernal-Mizrachi’s team translates basic discoveries into therapeutic strategies for T1D and T2D.
Recent DRIF-funded projects
Role of immunometabolism in the protection of T1D by mTOR/4E-BP2 signaling (2025): This project focuses on exploring the role of immunometabolism as a mechanism for the immunomodulatory effect induced by 4E-BP2 deletion. The proposed studies will fill an important knowledge gap by providing insights into the role of 4E-BP2/eIF4E activation as a pharmacological target for T1D treatment. Such results will have a positive impact because this target will serve as a platform for designing novel therapeutic strategies to expand drug development for T1D.

