In the study of congenital hyperinsulinism now enrolling phase III sunRIZE trial

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Adrian Vella, MD

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Dr. Vella is a Professor of Medicine in the Endocrinology Division at the Mayo Clinic College of Medicine. He is a leading expert in hypoglycemic disorders and was involved as an investigator in the early clinical trials of RZ358. Dr. Vella has published over 160 peer-reviewed articles related to endocrinology, metabolic disorders, and diabetes and currently serves as a member of the Clinical and Translational Science Awards Postdoctoral Programs Committee at the Mayo Clinic Graduate School of Biomedical Sciences and at the Mayo Clinic College of Medicine and Science. He was a Mayo Foundation Scholar and Visiting Research Fellow in the Diabetes & Inflammation Laboratory at the Cambridge Institute of Medical Research in Cambridge, UK. Dr. Vella completed his Endocrinology fellowship at the Clinician-Investigator Training Program at the Mayo School of Graduate Medical Education and his Internal Medicine residency at the Mayo Clinic in Rochester. He received his M.D. from the University of Malta.

Jerrold Olefsky, MD

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Dr. Olefsky is Distinguished Professor of Medicine at the University of California, San Diego (UCSD) Division of Endocrinology and Metabolism and the Associate Dean of Scientific Affairs for the UCSD School of Medicine.  He is also a member of the Institute of Medicine and the American Academy of Arts and Sciences. One of his seminal contributions to the field of Medicine has been the identification of the role of insulin resistance as a primary cause of Type II (non-insulin dependent, adult-onset) diabetes, polycystic ovarian syndrome, and other human diseases. His work has also helped develop insulin-sensitizing drugs that are now standard therapies for Type II diabetes. More recently, his lab has developed studies establishing the role of macrophage-mediated tissue inflammation as a key cause of obesity-related insulin resistance. He has conducted numerous studies to help define the basic genetic and cellular mechanisms underlying decreased insulin action in human pathophysiologic states.