William W. Hay

Chief Medical Officer at Astarte Medical

Dr. William W. Hay, Jr. served as Professor of Pediatrics (Neonatology) at the University of Colorado Denver (retired). He was Head of the Section of Neonatology from 1982-1992 and Director of the ACGME/RRC accredited Training Program in Neonatal-Perinatal Medicine from 1982 until 2003. He also served as Director of the Child Maternal Health Program, now the Early Life Exposures Program and was Director for 36 years of the Neonatal-Perinatal Clinical Translational Research Center, for the NIH-NCATS-Colorado Clinical and Translational Sciences Institute. Dr. Hay’s principal administrative role was Scientific Director of the UCDenver–Department of Pediatrics/Section of Neonatology Perinatal Research Center. He is principal investigator and program director for an NIH-NICHD T32 Training Grant in Perinatal Biology and Medicine. Dr. Hay is widely published, with his research and scholarship appearing in more than 400 articles and books.

Dr. Hay graduated from Dartmouth College with a BA degree (cum laude) in biology and was a Senior Fellow conducting independent study in philosophy for his senior year. He graduated from Yale University School of Medicine in 1971. From 1971-1974, he completed an internship and residency in pediatrics at the University of Colorado School of Medicine and then served as Chief of Pediatrics at the U.S. Air Force Regional Hospital, Minot, North Dakota. He returned to the University of Colorado School of Medicine in 1976 for a research fellowship in Perinatal Biology and Medicine and as an Instructor in Neonatology. He became a full time member of the faculty of the University of Colorado School of Medicine in 1978 as an Assistant Professor. He rose to Associate Professor in 1983, to Professor in 1988, and received tenure in 1989.

Dr. Hay has conducted and directed basic, translational, and clinical research in perinatal medicine and biology for more than 40 years. His research, supported by NIH and occasionally other funding sources (e.g., the Bill & Melinda Gates Foundation) has been focused on the mechanisms by which maternal nutrition and diseases (such as diabetes) that produce different plasma nutrient substrate and hormone concentrations regulate placental uptake, metabolism, and transfer to the fetus of essential nutrients (principally glucose and amino acids), and in turn, how these processes are interrelated to nutrition, metabolism of nutrient substrates, hormone balance, and growth rate in the fetus. A major focus over the years has been on placental and fetal intrauterine growth restriction and both acute and chronic fetal hypoglycemia and hypoxemia and how these conditions in the placenta and fetus adversely affect fetal insulin production, variable insulin action, hepatic glucose production, skeletal muscle metabolism and growth, and other aspects of fetal metabolism and growth. This research is fundamental for learning how they might provide selective nutrition to the pregnant mother and nutrients, hormones, growth factors, and oxygenation to the fetus in order to better nourish the fetus and prevent or correct acute and long-term adverse consequences of abnormal fetal nutrition, growth, and development. Dr. Hay’s original studies of fetal glucose and oxygen metabolism focused on placental glucose transport and fetal glucose utilization. He has done pioneering work in developing methods using tracers (glucose and lactate) to measure rates of fetal glucose utilization and oxidation. More recent studies have focused on fetal insulin production and action (with Paul Rozance MD) and how both hypoglycemia and hypoxia induce fetal hepatic insulin resistance (with Stephanie Wesolowski PhD), in contrast to peripheral insulin sensitivity, that promotes glucose production that serves to sustain fetal energy metabolism in the presence of reduced glucose supply. Other studies are focused on how amino acid supply regulates fetal myocyte development and growth of skeletal muscle (with Laura Brown MD).

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  • Chief Medical Officer

    Current role