About Will Holland
Will Holland, PhD
Associate Professor
Department of Nutrition and Integrative Physiology
Born in Maui and raised in Colorado, Dr. Holland completed graduate work at the University of Colorado, Colorado State University, and the University of Utah. He was drawn to Utah by the collaborative, interdisciplinary research approaches used to study Diabetes, Obesity and related co-morbidities. Dr. Holland recently returned to Utah after a decade of research at the University of Texas Southwestern Medical Center in Dallas, where he ran an independent research laboratory in the Touchstone Diabetes Center. He brings to Utah a strong background in lipid signaling, insulin action and diabetic physiology. His past research has highlighted the role for a lipid metabolite, termed ceramide, in the progression of diabetes, beta cell dysfunction, vascular dysfunction, and cardiomyopathy. Ceramide builds up in response to excess dietary intake of saturated fat, inflammatory factors, and environmental toxins. Will Holland completed his dissertation work with Scott Summers at the University of Utah in 2007. Together, they produced seminal work establishing the role of ceramide as an inhibitor of insulin action. During his subsequent postdoctoral work with Philipp Scherer, he uncovered the roles of adiponectin and FGF21, as potent regulators of ceramide metabolism which can maintain survival and promote regeneration of insulin-producing beta cells. He is currently an Associate Professor in the Department of Nutrition and Integrative Physiology, focusing efforts on the roles of ceramide catabolic enzymes on glucose and lipid metabolism. Will has recently uncovered an exciting result, that blocking the action of glucagon (a glucose-raising hormone) stimulates the regeneration of new beta cell mass and prevents cell death in human islets.
His current research focuses on: 1) protecting fragile insulin producing beta cells and heart muscle cells from the lipid burden encountered in diabetic individuals; 2) evaluating mechanisms by which adiponectin and FGF21 promote beta cell survival and regeneration; 3) evaluating novel means of opposing glucagon’s hyperglycemic effects in diabetes; 4) uncovering novel molecular mediators governing ceramide homeostasis; and 5) understanding the complex biophysical and signaling components by which the sphingolipid ceramide impairs insulin action and promotes cell death.