Elizabeth Parks, PhD

Parks, Elizabeth 2016_120Dr. Parks received her PhD from the University of California, Davis for where she worked with Barbara Schneeman, PhD in the Department of Nutrition. She then became a Postdoctoral Fellow at Berkeley/UCSF in the laboratory of Marc Hellerstein, MD, PhD. Dr. Parks has held academic positions at the University of Minnesota and the University of Texas Southwestern Medical Center in Dallas, where she collaborated to establish a highly successful research consortium for the study of obesity. In 2013 she moved to the University of Missouri at Columbia, where she is a Professor in the Department of Nutrition and Exercise Physiology and in the Division of Gastroenterology and Hepatology, both in the School of Medicine. She also serves as Associate Director of the Clinical Research Center in the Medical School's Institute for Clinical and Translational Science.

The major research contributions of Dr. Parks’ lab emanate from her development of novel techniques to quantitate the delivery and disposal of lipids in animal models and in humans. Over the past 16 years, her lab has developed methods using multiple stable isotopes and mathematical modeling to establish a non-steady state model of post-meal metabolism. Using this model she has shown that, in contrast to rodents, a significant amount of meal fat can cycle through the liver in healthy humans and that dietary sugars being made into liver fat, are a significant cause of non-alcoholic fatty liver disease (NAFLD). The model also includes quantitation of fatty acid flux through the intestine (fat absorption), from the intestine to other tissues, and also from adipose back out to other tissues. From a national service perspective, Dr. Parks holds leadership positions in the American Society for Nutrition and the Obesity Society. She is a fellow of the AHA and the Obesity Society and has been a standing member and ad hoc member of numerous NIH grant review committees. Her current research in humans focuses on how peripheral lipid metabolism can influence liver lipid deposition and injury.