Elinor Sullivan


Assistant Professor, Department of Human Physiology
Member, ION

Ph.D. Oregon Health and Science University

Lab Website


Research Interests: 


Elinor Sullivan’s teaching focus is in the areas of nutrition, endocrinology, and neurobiology.

Dr. Sullivan’s research focuses on examining the influence of maternal metabolic state and dietary environment on offspring behavioral regulation, with an emphasis on behaviors that relate to mental health and behavioral disorders including autism spectrum disorders, attention deficit hyperactivity disorder, anxiety, and depression.

Her areas of expertise include behavioral neuroscience, with training and expertise in human and nonhuman primate behavior, brain development, developmental programming, maternal nutrition, and neurodevelopmental disorders.

Dr. Sullivan received her Ph.D. in Physiology from Oregon Health and Science University. She received her postdoctoral training at the University of California San Francisco and Oregon Health and Science University. Prior to coming to the University of Oregon, Dr. Sullivan was an Assistant Professor in the Biology Department at the University of Portland. Dr. Sullivan is currently an Assistant Professor in the Divisions of Neuroscience and Cardiometabolic health at the Oregon National Primate Research Center. She joined the UO Department of Human Physiology in 2017.

Dr. Sullivan has received research grants from the National Institute of Health, the Bill and Melinda Gates Foundation, the Murdock Charitable Trust, and the Obesity Society.


Trends Neurosci. 2021 Mar 1:S0166-2236(21)00021-7. doi: 10.1016/j.tins.2021.01.008. Online ahead of print.


Early adversity influences brain development and emerging behavioral phenotypes relevant for psychiatric disorders. Understanding the effects of adversity before and after conception on brain development has implications for contextualizing current public health crises and pervasive health inequities. The use of functional magnetic resonance imaging (fMRI) to study the brain at rest has shifted understanding of brain functioning and organization in the earliest periods of life. Here we review applications of this technique to examine effects of early life stress (ELS) on neurodevelopment in infancy, and highlight targets for future research. Building on the foundation of existing work in this area will require tackling significant challenges, including greater inclusion of often marginalized segments of society, and conducting larger, properly powered studies.

PMID:33663814 | DOI:10.1016/j.tins.2021.01.008

Related Articles

Maternal Obesity and Western-Style Diet Impair Fetal and Juvenile Offspring Skeletal Muscle Insulin-Stimulated Glucose Transport in Nonhuman Primates.

Diabetes. 2020 07;69(7):1389-1400

Authors: Campodonico-Burnett W, Hetrick B, Wesolowski SR, Schenk S, Takahashi DL, Dean TA, Sullivan EL, Kievit P, Gannon M, Aagaard K, Friedman JE, McCurdy CE

Infants born to mothers with obesity have a greater risk for childhood obesity and metabolic diseases; however, the underlying biological mechanisms remain poorly understood. We used a Japanese macaque model to investigate whether maternal obesity combined with a Western-style diet (WSD) impairs offspring muscle insulin action. Adult females were fed a control or WSD prior to and during pregnancy through lactation, and offspring subsequently weaned to a control or WSD. Muscle glucose uptake and signaling were measured ex vivo in fetal (n = 5-8/group) and juvenile (n = 8/group) offspring. In vivo signaling was evaluated after an insulin bolus just prior to weaning (n = 4-5/group). Maternal WSD reduced insulin-stimulated glucose uptake and impaired insulin signaling at the level of Akt phosphorylation in fetal muscle. In juvenile offspring, insulin-stimulated glucose uptake was similarly reduced by both maternal and postweaning WSD and corresponded to modest reductions in insulin-stimulated Akt phosphorylation relative to controls. We conclude that maternal WSD leads to a persistent decrease in offspring muscle insulin-stimulated glucose uptake even in the absence of increased offspring adiposity or markers of systemic insulin resistance. Switching offspring to a healthy diet did not reverse the effects of maternal WSD on muscle insulin action, suggesting earlier interventions may be warranted.

PMID: 32354857 [PubMed - in process]