Elinor Sullivan

 

Assistant Professor, Department of Human Physiology
Member, ION

Ph.D. Oregon Health and Science University
 

elinors@uoregon.edu
Lab Website
Office: 
Phone: 485-215-0227

 

Research Interests: 

Overview: 

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.

RECENT PUBLICATIONS

Related Articles

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

Diabetes. 2020 Apr 30;:

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

Abstract
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 offspring (n=8/group). 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 post-weaning 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 - as supplied by publisher]

Related Articles

Accelerating the Evolution of Nonhuman Primate Neuroimaging.

Neuron. 2020 02 19;105(4):600-603

Authors: PRIMatE Data Exchange (PRIME-DE) Global Collaboration Workshop and Consortium. Electronic address: michael.milham@childmind.org, PRIMatE Data Exchange (PRIME-DE) Global Collaboration Workshop and Consortium

Abstract
Nonhuman primate neuroimaging is on the cusp of a transformation, much in the same way its human counterpart was in 2010, when the Human Connectome Project was launched to accelerate progress. Inspired by an open data-sharing initiative, the global community recently met and, in this article, breaks through obstacles to define its ambitions.

PMID: 32078795 [PubMed - indexed for MEDLINE]

Effects of Pre and Postnatal Protein Restriction on Maternal and Offspring Metabolism in the Nonhuman Primate.

Am J Physiol Regul Integr Comp Physiol. 2020 Mar 04;:

Authors: Kirigiti MA, Frazee T, Bennett BJ, Arik A, Blundell P, Bader LA, Bagley JL, Frias AE, Sullivan EL, Roberts CT, Kievit P

Abstract
Women in low and middle-income countries (LMICs) frequently consume a protein-deficient diet during pregnancy and breastfeeding. The effects of gestational malnutrition on fetal and early postnatal development can have lasting adverse effects on offspring metabolism. Expanding on previous studies in rodent models, we utilized a nonhuman primate model of gestational and early-life protein restriction in order to evaluate effects on the organ development and glucose metabolism of juvenile offspring. Offspring were born to dams who had either consumed a control diet containing 26% protein or a protein-restricted (PR) diet containing 13% protein. Offspring were maintained on a PR diet and were studied (body and serum measurements, iv glucose tolerance tests (GTTs), DEXA scans) up to 7 months of age, at which time tissues were collected for analysis. PR offspring had age-appropriate body weight and were euglycemic, but exhibited elevated fasting insulin and reduced initial but increased total insulin secretion during an ivGTT at 6 months of age. No changes were detected in pancreatic islets of PR juveniles; however, PR did induce changes in other peripheral organs, including reduced kidney size and changes in liver, adipose tissue, and muscle gene expression. Serum osteocalcin was elevated and bone mineral content and density were reduced in PR juveniles, indicating a significant impact of PR on early postnatal bone development.

PMID: 32130027 [PubMed - as supplied by publisher]

Related Articles

Neuroinflammation as a risk factor for attention deficit hyperactivity disorder.

Pharmacol Biochem Behav. 2019 07;182:22-34

Authors: Dunn GA, Nigg JT, Sullivan EL

Abstract
Attention Deficit Hyperactivity Disorder (ADHD) is a persistent, and impairing pediatric-onset neurodevelopmental condition. Its high prevalence, and recurrent controversy over its widespread identification and treatment, drive strong interest in its etiology and mechanisms. Emerging evidence for a role for neuroinflammation in ADHD pathophysiology is of great interest. This evidence includes 1) the above-chance comorbidity of ADHD with inflammatory and autoimmune disorders, 2) initial studies indicating an association with ADHD and increased serum cytokines, 3) preliminary evidence from genetic studies demonstrating associations between polymorphisms in genes associated with inflammatory pathways and ADHD, 4) emerging evidence that early life exposure to environmental factors may increase risk for ADHD via an inflammatory mechanism, and 5) mechanistic evidence from animal models of maternal immune activation documenting behavioral and neural outcomes consistent with ADHD. Prenatal exposure to inflammation is associated with changes in offspring brain development including reductions in cortical gray matter volume and the volume of certain cortical areas -parallel to observations associated with ADHD. Alterations in neurotransmitter systems, including the dopaminergic, serotonergic and glutamatergic systems, are observed in ADHD populations. Animal models provide strong evidence that development and function of these neurotransmitters systems are sensitive to exposure to in utero inflammation. In summary, accumulating evidence from human studies and animal models, while still incomplete, support a potential role for neuroinflammation in the pathophysiology of ADHD. Confirmation of this association and the underlying mechanisms have become valuable targets for research. If confirmed, such a picture may be important in opening new intervention routes.

PMID: 31103523 [PubMed - indexed for MEDLINE]