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

Evaluation of Maternal Inflammation as a Marker of Future Offspring ADHD Symptoms: A Prospective Investigation.

Brain Behav Immun. 2020 Jul 21;:

Authors: Gustafsson HC, Sullivan EL, A J Battison E, Holton KF, Graham AM, Karalunas SL, Fair DA, Loftis JM, Nigg JT

Abstract
Early life predictors of attention-deficit/hyperactivity disorder (ADHD) are critically needed; they could inform etiological theory and may help identify new prevention targets. The current study examined prospectively whether maternal cytokine levels during pregnancy predict offspring ADHD symptoms at age 4-6 years. Secondarily, we evaluated maternal cytokine levels as a possible common pathway through which prenatal risks exert influence on child ADHD. Data came from a sample of women recruited during the 2nd trimester of pregnancy (N=62) and followed postnatally until children were 4-6 years old. Maternal inflammation was assessed using 3rd trimester plasma concentrations of three indicators of nuclear factor kappa B signaling: interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 which were combined into a latent variable. Mothers and teachers reported on child ADHD symptoms, negative affect, and externalizing behaviors at 48-72 months of age. Maternal inflammation in the 3rd trimester predicted ADHD symptoms when children were 4-6 years old (β=0.53, 95% CI=0.154, 0.905, p=0.006). Further, maternal inflammation mediated the effect of prenatal distress on child ADHD (β=0.21, 95% CI=0.007, 0.419, p=0.04). The inflammation effect on ADHD was not explained by concurrent child negative affect, externalizing behavior, or familial ADHD status. This is the first human study to prospectively link maternal pregnancy cytokine levels and offspring ADHD symptoms, suggesting that cytokine levels are a possible marker of ADHD risk. Results also provides new evidence that maternal prenatal inflammation may be one common pathway by which prenatal risk factors influence offspring mental health outcomes.

PMID: 32707260 [PubMed - as supplied by publisher]

Related Articles

Effects of pre- and postnatal protein restriction on maternal and offspring metabolism in the nonhuman primate.

Am J Physiol Regul Integr Comp Physiol. 2020 05 01;318(5):R929-R939

Authors: Kirigiti MA, Frazee T, Bennett B, Arik A, Blundell P, Bader L, Bagley J, Frias AE, Sullivan EL, Roberts CT, Kievit P

Abstract
Women in low- and middle-income countries 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 (PR) to evaluate effects on the organ development and glucose metabolism of juvenile offspring. Offspring were born to dams that had consumed a control diet containing 26% protein or a PR diet containing 13% protein. Offspring were maintained on the PR diet and studied [body and serum measurements, intravenous glucose tolerance tests (ivGTTs), and dual-energy X-ray absorptiometry scans] up to 7 mo 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 mo of age. No changes were detected in pancreatic islets of PR juveniles; however, PR did induce changes, including reduced kidney size, and changes in liver, adipose tissue, and muscle gene expression in other peripheral organs. 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 - indexed for MEDLINE]

Neuroinflammation in psychiatric disorders: An introductory primer.

Pharmacol Biochem Behav. 2020 Jul 01;:172981

Authors: Dunn GA, Loftis JM, Sullivan EL

PMID: 32621927 [PubMed - as supplied by publisher]

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]