The causes and consequences of elevated glucocorticoids in wild animals

Open Access
- Author:
- Ensminger, David
- Graduate Program:
- Wildlife and Fisheries Science
- Degree:
- Doctor of Philosophy
- Document Type:
- Dissertation
- Date of Defense:
- February 27, 2019
- Committee Members:
- Tracy Langkilde, Dissertation Advisor/Co-Advisor
David Andrew Miller, Committee Chair/Co-Chair
W. David Walter, Committee Member
Matthew R. Marshall, Committee Member
Tracy Langkilde, Outside Member - Keywords:
- corticosterone
maternal stress
maternal programming
glucocorticoid
wild animal
Sceloporus undulatus
Cervus canadensis - Abstract:
- Stressors on organisms such as habitat alteration, climate change, and introduction of invasive species are integrated into a physiological response through the hypothalamus-pituitary-adrenal (HPA) axis and subsequent release of glucocorticoids (GCs). Understanding the causes and consequences of these GC elevations is integral to predicting how organisms will respond to environmental perpetrations and the cross-generational impacts of these hormones. However, few studies have examined this in the wild. In Chapter 2, I examined the impact of human hunting on GCs in a population of wild elk, Cervus canadensis. I measured GC non-invasively using fecal metabolite analysis and found no evidence of a positive relationship between hunting pressure GC metabolite concentrations in elk but a strong impact of yearly variation on GC metabolite. To gain a holistic understanding of effects of elevated maternal GC concentration during gestation, I examined impacts on maternal energetics and behavior, egg hormone and nutrient allocation, and ultimately offspring phenotype in the eastern fence lizard, Sceloporus undulatus. In Chapter 3, I report that daily exogenous GC elevations increased maternal anti-predator behavior and post-laying glucose, altered egg yolk hormone and nutrient content, and altered offspring morphology and stress-relevant physiology and behavior. In Chapter 4, I examined the impact of maternal GCs on offspring telomere length; the evolutionarily conserved endcaps of chromosomes. Shorter telomeres are associated with many disease states, cellular senescence, and are a proxy for lifespan. Using a modified RT-qPCR assay protocol to assess absolute telomere length, I report maternal telomeres were strongly heritable to offspring but not altered by the maternal CORT treatment. Elevated maternal GCs decreased offspring telomere length of sons but not daughters. Collectively, the results of my dissertation highlight that: 1) anthropogenic activities, such as hunting pressure, can affect GC concentrations, 2) maternally derived GCs can have a myriad of cross-generational impacts, and 3) there are potential long-term implications of maternally derived CORT. These findings allow better insight into the nature and potential mechanisms driving phenotypic responses to elevated maternal GC concentration.