Date Thesis Awarded


Access Type

Honors Thesis -- Access Restricted On-Campus Only

Degree Name

Bachelors of Science (BS)




Paul D. Heideman

Committee Members

John D. Griffin

Beverly Sher


A thorough understanding of genetic variation within a population as well as gene-environment interaction is essential in the clinical prediction and manipulation of physiological phenotypes. In a human population, many incidences of infertility are of a genetic origin, and up to 25% have no apparent cause (Roupa et al, 2009). Environmental cues interact with genetics to modulate reproductive status; a lack of sufficient nutrient intake can result in infertility in a genetically normal mouse or human (Mitan, 2004). In addition, increasing evidence indicates that genetic variability in the concentration of specific neurotransmitters and circulating hormones can confer varying degrees of vulnerability or resistance to the onset of obesity by regulating appetite and metabolism (Palmiter, 2009; Beck, 2000). The development of an animal model is essential for the examination of genetic variability, phenotypic plasticity and gene-environment interactions. However, many models, including lab mice and rats, are completely unlike human populations in genetic structure, providing little insight into genetic variability in appetite and fertility in humans (Smale et al, 2005). A wild-derived animal model, therefore, shows the most promise in elucidating the interaction between environmental and genetic contributions to infertility and obesity.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.


Thesis is part of Honors ETD pilot project, 2008-2013. Migrated from Dspace in 2016.

On-Campus Access Only