Thesis (Ph.D.) - Indiana University, Biology, 2015To ensure survival and reproductive success, animals must optimally allocate energy among various physiological and behavioral processes while inhabiting environments that change predictably across and unpredictably within seasons. In this dissertation, I examined the mechanisms by which a seasonally-breeding rodent allocates energy between the reproductive and immune systems within the breeding season and modulates intensity of its sickness responses to a simulated infection across seasons. Siberian hamsters (Phodopus sungorus) inhibit reproduction and display lower body masses, lower levels of the adipose hormone leptin, and less intense sickness responses when housed in short, winter-like days compared to long, summer-like days. I used several techniques to modulate the internal energetic state of the hamsters (i.e., food restriction, manipulation of the energetic hormones leptin and insulin, pharmacological induction of glucose deprivation) to determine its role in reproductive-immune trade-offs and seasonal regulation of sickness intensity. In the first chapter, I examined energetic mechanisms involved in regulating reproductive-immune trade-offs in reproductively-active female hamsters. I found that glucose deprivation resulted in reproductive suppression, however, suppression could be alleviated when animals were provided with a hormonal signal of increased fat stores (i.e., leptin). Alternatively, reproduction was not inhibited when animals experienced more severe glucose deprivation; yet, providing animals with the signal of increased fat stores during this period of severe glucose deprivation resulted in decreased allocation to humoral immunity. In the last three chapters, I examined the contributions of seasonal changes in energetic fuels and signals to seasonal variation in sickness intensity. I found that seasonal variation in sickness-induced hypothermia was regulated by seasonal changes in glucose availability and leptin levels; however, seasonal changes in sickness-induced anorexia and body mass loss were regulated by seasonal differences in body mass more generally. Finally, I observed that changes in insulin, a pancreatic hormone secreted in response to positive energy balance, had both suppressive and enhancing effects on sickness intensity depending on energetic context. These collective findings illustrate that physiological trade-offs and sickness intensity are sensitive to a variety of energetic modulators and that the effects of these modulators are dependent on their interactions with each other and the environment.