Animal Science, Department of


First Advisor

Dr. Jessica L. Petersen

Date of this Version


Document Type



A THESIS Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Master of Science, Major: Animal Science, Under the Supervision of Professor Jessica L. Petersen. Lincoln, Nebraska: July 2021

Copyright © 2021 Rachel R. Reith


Heat stress reduces livestock efficiency, induces inflammation, and alters adipose tissue metabolism through stress-induced epinephrine acting on beta-adrenoreceptors (β-AR). Supplementation of beta-adrenergic agonists (β-AA) improve livestock growth and carcass traits, also by acting on β-AR located in skeletal muscle and adipose tissue. The binding of β-AR in adipose tissue results in changes in adipose tissue metabolism including increased lipolysis and decreased fatty acid synthesis. Due to their similar effects on stress response pathways, the possible interaction of heat stress and β-AA could negatively impact animal well-being. The purpose of the first study was to understand how ractopamine (RAC), a beta-one adrenergic agonist, and heat stress alter the subcutaneous adipose tissue transcriptome in sheep, and to identify interaction between the two. Based on differential expression and pathway analysis, the interaction of RAC and heat stress was predicted to alter adipose tissue metabolism and inflammation, but physiological data did not show a negative impact due to interaction. The second study investigated possible interaction of zilpaterol hydrochloride (ZH), a beta-two adrenergic agonist, and heat stress in subcutaneous adipose tissue transcriptome in beef cattle. Transcriptomic evidence suggests that ZH did not exacerbate the negative effects of heat stress and instead moderated heat stress-induced inflammation and oxidative stress. The purpose of the third study was to understand the effects of chronic heat stress and ZH supplementation on fatty acid mobilization in ex vivo visceral adipose tissue with and without stimulation of the adipose tissue with epinephrine. All treatment groups responded to stimulation by epinephrine, with no interaction of heat stress and ZH being apparent. Heat stress decreased fatty acid concentration while ZH increased it. Overall, these findings indicate that while the interaction of heat stress and β-AA in ruminant adipose may impact gene expression, there was no evidence of a detriment to animal well-being based on the parameters measured; in fact, β-AA supplementation may moderate many negative effects of heat stress.

Advisor: Jessica L. Petersen