Degree Type


Date of Award


Degree Name

Doctor of Philosophy


Animal Science


Animal Science

First Advisor

Lance H. Baumgard


Nutrient partitioning towards productive processes (i.e., milk synthesis, growth, and reproduction) concomitant with diluting maintenance costs are key to profitable animal agriculture. During immune activation, the hierarchy of coordinated nutrient trafficking is reprioritized towards the immune system at the expense of production. Dairy cows encounter frequent immune challenges, as bacterial insults can originate from a myriad of sources including the uterus, mammary gland, lungs, and gastrointestinal tract. Regardless of origin, immune activation hinders animal welfare and mounting evidence suggests it plays a role in many undesirable phenotypes post-calving (i.e., decreased DMI, increased NEFA, hypocalcemia). Following activation, most leukocytes undergo a metabolic shift from oxidative phosphorylation to aerobic glycolysis (a phenomenon known as the “Warburg effect”) and begin consuming copious amounts of glucose. To ensure adequate glucose delivery to activated leukocytes, several well-characterized metabolic adjustments are employed including: increased insulin and glucagon levels, increased skeletal muscle catabolism, hypertriglyceridemia, and hypoketonemia. The energetic burden of immune activation is intensified by a simultaneous decrease in feed intake and thus reduced intestinally derived nutrients. Identifying dietary strateiges with potential to alleviate the negative consequences of immune activation on metabolism and production are of interest. As part of this dissertation, supplementation of dietary zinc hydroxychlrode, zinc amino acid complex, and chromium propionate were evaluated in feed-restricted or LPS-infused cows. In addition to energetic metabolism, immune activation induces a marked and sustained decrease in circulating calcium (Ca). In this dissertation we have demonstrated that the total Ca deficit was ~20 g during an acute (12 hour) and intense model of immune activation. Infection-induced hypocalcemia is a species conserved response, yet, it remains largely unknown what role Ca plays during infection and why it abruptly decreases during immune activation. Evidence suggests it may be a protective strategy to prevent a hyperinflammatory systemic response. Based upon the literature and our supporting work we suggest that post-calving hypocalcemia can be explained, at least partially, by inflammation. In addition to hypocalcemia, research in rodents suggests that inflammation may also be involved in fatty liver development. A final objective of this dissertation was to evaluate if inflammation affected liver fat accumulation in artificially-induced hyperlipidemic cows. In summary, immune activation negatively influences metabolic, hormonal, and Ca homeostasis and these alterations closely mimic changes observed in poorly transitioning dairy cows. Having a better understanding of the impact of immune activation on nutrient trafficking and Ca homeostasis will provide foundational information for developing strategies aimed at minimizing production losses during infection.


Copyright Owner

Erin Andrea Horst



File Format


File Size

342 pages