131 Zilpaterol Hydrochloride and Heat Stress Each Alter the Cattle Adipose Transcriptome and Predicted to Alter Molecular Pathways After 21 Days

Heat stress reduces livestock performance while supplementation of beta-adrenergic agonists (βAA) such as zilpaterol hydrochloride (ZH) improve production efficiency; both stimulate lipolysis. The objective of this study was to understand the effects (independent, interacting) of heat stress and ZH on the subcutaneous adipose transcriptome in fed steers. 24 Red Angus steers were assigned to thermoneutral (TN; THI=68) or heat stress (HS; THI=83) conditions and fed no supplement (NS) or ZH (8.33 mg/kg/day) for 21d in a 2x2 factorial. TN steers were pair-fed the HS daily average. Subcutaneous adipose samples were collected at day -3, 3, 10, and 21. RNA was isolated and sequenced using 3’ Tag-Seq reads to a depth of 3.6 million reads/sample. Transcripts were mapped to ARS-UCD1.2 and quantified. After quality control, differential expression (DE) analyses were performed in DESeq2 with a significance threshold (FRD) of 0.05. Pathway analysis was used to explore pathways affected by HS, ZH, and their interaction using DE loci (P < 0.05). The acute phase response signaling pathway was predicted to be activated at 3d, but inhibited at 10d and 21d by the combination of HS and ZH. At multiple time points, inflammatory pathways including those for interferon and IL-8 were predicted to be activated by HS. Mitochondrial function pathways including oxidative phosphorylation, mitochondrial dysfunction, and TCA cycle II were altered by ZH. Adipose centric pathways for phospholipase-C and protein kinase-A signaling were altered by HS/ZH interaction while glycolysis was altered solely by HS. These data support the hypothesis that exposing cattle to HS conditions and ZH supplementation alters the subcutaneous adipose transcriptome, but not necessarily in an additive fashion. These data provide information regarding the supplementation of βAA in heat stress environments, especially if it mediates the effects of HS.

Productivity-Enhancing Technologies. Can Consumer Choices Affect the Environmental Footprint of Beef?

Use of productivity-enhancing technologies (PET: growth hormones, ionophores, and beta-adrenergic agonists) to improve productivity has recently garnered public attention regarding environmentally sustainability, animal welfare, and human health. These consumer perceptions and increased demand for PET-free beef offer opportunities for the beef industry to target niche premium markets, domestically and internationally. However, there is a need to critically examine the trade-offs and benefits of beef raised with and without the use of PETs. This review contains a summary of the current literature regarding PET products available. The implications of their use on resource utilization, food safety and security, as well as animal health and welfare are discussed. Furthermore, we identified gaps in knowledge and future research questions related to the sustainability of these technologies in beef production systems. This work highlights the tradeoffs between environmental sustainability of beef and supplying the dietary needs of a growing population.

159 Effect of ionophore, implant, and beta-adrenergic agonists on key indicators of sustainable beef production

Net protein contribution (NPC) of the beef value chain has been evaluated and it has been demonstrated that the beef value chain positively contributes to NPC; however, the specific role of growth-enhancing technologies has not be evaluated. To compare effects of technology on NPC baseline, performance data from 8 commercial feedlots located in the Texas panhandle (n = 6) and Kansas (n = 2) were used to create 8 scenarios: 1) no technology (NT), 2) ionophore (ION), 3) implant (IMP), 4) beta-agonist (B), 5) ionophore and implant (ION+IMP), 6) ionophore and beta-agonist (ION+B), 7) implant and beta-agonist (IMP+B), and 8) ionophore, implant and beta-agonist (I+I+B). An IMP×B interaction was observed for human-edible protein conversion efficiency (HePCE) and NPC (P ≤ 0.03). Implants and beta-agonists increased HePCE and NPC compared to NT (P < 0.01), and IMP+B was greater than combined effects of IMP and B. Ionophore scenarios had greater HePCE and NPC compared to NT (P < 0.01). Interactions for ION×IMP and IMP×B were observed for NPC of beef value chain (P < 0.03), but an ION×B interaction was not observed (P = 0.07). All technology scenarios were lower than NT for NPC (3.21 vs 3.74, respectively; P < 0.01) because HePCE for the beef value chain was reduced when cattle were fed longer in the technology scenarios. Interactions for ION×IMP, IMP×B, and ION×B were observed for enteric CH4 production feedlot cattle (P ≤ 0.03), and a three-way interaction was observed for enteric CH4 production of the beef value chain (P < 0.01). All technologies reduced enteric CH4 produced per kg of HePg compared to NT (P < 0.01). Net protein contribution should be balanced with other indicators of sustainability for a representative understanding of technology impacts on sustainable beef production.

271 Beta-adrenergic agonists increase maximal output of oxidative phosphorylation in bovine satellite cells

Beta-adrenergic agonists (βAA) are widely used supplements in beef production to improve feed efficiency and increase lean muscle mass, yet little is known about the molecular mechanism by which βAA achieve this outcome. Our objective was to identify the influence of Ractopamine HCl (RH) and Zilpaterol HCl (ZH) on mitochondrial function in muscle stem cells. Satellite cells were isolated from skeletal muscle of cattle (n = 4) and yak (n = 1) at harvest. Cells were exposed to ZH, RH, or no βAA in replicates of four. Real-time measurements of oxygen consumption rates (OCR) and extracellular acidification rates (ECAR) were recorded using intracellular flux analysis. Incubation of bovine (n = 4) cells with either ZH or RH increased maximal respiration (P = 0.004) and spare respiratory capacity (P = 0.013). When yak cells were included, the response to treatment was similar (P = 0.006 and P = 0.006), but an animal effect was also observed (P < 0.02), presumably due to differences in genetic background. These findings indicate that βAA-treated cells have the capacity to respond more efficiently to increased energy demands than non-supplemented cells. Beta-adrenergic agonists improve the efficiency of muscle stem cells in part by modifying mitochondrial function.