245 Fish Oil and Dexamethasone Administration Each Partially Improve Indicators of Glucose Metabolism and Fat Homeostasis By Reducing Systemic Inflammation in Heat-Stressed Feedlot Wethers
Authors: Grijalva Pablo Cesar C , Most Micah S , Beer Haley N , Gibbs Rachel L , Hicks Zena M , Lacey Taylor A , White Melanie R , Schmidt Ty B B , Peterson Jessica L L , Yates Dustin T 
Published: November 2023

Abstract
Heat stress is costly for livestock production due to its impact on metabolism, which negatively affects health and growth. Previous pair-fed studies demonstrated that heat stress-induced inflammation is associated with disruptions in metabolism and growth. Therefore, the objective of this study was to determine whether targeting systemic inflammation in heat-stressed wethers improves metabolic and stress indicators. Feedlot wethers were randomly assigned to 30-d heat stress (40°C; THI = 85) or were pair-fed under thermoneutral conditions (controls; 25°C; n = 11). Heat-stressed wethers were administered oral fish oil capsules twice daily (HeatStress+FO; 2,400 mg/d; n = 11), injected with dexamethasone every 3 d (HeatStress+DEX; 0.15 mg/kg, i.m.; n = 11), or received no intervention (HeatStress; n = 11). Plasma hormones and lipids were assessed over the 30-d period, and soleus muscle and adipose tissue were collected at necropsy for ex vivo glucose metabolism studies and non-esterified fatty acid (NEFA) mobilization analyses, respectively. Plasma TNFα was up to 3-fold greater (P &lt; 0.05) in HeatStress wethers than controls throughout the study. By the end of the study, plasma TNFα in HeatStress+DEX and HeatStress+FO was reduced (P &lt; 0.05) by 38% and 47%, respectively, compared with HeatStress and did not differ from controls. Plasma insulin did not differ among groups early in the study but by d 30 were increased (P &lt; 0.05) in HeatStress and HeatStress+DEX compared with controls and HeatStress+FO. Blood glucose-to-insulin ratios were less (P &lt; 0.05) for HeatStress wethers than controls throughout the study and were intermediate for HeatStress+DEX and HeatStress+FO. Plasma cortisol did not differ among groups and was less (P &lt; 0.05) at d 30 than d -3 for all weathers. Plasma eicosapentaenoic acid and triglycerides were 15% to 22% less (P &lt; 0.05) for HeatStress and HeatStress+DEX but not HeatStress+FO than for controls throughout the study. High density lipoprotein-bound cholesterol was 8% and 22% less (P &lt; 0.05), respectively, for HeatStress and HeatStress+DEX wethers but not HeatStress+FO wethers compared with controls. Ex vivo basal and insulin-stimulated glucose oxidation rates were reduced (P &lt; 0.05) by 32% in muscle from HeatStress wethers but not HeatStress+DEX, or HeatStress+FO wethers compared with muscle from controls. Glucose uptake rates did not differ among groups. Mobilization of NEFA was reduced (P &lt; 0.05) by 19% and 37%, respectively, in fat from HeatStress wethers and HeatStress+DEX wethers compared with controls and was intermediate in fat from HeatStress+FO wethers. These data indicate that supplementation of DEX and FO partially improve muscle-specific glucose metabolism as well as lipid homeostasis and stress indicators, which provides a fundamental basis for heat stress interventions that utilize anti-inflammatory supplements.