255. Anti-inflammatory Intervention via Dietary ω-3 Polyunsaturated Fatty Acids Partially Resolves Poor Adipose Lipolytic Responsiveness in Heat-stressed Beef Heifers.

Abstract Heat stress in livestock disrupts lipid mobilization, utilization, and tissue partitioning. Heightened inflammation due to heat stress may contribute to metabolic dysfunction, but these effects remain undefined. Therefore, the objective of this study was to determine if targeting heat stress-induced inflammation would improve adipose lipolytic responsiveness to adrenergic stimulation and intramuscular fat (IMF) deposition in heifers. Red Angus heifers (244.7 ± 3.9 kg) were heat stressed (40 °C; 35% relative humidity) for 5 days. Heat-stressed heifers were randomly assigned to receive daily oral ω-3 polyunsaturated fatty acid Ca2+ salt (ω-3 PUFA) supplementation (n = 12) or molasses placebo (n = 12). Thermoneutral controls (19 °C, 15% relative humidity; n = 12) were pair fed. Circulating tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6) concentrations were measured via ELISA to evaluate systemic inflammation. Circulating adiponectin was measured via ELISA to assess metabolic regulation. Subcutaneous adipose tissue was biopsied on day 5 and incubated with 0, 100, or 1000 nM epinephrine. Non-esterified fatty acids (NEFA) and glycerol in the media were measured by ELISA. Ultrasounds of the 12th/13th rib interface were performed before and after heat stress to determine lipid area and average lipid droplet size using ImageJ. Heat stress increased (P < 0.05) circulating TNFα throughout the 5-day period and IL-6 on day 2, and supplementing ω-3 PUFA attenuated these increases. Heat stress also reduced (P < 0.05) circulating adiponectin on day 2, but ω-3 PUFA did not resolve this deficit. Subcutaneous adipose tissue exhibited a dose-dependent lipolytic response to epinephrine: heat stress reduced (P < 0.05) NEFA mobilization at 100 and 1000 nM epinephrine and tended to reduce (P = 0.06) glycerol release at all concentrations, showing impaired lipolytic capacity under heat-stress conditions. Supplementing ω-3 PUFA recovered NEFA mobilization at 100 nM epinephrine only and did not recover glycerol release, perhaps indicative of concurrent intracellular fatty acid recycling through re-esterification. Ultrasound-estimated IMF lipid area and droplet size did not differ due to heat stress or ω-3 PUFA supplementation. These findings demonstrate that heat stress-induced systemic inflammation disrupts lipid flux by reducing adipose lipolytic responsiveness, thus disrupting tissue lipid partitioning. Attenuating inflammatory signaling via anti-inflammatory dietary intervention partially restored adipose lipid turnover dynamics, which may benefit lipid utilization by other tissues. Thus, anti-inflammatory nutritional interventions represent a viable strategy to stabilize lipid flux and metabolic resilience in heat-stressed cattle.