Work

66 Targeting inflammation with ω-3 polyunsaturated fatty acid nutraceutical interventions improved lipid flux and partially restored lipid metabolic indicators in heat-stressed finishing wethers.

Year: 2025

Type: article

Abstract: Chronic heat stress disrupts fat mobilization and metabolism, leading to reduced energy availability and metabolic inefficiencies in livestock. The present study aimed to determine if targeting heat stress-induced inflammation with anti-inflammatory nutraceutical supplements would improve lipid homeostasis in finishing wethers. We hypothesized that ω-3 polyunsaturated fatty acid (ω-3 PUFA) nutraceuticals would reduce systemic inflammation and in turn mitigate the adverse effects of heat stress on key indicators of lipid storage, mobilization, and metabolism. In Experiment 1, commercial Polypay-cross wether lambs (40.8 ± 0.7 kg) were maintained under heat stress (40 °C, 35% humidity) or were pair-fed under thermoneutral conditions (19 °C, 15% humidity; n = 11) for 30 d. Heat-stressed lambs were randomly assigned to receive: 1) clinical-dose dexamethasone injections (0.15 mg/kg, IM) every 72 h (n = 11), 2) oral 1200-mg boluses of ω-3 PUFA-rich fish oil capsules twice daily (n = 11), or 3) placebo injections/capsules (n = 11). In Experiment 2, heat-stressed wethers received daily oral ω-3 PUFA Ca2+ salts supplementation (0.42 g/kg bodyweight; n = 11) or a placebo (n = 12). Lipid mobilization was assessed ex vivo from primary visceral adipose tissue by measuring epinephrine-stimulated release of non-esterified fatty acids (NEFA) and glycerol. Semitendinosus muscle lipid content and lipid droplet dynamics were quantified by Oil Red O staining, and expression of lipid metabolism enzymes (CD36, PPARα, PPARγ, ACSL1) were analyzed via protein immunoblot. Heat stress reduced (P ≤ 0.05) fatty acid mobilization at all epinephrine concentrations, indicating limited energy availability. Fish oil restored (P ≤ 0.05), and ω-3 Ca2+ salts tended to restore (P = 0.06) ex vivo NEFA release. All three interventions improved (P ≤ 0.05) ex vivo glycerol mobilization. Following heat stress, semitendinosus lipid droplet density was reduced (P ≤ 0.05) by 34% in Experiment 1 and total lipid area tended to be reduced (P = 0.09) by 21% in Experiment 2, with no recovery from any of the interventions. Semitendinosus CD36 content was suppressed (P ≤ 0.05) and PPARγ tended to be suppressed (P = 0.08) by heat stress in Experiment 2, and PPARα was elevated (P ≤ 0.05) by heat stress in Experiment 1. This indicates a metabolic shift toward greater fatty acid oxidation. Moreover, ACSL1 content was unchanged in either experiment, indicating stable fatty acid activation capacity. These findings show that heat stress-induced systemic inflammation impairs lipid mobilization but may increase muscle lipid metabolism. Anti-inflammatory interventions mitigated some of these effects, but unresolved deficits in glycerol mobilization and some metabolic pathways suggest that inflammation is not the sole driver of heat stress-induced lipid dysregulation. Nevertheless, targeting inflammation clearly benefited lipid flux in heat-stressed livestock.

Source: Journal of Animal Science

DOI: 10.1093/jas/skaf300.187