# Targeting Inflammation with Dietary ω-3 Polyunsaturated Fatty Acids Improved Lipid Mobilization and Flux in Heat-Stressed Wether Lambs

## TL;DR

This study shows that reducing inflammation with dietary ω-3 fatty acids can help heat-stressed lambs better mobilize lipids for energy.

## Contribution

The study demonstrates that targeting inflammation with ω-3 fatty acids improves lipid mobilization in heat-stressed lambs.

## Key findings

- Heat stress reduced lipid mobilization from visceral adipose tissue, which was partially or fully resolved by fish oil or ω-3 PUFA.
- Fish oil and dexamethasone reduced muscle PPARα, suggesting less lipid utilization.
- ω-3 PUFA improved muscle CD36 and PPARγ, indicating better lipid uptake, but did not restore intramuscular lipid content.

## Abstract

Background/Objectives: Chronic heat stress impairs lipid mobilization from adipocytes, which reduces substrate availability for muscle metabolism. Systemic inflammation is a key facilitative response to heat stress, and we sought to determine if mitigating inflammation in heat-stressed wether lambs would improve lipid flux. Methods: Two cohorts of commercial feedlot lambs were heat stressed for 30 days. In study 1, heat-stressed lambs received dexamethasone injections every 3 days, fish oil capsules twice daily, or no intervention. In study 2, heat-stressed lambs received daily boluses of ω-3 polyunsaturated fatty acid Ca2+ salts (ω-3 PUFA) or no intervention. Results: In both studies, heat stress reduced ex vivo epinephrine-stimulated free fatty acid and glycerol mobilization from visceral adipose tissue. These deficits were partially resolved by fish oil and fully resolved by ω-3 PUFA. In study 1, fish oil recovered heat stress-induced deficits in circulating triglycerides and HDL-cholesterol but not in circulating free fatty acids. Fish oil and dexamethasone resolved the increase in muscle PPARα, indicating less lipid utilization for metabolism. In study 2, ω-3 PUFA resolved heat stress-induced deficits in muscle CD36 and PPARγ, indicating improved lipid uptake capacity. However, interventions did not resolve reduced intramuscular lipid content in either study. Conclusions: We conclude that inflammation was a primary facilitator of impaired lipid mobilization in heat-stressed lambs but was not the sole driver of lipid dysregulation. Nevertheless, targeting inflammation was a beneficial strategy for improving lipid flux during chronic heat stress.