Effect of dietary alpha-linolenic acid on equine monocyte procoagulant activity and eicosanoid synthesis.

This research conducted an 8-week trial on horses to examine the impact of omega-3 fatty acid-enriched diet specifically containing alpha-linolenic acid, from linseed oil, on a particular cell response to endotoxin. The study revealed that this diet could potentially reduce the production of cellular mediators deemed harmful following an endotoxin exposure.

Study Design and Methodology

• An 8-week feeding trial was performed involving two groups of horses to study the effects of an omega-3 fatty acid-enriched diet on endotoxin response by equine monocytes.
• One group of horses was given a control pelleted ration while the other group was fed an 8% linseed oil-enriched pelleted ration.
• Linseed oil was used in the diet due to its high content of the omega-3 fatty acid, alpha-linolenic acid.
• After the feeding period, monocytes were isolated and incubated in the presence of Escherichia coli O55:B5 endotoxin for 6 hours.

Results and Findings

• After 8 weeks, monocytes from horses fed the linseed oil-enriched diet showed a 51% decrease in procoagulant activity and a 71% decrease in the production of thromboxane B2 in response to endotoxin stimulus, compared to cells from horses fed the control diet.
• There was no significant difference observed in the monocyte synthesis of 12-hydroxyeicosatetraenoic acid or leukotriene B4 between the two groups.
• Fatty acid analysis of membrane phospholipids disclosed a reduction in the omega-6 to omega-3 ratio in monocytes from horses fed the linseed oil-enriched ration.

Conclusion of the Study

• The observed reduction in procoagulant activity and thromboxane B2 production is significant because these factors are known as potentially harmful cellular mediators that are synthesized in response to endotoxin exposure.
• The results imply that dietary supplementation with alpha-linolenic acid, an omega-3 fatty acid, may modify the equine monocyte response to endotoxin by reducing the production of these harmful cellular mediators.