Abstract
The composition of fatty acids in the diets of both human and domestic animal species can regulate inflammation through the biosynthesis of potent lipid mediators. The substrates for lipid mediator biosynthesis are derived primarily from membrane phospholipids and reflect dietary fatty acid intake. Inflammation can be exacerbated with intake of certain dietary fatty acids, such as some ω-6 polyunsaturated fatty acids (PUFA), and subsequent incorporation into membrane phospholipids. Inflammation, however, can be resolved with ingestion of other fatty acids, such as ω-3 PUFA. The influence of dietary PUFA on phospholipid composition is influenced by factors that control phospholipid biosynthesis within cellular membranes, such as preferential incorporation of some fatty acids, competition between newly ingested PUFA and fatty acids released from stores such as adipose, and the impacts of carbohydrate metabolism and physiological state. The objective of this review is to explain these factors as potential obstacles to manipulating PUFA composition of tissue phospholipids by specific dietary fatty acids. A better understanding of the factors that influence how dietary fatty acids can be incorporated into phospholipids may lead to nutritional intervention strategies that optimize health.
Highlights
Dietary fatty acids can control the incidence and severity of inflammation in some diseases of humans and domestic animals
The link between dietary polyunsaturated fatty acids (PUFA), inflammation, and disease susceptibility is partially due to changes in the PUFA content of phospholipids in cells involved in the inflammatory response, such as monocytes, macrophages, and vascular endothelial cells [33,34]
Human adipose expression of a CCT gene, Pcyt1a, is positively correlated with adipose mass [110]. These findings indicate that the capacity for de novo biosynthesis of phospholipids may change by reproductive state and adipose mass, and warrant further investigation at all levels of enzyme regulation
Summary
Dietary fatty acids can control the incidence and severity of inflammation in some diseases of humans and domestic animals. Associations between dietary fatty acids and diseases are partially explained by the incorporation of dietary n-6 and n-3 PUFA into membrane phospholipids [6]. The objectives of this review are to explain how dietary n-6 and n-3 PUFA are incorporated into membrane phospholipids, explain how the subsequent biosynthesis of lipid mediators can influence inflammatory responses, and describe factors confounding the influence of dietary PUFA on phospholipid composition. Future studies of these confounding factors will improve knowledge of phospholipid biosynthesis in humans and domestic animals and will reveal all health outcomes of n-3 PUFA dietary supplements
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