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Phospholipid-mediated routing of omega-3 fatty acids in the postprandial state

作者
Emma Burnett
出处
期刊:Memorial University - Memorial University Research Repository [Memorial University of Newfoundland]
标识
DOI:10.48336/463
摘要

Omega-3 long-chain polyunsaturated fatty acids (PUFA), also referred to as n-3 PUFA, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), play key roles in cardiometabolic health, neurodevelopment, and inflammatory regulation. Although fish oil (FO) supplementation is widely used to increase n-3 PUFA intake, the molecular form in which EPA and DHA are delivered may influence their postprandial metabolic handling. Most studies rely on long-term supplementation or high-fat challenges, limiting insight into early postprandial handling under physiologically relevant conditions. The goal of my study was to evaluate whether molecular lipid structure and phospholipid co-ingestion differentially influence early postprandial handling and partitioning of n-3 PUFA using a controlled mixed-meal design in growing piglets. Piglets received meals containing TAG-rich FO, PL-rich krill oil (KO), FO plus phosphatidylcholine (PC), or control fats enriched in n-6 or n-9 fatty acids. Serial blood sampling over eight hours assessed glucose, TAG, total plasma fatty acids, and detailed PC profiles. Marine oils significantly increased circulating n-3 PUFA, with EPA exhibiting greater postprandial responsiveness than DHA. When normalized for dose, EPA kinetics were similar across marine oil sources, whereas DHA concentrations declined over time. KO supplementation preferentially enriched plasma PC species with n-3 PUFA, whereas FO co-ingested with PC was associated with greater enrichment of EPA-containing LPC species. Despite these differences in lipid-class partitioning, overall plasma n-3 PUFA concentrations were not significantly different between marine oil treatments. Together, these findings demonstrate that dietary lipid structure influences early postprandial partitioning of n-3 PUFA into circulating phospholipid pools independent of total acute systemic availability.

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