Here we report the changes in fatty acid concentrations in plasma over 10 hours following consumption of a high fat breakfast plus supplements providing LC n-3 PUFAs. Some fatty acids in plasma are in the “free” (i.e. non-esterified) form but the bulk are esterified to produce more complex lipids mainly TAGs, PhLs, and cholesteryl esters. In turn, the complex lipids are components of lipoproteins whose role is to transport lipids, especially the fatty acid constituents, between tissues. In lipoproteins, the non-polar lipids (TAGs, cholesteryl esters) form a core which is surrounded by a PhL monolayer. The TAGs, cholesteryl esters and PhLs have characteristic fatty acid compositions but both the complex lipid content and the fatty acid composition of lipoproteins changes as they are metabolised. After eating, the bulk of fatty acids derived from the meal appear in the circulation as components of TAGs within chylomicrons. In the current study fatty acids of 14 to 18 carbons derived from the meal appeared quickly in plasma and reached their maximal concentration around 3 hours after consuming the breakfast. This is entirely consistent with the time course of the change in concentration of total TAGs [35–37] and of chylomicrons [35, 37]. The changes in the concentrations of 14 to 18 carbon fatty acids in plasma are in accordance with the relative amounts of those fatty acids in the breakfast. This agrees with the data presented by Burdge et al.  and fits with current concepts on the handling of dietary fat . Most of these fatty acids had returned to their starting concentrations by 8 hours following the breakfast.
In contrast to 14 to 18 carbon fatty acids, 20 and 22 carbon PUFAs demonstrated a slower rise in concentration in plasma and reached their maximum concentrations 6 to 8 hours after consuming the breakfast. Again this pattern of appearance is in agreement with the literature. Burdge et al.  reported appearance of EPA and DHA in plasma TAGs after subjects consumed a high fat breakfast containing EPA and DHA and saw that the maximum concentrations were not reached until 4 hours after completing the meal and then were sustained for a further two hours. They did not make measurements beyond that time point. In the current study EPA and DHA concentrations were maintained at their maximum until 10 hours after the meal was consumed. Heath et al.  reported EPA and DHA in chylomicron-like particles, chylomicron remnants, very low density lipoproteins (VLDLs) and non-esterified fatty acids (NEFAs) over 6 hours following their consumption. The appearance of EPA and DHA in chylomicron-like particles was maximal at 3 and 4 hours. They then tracked into chylomicron remnants peaking in concentration at 4.5 hours. Finally, they appeared in VLDLs peaking in concentration at 5-6 hours. EPA concentration was greater than DHA in the chylomicron-like particles and the chylomicron remnants, reflecting the higher content of EPA than DHA in the test meal . However, DHA concentration was greater than that of EPA in VLDLs , indicating different pathways of metabolism and handling of EPA and DHA over the 6 hours following their consumption in a meal. Heath et al.  also reported appearance of EPA and DHA, with the concentration of DHA being greater, in NEFAs in the late phase of their study. The sequential movement of EPA and DHA through the various lipoproteins and the relative enrichment of VLDLs in DHA were confirmed in a second study by Heath et al. . The later appearance of EPA and DHA in plasma compared with shorter chain fatty acids observed in the current study is consistent with the findings of Burdge et al. and Heath et al. in relation to the late appearance of EPA and DHA in plasma TAGs and TAG-rich lipoproteins. It seems likely that in the current study the EPA and DHA appearing in the plasma over the first hours is within chylomicrons, as seen by Heath et al. , but that later on these fatty acids are within remnant particles, VLDLs and NEFAs.
Plasma EPA concentration increased with both algal and krill oils, but was higher with algal oil reflecting its higher EPA content. The mean increase in plasma EPA with algal oil was 100% higher than with krill oil. Participants consumed 1.5 g EPA from algal oil and 1 g EPA from krill oil. This suggests that on a gram-per-gram basis algal oil may be a more effective source of EPA than krill oil. It is possible that the presence of DHA in krill oil limits the incorporation of EPA into plasma lipids. Another possibility is that n-3 PUFAs within glycolipids, as found in algal oil but not krill oil, are an effective system for delivering EPA to humans. The apparently higher incorporation of EPA with algal compared with krill oil is particularly interesting because a recent study reported better incorporation of EPA into plasma over 72 hours if participants consumed krill oil compared with if they consumed TAGs, both providing the same amounts of EPA and DHA . Taking this finding together with that of the current study suggests that an EPA-rich algal oil may be a very effective way of enhancing EPA status in humans. This will need to be studied in longer term intervention studies that assess other functional pools such as leukocytes and red cells  and link the fatty acid changes observed to physiological effects of relevance to human health .
Plasma DHA concentration clearly increased with krill oil as shown by the significant relationship between time and DHA concentration and by the significant differences in DHA concentration between time zero and all time points from 3 hours on when the participants consumed krill oil. Nevertheless, plasma DHA concentration did not differ between algal and krill oils at any time point, even though krill oil contains DHA and the algal oil does not. This is because there was a small increase in concentration of DHA with algal oil seen as a significant relationship between time and DHA concentration. It is not clear why this might be, although the effect is sufficiently small that there was no difference in DHA concentration between time zero and any subsequent time point when participants consumed algal oil. It is generally considered that there is poor conversion of EPA to DPA and especially to DHA [2, 40]. It is possible that enterocytes may be able to carry out this metabolic transformation, but the rather late appearance of DPA and DHA with algal oil suggests that enterocyte biosynthesis of these two fatty acids is not likely to be involved. There is more likely to be a metabolic explanation for these observations. It is possible that DHA, and perhaps also DPA, become preferentially concentrated in VLDLs late in the post-prandial period, as suggested by the observations of Heath et al. . Thus, the appearance of increasing concentrations of DHA in plasma beyond 5 to 6 hours with algal oil may reflect continued accumulation of DHA in lipoproteins synthesised in the liver (VLDLs) using DHA from remnant lipoproteins and NEFAs while at the same time limiting, or perhaps preventing, DHA oxidation.