EPA and DHA are required for normal cell function and can also induce health benefits. Oily fish are the main source of EPA and DHA for human consumption. However, food choices and concerns about the sustainability of marine fish stocks limit the effectiveness of dietary recommendations for EPA + DHA intakes. Seed oils from transgenic plants that contain EPA + DHA are a potential alternative source of EPA and DHA. The present study investigated whether dietary supplementation with transgenic Camelina sativa seed oil (CSO) that contained EPA and DHA was as effective as fish oil (FO) in increasing EPA and DHA concentrations when consumed as a dietary supplement in a blinded crossover study. Healthy men and women (n 31; age 53 (range 20–74) years) were randomised to consume 450 mg/d EPA + DHA provided either as either CSO or FO for 8 weeks, followed by 6 weeks washout and then switched to consuming the other test oil. Fasting venous blood samples were collected at the start and end of each supplementation period. Consuming the test oils significantly (P < 0·05) increased EPA and DHA concentrations in plasma TAG, phosphatidylcholine and cholesteryl esters. There were no significant differences between test oils in the increments of EPA and DHA. There was no significant difference between test oils in the increase in the proportion of erythrocyte EPA + DHA (CSO, 12 %; P < 0·0001 and FO, 8 %; P = 0·02). Together, these findings show that consuming CSO is as effective as FO for increasing EPA and DHA concentrations in humans.

The aim of this work was to study the bioavailability of fatty acids (FA), focusing on n-3 long-chain (LC) PUFA, carried by different molecular lipid species, that is, phospholipids (PL) or TAG, with three formulations based on fish oils or marine PL, providing a similar n-3 LC PUFA amount. The digestive lipolysis was first assessed using an in vitro enzymatic model. Then, intestinal absorption and enterocyte metabolism were investigated in vivo, on male Wistar rats through lymph lipid analysis. The in vitro results showed that the release of n-3 LC PUFA from lipolysis was increased by 48 % when FA were provided as PL rather than TAG. The in vivo results demonstrated that EPA and DHA from both TAG and PL were similarly absorbed and incorporated into lymph lipids. However, DHA was mainly distributed at the sn-1/3 positions of lymph TAG when provided as marine PL, whereas it was equally distributed at the three positions with marine TAG. On the whole, even if the molecular lipid species of n-3 LC PUFA did not greatly modify the in vivo digestion and absorption steps, it modulated the rearrangement of DHA on the glyceride positions of the lymph TAG, which may further impact the DHA metabolic fate and tissue accretion. Consequently, the present study has provided data which may be used to formulate lipid diets rich in DHA in the context of an insufficient consumption of n-3 PUFA in Western countries.

Postprandial hypertriacylglycerolaemia is associated with an increased risk of developing CVD. How fat quality influences postprandial lipid response is scarcely explored in subjects with familial hypercholesterolaemia (FH). The aim of this study was to investigate the postprandial response of TAG and lipid sub-classes after consumption of high-fat meals with different fat quality in subjects with FH compared with normolipidaemic controls. A randomised controlled double-blind cross-over study with two meals and two groups was performed. A total of thirteen hypercholesterolaemic subjects with FH who discontinued lipid-lowering treatment 4 weeks before and during the study, and fourteen normolipidaemic controls, were included. Subjects were aged 18–30 years and had a BMI of 18·5–30·0 kg/m2. Each meal consisted of a muffin containing 60 g (70 E%) of fat, either mainly SFA (40 E%) or PUFA (40 E%), eaten in a random order with a wash-out period of 3–5 weeks between the meals. Blood samples were collected at baseline (fasting) and 2, 4 and 6 h after intake of the meals. In both FH and control subjects, the level of TAG and the largest VLDL sub-classes peaked at 2 h after intake of PUFA and at 4 h after intake of SFA. No significant differences were found in TAG levels between meals or between groups (0·25≤P≤0·72). The distinct TAG peaks may reflect differences in the postprandial lipid metabolism after intake of fatty acids with different chain lengths and degrees of saturation. The clinical impact of these findings remains to be determined.

Chylomicron particles are continually synthesised and secreted from the intestine even in the absence of ingested fat. It is possible that following consumption of low doses of fat the basal level of chylomicron secretion and subsequent metabolism are sufficient to metabolise this fat without an increase in postprandial chylomicron concentrations. To test this hypothesis, healthy male subjects were randomised to receive, on three separate occasions, meals containing a range of doses of fat (average 8·1–19 g) and effects on postprandial lipaemia and chylomicron concentration were determined. Furthermore, to delineate the effect on lipid-rich v. lipid-poor (remnant) forms lipid levels were also determined in a density <1·006 g/ml fraction. Following consumption of the very low dose of fat the postprandial concentration of chylomicrons was unaltered, whereas following the medium dose postprandial chylomicron concentrations were significantly increased. Interestingly, this increase was only detected in the lipid-rich chylomicron fraction, with postprandial levels of chylomicron remnants remaining unchanged. In conclusion, it appears that consumption of what would be considered low to medium doses of fat are not associated with transient postprandial increases in chylomicron remnants in healthy male subjects.

Dietary cholesterol may influence Alzheimer's disease risk, because it regulates the synthesis of amyloid-β. It was recently demonstrated in enterocytes of wild-type mice that intracellular amyloid-β expression is enhanced in response to a high-fat diet made up of SFA and cholesterol. Intestinally derived amyloid-β may be associated with postprandial lipoproteins in response to dietary fats and could be a key regulator in chylomicron metabolism. The present study was designed to investigate the role of cholesterol in modulating amyloid-β abundance in enterocytes. Wild-type mice were fed a low-fat diet supplemented with 2 % (w/w) cholesterol. The effects of cholesterol absorption inhibition and cholesterol biosynthesis inhibition utilising ezetimibe and atorvastatin, respectively, were also studied. Quantitative immunohistochemistry was utilised to determine enterocytic amyloid-β homeostasis. We found that enterocytic amyloid-β concentration was significantly attenuated in mice fed the 2 % (w/w) cholesterol diet. However, blocking cholesterol absorption reversed the cholesterol-feeding effect. Consistent with a suppressive effect of cholesterol on enterocytic amyloid-β abundance, atorvastatin, an inhibitor of cholesterol biosynthesis, enhanced amyloid-β. However, providing exogenous cholesterol abolished the atorvastatin-induced effect. In contrast to the suppression of enterocytic amyloid-β by dietary cholesterol, mice fed a diet enriched in SFA had markedly greater abundance. Collectively, the findings suggest that exogenous and endogenous cholesterol reduce amyloid-β concentration in enterocytes by suppressing production, or enhancing secretion associated with postprandial lipoproteins. Intestinally derived amyloid-β will contribute to the pool of plasma protein and may influence cerebral amyloid homeostasis by altering the bi-directional transfer across the blood–brain barrier.

Vitamin E absorption requires the presence of fat; however, limited information exists on the influence of fat quantity on optimal absorption. In the present study we compared the absorption of stable-isotope-labelled vitamin E following meals of varying fat content and source. In a randomised four-way cross-over study, eight healthy individuals consumed a capsule containing 150 mg 2H-labelled RRR-α-tocopheryl acetate with a test meal of toast with butter (17·5 g fat), cereal with full-fat milk (17·5 g fat), cereal with semi-skimmed milk (2·7 g fat) and water (0 g fat). Blood was taken at 0, 0·5, 1, 1·5, 2, 3, 6 and 9 h following ingestion, chylomicrons were isolated, and 2H-labelled α-tocopherol was analysed in the chylomicron and plasma samples. There was a significant time (P<0·001) and treatment effect (P<0·001) in 2H-labelled α-tocopherol concentration in both chylomicrons and plasma between the test meals. 2H-labelled α-tocopherol concentration was significantly greater with the higher-fat toast and butter meal compared with the low-fat cereal meal or water (P<0·001), and a trend towards greater concentration compared with the high-fat cereal meal (P=0·065). There was significantly greater 2H-labelled α-tocopherol concentration with the high-fat cereal meal compared with the low-fat cereal meal (P<0·05). The 2H-labelled α-tocopherol concentration following either the low-fat cereal meal or water was low. These results demonstrate that both the amount of fat and the food matrix influence vitamin E absorption. These factors should be considered by consumers and for future vitamin E intervention studies.

We investigated the dietary influence of low and high levels of fish oil, supplemented with or without dietary cholesterol, on the plasma lipoprotein profile in Bio F1B hamsters, a model susceptible to diet-induced hyperlipidaemia. The MIX diet, a diet supplemented with a mixture of lard and safflower-seed oil, was used as the control diet to maintain the saturated MUFA and PUFA levels similar to the fish-oil diet. The animals were fed the specific diets for 2 weeks and fasted for 14h before killing. The plasma from the animals fed high levels of fish oil was milky and rich in chylomicron-like particles. The plasma total cholesterol, VLDL- and LDL-cholesterol and -triacylglycerol concentrations were significantly higher, whereas HDL-cholesterol was lower in hamsters fed fish oil compared with the MIX-diet-fed hamsters. Increasing the amount of fat in the diet increased plasma lipids in both the fish-oil- and the MIX-diet-fed hamsters; however, this hyperlipidaemic effect of dietary fat level was greater in the hamsters fed the fish-oil diet. The hepatic lipid concentrations were not dramatically different between the fish-oil-fed and the MIX-diet-fed hamsters. However, the hepatic LDL-receptor mRNA levels were significantly low in the fish-oil-fed hamsters compared with the MIX-diet-fed hamsters. Increasing the amount of fish oil in the diet further decreased the hepatic LDL-receptor mRNA expression. It is concluded that F1B hamsters are susceptible to fish-oil-induced hyperlipidaemia, especially at high fat levels, and this increase is partially explained by the inhibition of hepatic LDL-receptor mRNA expression.

The aim of the present study was to investigate the effects of stearic acid-, oleic acid- and linoleic acid-rich meals on postprandial haemostasis in young healthy volunteers whose background diets had been controlled for 14 d in a residential study. Six healthy male volunteers were assigned randomly to consume diets rich in stearic acid, oleic acid or linoleic acid for 14 d. On day 15, plasma lipids and haematological variables were measured in the fasted state, and 3 and 7 h (factor VII and prothrombin activation peptide fragments, 1 and 2 only) after consumption of a test meal. Test meals provided 40 % of the subjects' daily energy requirement, with 41 % of the energy provided as fat, 17 % energy as protein and 42 % energy as carbohydrate. The mean fat content of the meal was 45 (SD 5) g. Significant alterations from fasted values were observed for activated factor VII (P<0·05 after 7 h), factor VII antigen (P<0·05 after 7 h), prothrombin activation peptide fragments 1 and 2 (P<0·05 after 7 h) and plasminogen activator inhibitor type 1 activity (P<0·01 after 3 h) after consumption of each of the three meals. No significant differences were observed in haemostatic values (factor VII coagulant activity, factor VII antigen, tissue plasminogen activator activity prothrombin activation peptide fragment and plasminogen activator inhibitor type-1) with regard to diet except for activated factor VII at 3 h; values were higher after the oleic acid- and linoleic acid-rich meals than after the stearic acid-rich meal (P<0·05). After consumption of each of the three meals, chylomicrons contained proportionately more palmitic acid than the lipids ingested. The present study shows that there are demonstrable changes in postprandial haemostasis when young healthy volunteers with controlled dietary backgrounds are challenged with a physiological fat load. These changes are independent of the fatty acid composition of the test meals.

The uptake and metabolism of [14C]oleate-labelled chylomicron remnants derived from olive oil, maize oil, palm oil, fish oil or butter fat was investigated using perfused livers from rats fed on the corresponding fat-supplemented diet (providing 40 % of the dietary energy) or a low-fat diet for 21 d. The percentage of added [14C]oleate-labelled remnant removed from the perfusate was similar for livers from rats fed on the fat-supplemented diets irrespective of the type of fat fed, whereas livers from rats fed on the low-fat diet removed more labelled fish oil and butter fat remnants than olive, maize or palm oil remnants. Following hepatic uptake in the fat-supplemented groups, the oxidation of [14C]oleate-labelled remnant lipid from maize oil, fish oil, and butter fat remnants was greater than that of the lipids from olive and palm oil remnants, although only the oxidation of lipids from maize and palm oil remnants was increased by prior fat-supplementation of the diet. In addition, the livers from rats fed on the fish-oil-supplemented diet incorporated more [14C]oleate-labelled remnant lipid into phospholipid compared with the livers from rats fed on the other fat-supplemented diets or the low-fat diets. These investigations show that both prior fat feeding and the composition of the fat fed, as well as the fatty acid composition of the chylomicron remnant particles themselves, influence the uptake and metabolism of chylomicron remnants by the liver.

Possible changes in the fatty acid composition of dietary fats and oils which might occur during digestion, absorption and formation of chylomicrons and chylomicron remnants were investigated. Chylomicrons were collected from the thoracic duct of rats tube-fed with olive, maize, palm or fish oil or butter fat, and their fatty acid composition was determined and compared with that of their parent lipids. In turn, these lipoproteins were converted to chylomicron remnants infunctionally hepatectomized rats and their composition re-determined. The predominant fatty acids in each of the oils and fats also predominated in their respective chylomicrons, but their proportions were reduced during the processes leading to their formation. Endogenous contributions of linoleic, eicosapentaenoic, and docosahexaenoic acids were particularly noted when these fatty acids were not well-represented in the original oils and fats, suggesting that they may be obligatory constituents in the formation of chylomicrons. The conversion of chylomicrons to remnants further attenuated the extremes in fatty acid composition of the dietary oils and fats. These results indicate that following an acute intake of oil or fat, the resulting chylomicrons and chylomicron remnants presented to the tissues contain a more balanced distribution of saturated, mono-and polyunsaturated fatty acids than the oils and fats from which they were derived.

The changes in lipoprotein metabolism which follow the ingestion of a large fat load have been well described. The hypothesis was tested that similar changes in lipoprotein metabolism would occur after a relatively normal meal. Plasma and lipoprotein triacylglycerol, cholesterol and apolipoprotein concentrations were determined in twenty subjects (ten female) given a mixed meal containing approximately one-third of the daily intake of major nutrients in the typical Western diet. Fasting plasma triacylglycerol concentrations (range 0.38–2.70 mm/l) and the postprandial rise in plasma triacylglycerol varied considerably between subjects and were significantly associated (P < 0.01). The rise in plasma triacylglycerol corresponded to marked increases in the triacylglycerol concentration of the triacylglycerol-rich lipoproteins (TRL; chylomicrons and very-low-density lipoproteins). TRL cholesterol also increased after the meal. An increase in high-density-lipoprotein (HDL)-triacylglycerol following the meal was accompanied by a decrease in HDL-cholesterol concentration, presumably due to the action of the cholesteryl-ester transfer protein. The increases in HDL-triacylglycerol and in TRL- cholesterol were correlated with the postprandial rise in triacylglycerol in the TRL (P < 0.01). We conclude that potentially adverse changes occur in both triacylglycerol-rich and high-density lipoproteins following a typical mixed meal, as they do after large fat loads. The changes are exaggerated in those subjects with greater fasting plasma triacylglycerol concentrations.