Sex differences in the response of postprandial lipemia to a change from a low-fat low-cholesterol diet to a high-fat high-cholesterol diet

To determine whether a short-term change in dietary habits affects postprandial lipemia in men and women in the same way, postprandial triglyceridemia was measured in age- and BMI-matched young healthy men and women after two weeks on the self-selected low-fat low-cholesterol (LF) diet and after another two weeks on the self-selected high-fat high-cholesterol (HF) diet. After a standardized challenge meal (1.4 g fat/kg of body weight), men had higher postprandial triglyceridemia than women on the HF diet but no such difference was observed on the LF diet. The results of this preliminary study suggest that there may be important sex differences in the mechanisms regulating the postprandial lipemia response to different diets, women being able to adapt better to the HF diet with respect to postprandial lipemia.     

Chronic supplementation of proanthocyanidins reduces postprandial lipemia and liver miR-33a and miR-122 levels in a dose-dependent manner in healthy rats

Elevated postprandial triglycerides are associated with an increased risk of cardiovascular disease. Acute proanthocyanidin supplementation improves postprandial lipemia. Therefore, in this study, we evaluated whether a chronic treatment (3 weeks) of grape seed proanthocyanidins (GSPE) improves tolerance to lipid overload and represses liver microRNA (miRNA)-33a and miRNA-122 and their target genes as a mechanism to soften the elevated postprandial triglycerides in healthy rats. Additionally, the minimal GSPE chronic dose required to alter miRNA levels was determined by means of a dose–response experiment using 5, 15, 25 or 50 mg of GSPE/kg body weight. GSPE repressed miR-33a and miR-122 liver expression and reduced postprandial lipemia in a dose-dependent manner. Significant effects were only observed at high levels of proanthocyanidin consumption, but moderate doses of proanthocyanidins were still able to modulate miRNA expression. Therefore, it can be suggested that a population with a normal intake of proanthocyanidin-rich foods can benefit from the modulation of miRNA expression. At the molecular level, this action can confer homeostatic robustness and will thus exert subtle changes in lipid metabolism, thereby reducing the risk associated with postprandial hyperlipemia.     

The Effect of Lipemia on Peripheral Blood Flow

The effect of lipemia on peripheral blood flow was studied in patients with and without peripheral vascular disease. Blood flow was measured by venous occlusion plethysmography in the calf and/or finger four to six hours after a fatty meal and after intravenous heparin. The abolition of postprandial lipemia by heparin was determined by measuring the plasma lactescence.Heparin resulted in no change in finger flow of either group or in calf flow in the control group. In nine out of 10 patients with occlusive vascular disease of the legs, it resulted in a small but significant increase of calf blood flow. No such alteration was found when heparin was given following a non-fatty meal.In 12 patients with intermittent claudication the clearing of postprandial lipemia by heparin caused prolongation of claudication time, as measured by the appearance of pain on treadmill exercise.It is concluded that, in some cases, postprandial lipemia is associated with a decrease in blood flow in a limb which is already the site of occlusive vascular disease.     

Apolipoprotein E polymorphism influences postprandial retinyl palmitate but not triglyceride concentrations.

To quantify the effect of the apolipoprotein (apo) E polymorphism on the magnitude of postprandial lipemia, we have defined its role in determining the response to a single high-fat meal in a large sample of (N = 474) individuals taking part in the biethnic Atherosclerosis Risk in Communities Study. The profile of postprandial response in plasma was monitored over 8 h by triglyceride, triglyceride-rich lipoprotein (TGRL)-triglyceride, apo B-48/apo B-100 ratio, and retinyl palmitate concentrations, and the apo E polymorphism was determined by DNA amplification and digestion. The frequency of the apo E alleles and their effects on fasting lipid levels in this sample were similar to those reported elsewhere. Postprandial plasma retinyl palmitate response to a high-fat meal with vitamin A was significantly different among apo E genotypes, with delayed clearance in individuals with an epsilon 2 allele, compared with epsilon 3/3 and epsilon 3/4 individuals. In the sample of 397 Caucasians, average retinyl palmitate response was 1,489 micrograms/dl in epsilon 2/3 individuals, compared with 1,037 micrograms/dl in epsilon 3/3 individuals and 1,108 micrograms/dl in epsilon 3/4 individuals. The apo E polymorphism accounted for 7.1% of the interindividual variation in postprandial retinyl palmitate response, a contribution proportionally greater than its well-known effect on fasting LDL-cholesterol. However, despite this effect on postprandial retinyl palmitate, the profile of postprandial triglyceride response was not significantly different among apo E genotypes. The profile of postprandial response was consistent between the sample of Caucasians and a smaller sample of black subjects. While these data indicate that the removal of remnant particles from circulation is delayed in subjects with the epsilon 2/3 genotype, there is no reported evidence that the epsilon 2 allele predisposes to coronary artery disease (CAD). The results of this study provide not only a reliable estimate of the magnitude of the effect of the apo E polymorphism on various measurements commonly used to characterize postprandial lipemia, but also provide mechanistic insight into the effects of the apo E gene polymorphism on postprandial lipemia and CAD.     

Effects of glucose ingestion on postprandial lipemia and triglyceride clearance in humans

To determine whether the metabolism of diet-derived triglycerides (TG) is acutely regulated by the consumption of insulinogenic carbohydrates, we measured the effects of glucose ingestion on oral and intravenous fat tolerance, and on serum triglyceride concentrations obtained during duodenal fat perfusion. Postprandial lipemia was diminished by the ingestion of 50 g (148 +/- 121 mg.dl-1 x 7 h-1 vs 192 +/- 124 mg.dl-1 x 7 h-1, P less than 0.05) and 100 g (104 +/- 106 mg.dl-1 x 7 h-1 vs 171 +/- 104 mg.dl-1 x 7 h-1, P less than 0.05) glucose. Peak postprandial TG concentrations occurred later after meals containing glucose and fat than after meals containing fat alone. This effect could be reproduced when an iso-osmotic quantity of urea was substituted for glucose in the test meal. Starch ingestion had no discernible effect on postprandial lipemia. Intravenous fat tolerance was similar before (4.9 +/- 1.2%.min-1) and 2 h (4.4 +/- 1.3%.min-1) and 4 h (4.8 +/- 1.5%.min-1) after 50 g glucose ingestion. During duodenal fat perfusion, glucose ingestion caused a progressive decrease in plasma triglyceride concentrations. These data suggest that glucose ingestion diminishes postprandial lipemia in a dose-dependent manner, but that this effect is not due to increased clearance of triglyceride from the circulation. The hypotriglyceridemic effects of glucose appear to reflect delayed gastric emptying and decreased hepatic secretion of triglyceride.     

Exercise and postprandial lipid metabolism: an update on potential mechanisms and interactions with high-carbohydrate diets (review)

Endurance trained people exhibit low levels of postprandial lipemia. However, this favorable situation is rapidly reversed with de-training and it is likely that the triglyceride (TG) lowering effects of exercise are mainly the result of acute metabolic responses to recent exercise rather than long-term training adaptations. A large body of evidence suggests that postprandial lipemia can be attenuated following an individual exercise session, with the energy expended during exercise being an important determinant of the extent of TG lowering. Increased lipoprotein lipase-mediated TG clearance and reduced hepatic TG secretion are both likely to contribute to the exercise-induced TG reductions. These changes may occur in response to post-exercise substrate deficits in skeletal muscle and/or the liver. In addition, regular exercise can oppose the hypertriglyceridaemia sometimes seen with low-fat, high-carbohydrate diets. Levels of physical activity should therefore be taken into account when considering nutritional strategies for reducing the risk of cardiovascular disease.     

Postprandial lipoprotein metabolism, genes and risk of cardiovascular disease

PURPOSE OF REVIEW: Several lines of evidence suggest that postprandial lipemia increases the risk of atherogenesis, and in each of the systems involved in postprandial metabolism the roles of many genes have been explored in order to establish the possible implications of their variability in coronary heart disease risk. RECENT FINDINGS: This report focuses on recent results pertaining to postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and coronary heart disease. The postprandial lipid response was modified by polymorphisms within the genes for apolipoprotein AI, apolipoprotein E, apolipoprotein B, apolipoprotein CI, apolipoprotein CIII, apolipoprotein AIV, apolipoprotein AV, lipoprotein lipase, hepatic lipase, fatty acid-binding protein-2, the fatty acid transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I. We also discuss recent advances in the effects of gene regulation using knockdown animal models on postprandial lipoprotein metabolism. SUMMARY: The review discusses several of these factors as well as the potential impact of gene polymorphism on the variability of postprandial lipoprotein metabolism as intermediate phenotypes for coronary heart disease. The variability in postprandial lipid response is highly complex. Future studies will need to be large if they are to assess the effects of multiple polymorphisms.     

High postprandial triglyceridemia in patients with type 2 diabetes and microalbuminuria

Microalbuminuria (MA) is an independent risk factor for atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Postprandial lipemia is also associated with excess cardiovascular risk. However, the association between MA and postprandial lipemia in diabetes has not been investigated. A total of 64 patients with T2DM, 30 with and 34 without MA, were examined. Plasma total triglycerides (TGs), triglycerides contained in chylomicrons (CM-TG), and TGs in CM-deficient plasma were measured at baseline and every 2 h for 6 h after a mixed meal. Postheparin LPL and HL activities were also determined. Plasma levels of apolipoprotein A-V (apoA-V), apoC-II, and apoC-III were measured in the fasting state and 2 h postprandially. Patients with MA had higher postprandial total TG levels than those without MA (P < 0.001); this increase been attributed mainly to CM-TG. LPL activity and fasting concentrations of the measured apolipoproteins were not different between the studied groups, whereas HL activity was higher in the patients with MA. ApoC-II and apoC-III levels did not change postprandially in either study group, whereas apoA-V increased more in the patients with MA. These data demonstrate for the first time that MA is characterized by increased postprandial lipemia in patients with T2DM and may explain in part the excess cardiovascular risk in these patients.     

Postprandial plasma lipidome responses to a high-fat meal among healthy women

Postprandial lipemia consists of changes in concentrations and composition of plasma lipids after food intake, commonly presented as increased levels of triglyceride-rich lipoproteins. Postprandial hypertriglyceridemia may also affect high-density lipoprotein (HDL) structure and function, resulting in a net decrease in HDL concentrations. Elevated triglycerides (TG) and reduced HDL levels have been positively associated with risk of cardiovascular diseases development. Here, we investigated the plasma lipidome composition of 12 clinically healthy, nonobese and young women in response to an acute high-caloric (1135 kcal) and high-fat (64 g) breakfast meal. For this purpose, we employed a detailed untargeted mass spectrometry-based lipidomic approach and data was obtained at four sampling points: fasting and 1, 3 and 5 h postprandial. Analysis of variance revealed 73 significantly altered lipid species between all sampling points. Nonetheless, two divergent subgroups have emerged at 5 h postprandial as a function of differential plasma lipidome responses, and were thereby designated slow and fast TG metabolizers. Late responses by slow TG metabolizers were associated with increased concentrations of several species of TG and phosphatidylinositol (PI). Lipidomic analysis of lipoprotein fractions at 5 h postprandial revealed higher TG and PI concentrations in HDL from slow relative to fast TG metabolizers, but not in apoB-containing fraction. These data indicate that modulations in HDL lipidome during prolonged postprandial lipemia may potentially impact HDL functions. A comprehensive characterization of plasma lipidome responses to acute metabolic challenges may contribute to a better understanding of diet/lifestyle regulation in the metabolism of lipid and glucose.     

Proton nuclear magnetic resonance methyl and methylene linewidths from plasma decrease during postprandial lipemia

Narrow proton nuclear magnetic resonance (1H-NMR) linewidths from plasma have been associated with the presence of malignancy (Fossel et al., New Engl. J. Med. (1986) 315, 1369-1376). In that study, subjects and controls were not fasted. In the present study, 1H-NMR methyl and methylene linewidths were measured in plasma from normolipemic individuals without cancer both during fasting and every 90 min after eating a fat meal. Plasma lipoprotein levels were measured in order to relate results to postprandial lipemia. Methyl, methylene, and average 1H-NMR linewidths were strongly positively correlated with high-density lipoprotein levels and inversely correlated with triacylglycerol-rich lipoprotein levels in both the fasting and postprandial states. Linewidths decreased postprandially, reaching a nadir at the peak of plasma triacylglycerol levels. This study demonstrated that postprandial lipemia can lead to narrowing of plasma methyl and methylene resonances comparable to that reported for subjects with cancer.     

Effects of acute sprint interval cycling and energy replacement on postprandial lipemia

High postprandial blood triglyceride (TG) levels increase cardiovascular disease risk. Exercise interventions may be effective in reducing postprandial blood TG. The purpose of this study was to determine the effects of sprint interval cycling (SIC), with and without replacement of the energy deficit, on postprandial lipemia. In a repeated-measures crossover design, six men and six women participated in three trials, each taking place over 2 days. On the evening of the first day of each trial, the participants either did SIC without replacing the energy deficit (Ex-Def), did SIC and replaced the energy deficit (Ex-Bal), or did not exercise (control). SIC was performed on a cycle ergometer and involved four 30-s all-out sprints with 4-min active recovery. In the morning of day 2, responses to a high-fat meal were measured. Venous blood samples were collected in the fasted state and at 0, 30, 60, 120, and 180 min postprandial. There was a trend toward a reduction with treatment in fasting TG (P = 0.068), but no significant treatment effect for fasting insulin, glucose, nonesterified fatty acids, or betahydroxybutryrate (P > 0.05). The postprandial area under the curve (mmol·l(-1)·3 h(-1)) TG response was significantly lower in Ex-Def (21%, P = 0.006) and Ex-Bal (10%, P = 0.044) than in control, and significantly lower in Ex-Def (12%, P = 0.032) than in Ex-Bal. There was no treatment effect (P > 0.05) observed for area under the curve responses of insulin, glucose, nonesterified fatty acids, or betahydroxybutryrate. SIC reduces postprandial lipemia, but the energy deficit alone does not fully explain the decrease observed.     

Impaired glucose tolerance without hypertriglyceridemia does not enhance postprandial lipemia.

Postprandial lipemia has been thought to be one of risk factors for coronary heart disease, and enhances in potential patients for atherosclerotic disease. Patients with impaired glucose tolerance (IGT) often show hypertriglyceride, which is caused by enhanced portprandial lipemia. Therefore, postprandial lipemia in patients with IGT and without hypertriglyceridemia has not been cleared. We have examined the levels of plasma triglyceride and chylomicron remnants after a high fat meal load (1250 kcal, 40% fat and 420 mg cholesterol) in 13 normotriglyceridemic subjects with IGT and 10 controls with normal glucose tolerance (NGT). Chylomicron remnants were evaluated as remnant-like particles (RLP) that were not bound to an immunoaffinity gel mixture containing apo A-I and apo B-100 monoclonal antibody. RLP cholesterol levels 4 hours after the fat load were significantly lower in IGT subjects than in NGT subjects. Increase of RLP cholesterol after the fat meal load only significantly correlated with increase of insulin during the first 30 min after a 75 g oral glucose tolerance test, but not fasting lipid, insulinogenic index and HOMA-R (homeostasis model) in all subjects. These results suggest that postprandial response does not enhance in IGT subjects, and may associate with early-phase insulin secretion and without insulin resistance in normotriglyceridemic men with IGT or NGT.     

Postprandial lipemia enhances the capacity of large HDL2 particles to mediate free cholesterol efflux via SR-BI and ABCG1 pathways in type IIB hyperlipidemia

Lipid and cholesterol metabolism in the postprandial phase is associated with both quantitative and qualitative remodeling of HDL particle subspecies that may influence their anti-atherogenic functions in the reverse cholesterol transport pathway. We evaluated the capacity of whole plasma or isolated HDL particles to mediate cellular free cholesterol (FC) efflux, cholesteryl ester transfer protein (CETP)-mediated cholesteryl ester (CE) transfer, and selective hepatic CE uptake during the postprandial phase in subjects displaying type IIB hyperlipidemia (n = 16). Postprandial, large HDL2 displayed an enhanced capacity to mediate FC efflux via both scavenger receptor class B type I (SR-BI)-dependent (+12%; P < 0.02) and ATP binding cassette transporter G1 (ABCG1)-dependent (+31%; P < 0.008) pathways in in vitro cell systems. In addition, the capacity of whole postprandial plasma (4 h and 8 h postprandially) to mediate cellular FC efflux via the ABCA1-dependent pathway was significantly increased (+19%; P < 0.0003). Concomitantly, postprandial lipemia was associated with elevated endogenous CE transfer rates from HDL2 to apoB lipoproteins and with attenuated capacity (−17%; P < 0.02) of total HDL to deliver CE to hepatic cells. Postprandial lipemia enhanced SR-BI and ABCG1-dependent efflux to large HDL2 particles. However, postprandial lipemia is equally associated with deleterious features by enhancing formation of CE-enriched, triglyceride-rich lipoprotein particles through the action of CETP and by reducing the direct return of HDL-CE to the liver.     

Menstrual cycle exhibits no effect on postprandial lipemia.

Menstrual cycle effects on postprandial lipemia were investigated in 13 healthy women. They were monitored (dietary intake, basal body temperature) for a period of one cycle. Statistically significant follicular-luteal differences were neither observed between fasting triglyceride serum levels nor between areas under triglyceride response curves after a standardized oral fat load.     

Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation

Low-grade inflammation is a risk factor for the onset of atherosclerosis. Little is known about the involvement of endotoxin absorption from the gut during the digestion of lipids. In the present study, we first investigated in humans the impact of a mixed meal containing dispersed lipids on postprandial endotoxemia and inflammation. We then investigated the effect of (i) oil emulsification in vivo in rats and (ii) fatty acid amounts in vitro using Caco-2 cells on postprandial endotoxemia. In humans, postprandial endotoxemia increased early after the meal. Moreover, we evidenced that the endotoxin receptor sCD14 increased during digestion and that chylomicrons could contribute to absorbed endotoxin transport. This could explain the significant peak of inflammatory cytokine IL-6 that we observed 2 h after the mixed meal. Interestingly, in rats, the emulsion led to both higher endotoxemia and hypertriglyceridemia than oil and compared to a control saline load. In vitro, incubation of Caco-2 cells with increasing fatty acid concentrations enhanced epithelial absorption of endotoxin. To our knowledge, this is the first study evidencing in healthy humans that, following a mixed meal containing lipids, increased endotoxemia is associated with raised sCD14 and a peak of IL-6. On a repeated basis, this may thus be a triggering cascade for the onset of atherosclerosis. In this respect, optimizing both dietary fat amount and structure could be a possible strategy to limit such low-grade endotoxemia and inflammation by the control of postprandial lipemia.     

Hypertriglyceridemia Influences the Degree of Postprandial Lipemic Response in Patients with Metabolic Syndrome and Coronary Artery Disease: From the Cordioprev Study

Objective

To determine whether metabolic syndrome traits influence the postprandial lipemia response of coronary patients, and whether this influence depends on the number of MetS criteria.

Materials and Methods

1002 coronary artery disease patients from the CORDIOPREV study were submitted to an oral fat load test meal with 0.7 g fat/kg body weight (12% saturated fatty acids, 10% polyunsaturated fatty acids, 43% monounsaturated fatty acids), 10% protein and 25% carbohydrates. Serial blood test analyzing lipid fractions were drawn at 0, 1, 2, 3 and 4 hours during the postprandial state. Total and incremental area under the curves of the different postprandial parameters were calculated following the trapezoid rule to assess the magnitude of change during the postprandial state

Results

Postprandial lipemia response was directly related to the presence of metabolic syndrome. We found a positive association between the number of metabolic syndrome criteria and the response of postprandial plasma triglycerides (p<0.001), area under the curve of triglycerides (p<0.001) and incremental area under the curve of triglycerides (p<0.001). However, the influence of them on postprandial triglycerides remained statistically significant only in those patients without basal hypertriglyceridemia. Interestingly, in stepwise multiple linear regression analysis with the AUC of triglycerides as the dependent variable, only fasting triglycerides, fasting glucose and waist circumference appeared as significant independent (P<0.05) contributors. The multiple lineal regression (R) was 0.77, and fasting triglycerides showed the greatest effect on AUC of triglycerides with a standardized coefficient of 0.75.

Conclusions

Fasting triglycerides are the major contributors to the postprandial triglycerides levels. MetS influences the postprandial response of lipids in patients with coronary heart disease, particularly in non-hypertriglyceridemic patients.     

The influence of the apolipoprotein E gene promoter (-219G/ T) polymorphism on postprandial lipoprotein metabolism in young normolipemic males

The apolipoprotein E (apoE) gene promoter (-219G/T) polymorphism has been associated with increased risk of myocardial infarction, premature coronary heart disease, and decreased plasma apoE concentrations. We examined whether the -219G/T polymorphism could modify the postprandial response of triacylglycerol-rich lipoproteins (TRLs). Fifty-one healthy apoE 3/3 male volunteers (14GG, 29GT, and 8TT) were given a vitamin A fat-loading test consisting of 1 g of fat/kg body weight and 60,000 IU of vitamin A per m2 of body surface area. Blood samples were taken at time 0 and every hour until the sixth hour, and every 2 hours and 30 minutes until the eleventh hour. Cholesterol, triacylglycerols (TGs), and apoE were determined in plasma; and cholesterol, TG, apoB-100, apoB-48, and retinyl palmitate (RP) were analyzed in lipoprotein fractions. Postprandial lipemia data revealed that subjects with the -219TT genotype had a higher postprandial response of large TRL-cholesterol (P < 0.03), large TRL-triacylglycerols (P < 0.001), large TRL-RP (P < 0.004), and small TRL-apoB-48 (P < 0.03) than carriers of the -219G allele. Moreover, the -219TT subjects had the lowest postprandial levels of serum apoE (P < 0.05). In conclusion, the -219G/T polymorphism may influence TRL metabolism during the postprandial period, thus prolonging postprandial lipemia in subjects with the TT genotype.     

Intestinal lipoprotein overproduction in insulin-resistant states

PURPOSE OF REVIEW: Excessive postprandial lipemia is highly prevalent in obese and insulin-resistant/type 2 diabetic individuals and substantially increases the risk of atherosclerosis and cardiovascular disease. This article will review our current understanding of the link between insulin resistance and intestinal lipoprotein overproduction and highlight some of the key recent findings in the field. RECENT FINDINGS: Emerging evidence from several animal models of insulin resistance as well as insulin-resistant humans clearly supports the link between insulin resistance and aberrant intestinal lipoprotein metabolism. In insulin-resistant states, elevated free fatty acid flux into the intestine, downregulation of intestinal insulin signaling and upregulation of microsomal triglyceride transfer protein all appear to stimulate intestinal lipoprotein production. Gut peptides, GLP-1 and GLP-2, may be important regulators of intestinal lipid absorption and lipoprotein production. SUMMARY: Available evidence in humans and animal models strongly favors the concept that the small intestine is not merely an absorptive organ but rather plays an active role in regulating the rate of production of triglyceride-rich lipoproteins. Metabolic signals in insulin resistance and type 2 diabetes and in some cases an aberrant intestinal response to these factors all contribute to the enhanced formation and secretion of triglyceride-rich lipoproteins.     

Chronic dietary fat and cholesterol inhibit the normal postprandial stimulation of plasma cholesterol metabolism

The response of parameters of plasma cholesterol metabolism was studied in baboons adapted either to a low-fat, low-cholesterol diet or a high-fat, high-cholesterol diet. Animals adapted to the low-fat diet responded to a single low-fat or high-fat meal, as do normal humans, by a stimulation of cholesterol transport from blood cells to plasma, a stimulation of esterification of cholesterol, and a stimulation of cholesteryl ester transfer to very low and low density lipoproteins. While fasting rates of esterification and transfer increased as a result of diet-induced hypercholesterolemia, the postprandial response was reversed, so that postprandial metabolism was characterized by a movement of cholesterol from plasma to blood cells, an inhibition of cholesterol esterification, and a net transfer of cholesteryl esters from VLDL and LDL to HDL. These data indicate that the effects of postprandial lipemia on plasma cholesterol metabolism critically depend upon fasting plasma cholesterol levels.     

Effects of exercise and n-3 fatty acids on postprandial lipemia.

Because n-3 fatty acid ingestion and aerobic exercise each has been associated with diminished postprandial lipemia (PPL), the purpose of this study was to evaluate the effect of a combination of these two factors on PPL. Sedentary men underwent a standard dietary preparation, including a 12-h fast before each trial. Six subjects performed a control trial (fat meal, 100 g fat) and an n-3 fatty acid trial (fat meal after 3 wk of n-3 fatty acid supplementation at 4 g/day). In a parallel experiment, six different subjects underwent a control trial and n-3 fatty acid supplementation + 60 min of exercise before ingestion of the fat meal. Supplementation with n-3 fatty acid significantly decreased baseline triglyceride (TG) concentrations but did not significantly affect PPL. The combination of n-3 fatty acid and exercise had no effect on the postprandial TG response. The present study suggests that n-3 fatty acid supplementation lowers resting TG concentrations but inhibits the beneficial effect of aerobic exercise on the postprandial TG response.