Postprandial Triacylglycerol Response Research Articles

Impact of Saturated, Polyunsaturated and Monounsaturated Fatty Acid‐Rich Micelles on Lipoprotein Synthesis and Secretion in Caco‐2 Cells

Meal fatty acids have been shown to modulate the size and composition of triacylglycerol (TAG)-rich lipoproteins influencing the magnitude and duration of the postprandial plasma TAG response. As a result there is considerable interest in the origin of these meal fatty-acid induced differences in particle composition. Caco-2 cells were incubated over 4 days with fatty acid mixtures resembling the composition of saturated (SFA), monounsaturated (MUFA) and polyunsaturated fatty acid (PUFA)-rich meals fed in a previous postprandial study to determine their impact on lipoprotein synthesis and secretion. The MUFA- and PUFA-rich mixtures supported greater intracellular TAG, but not cholesterol accumulation compared with the SFA-rich mixture (P < 0.001). The MUFA-rich mixture promoted significantly greater TAG and cholesterol secretion than the other mixtures and significantly more apolipoprotein B-100 secretion than the PUFA-rich mixture (P < 0.05). Electron microscopy revealed the SFA-rich mixture had led to unfavourable effects on cellular morphology, compared with the unsaturated fatty acid-rich mixtures. Our findings suggest the MUFA-rich mixture, may support the formation of a greater number of TAG-rich lipoproteins, which is consistent with indirect observations from our human study. Our electron micrographs are suggestive that some endocytotic uptake of MUFA-rich taurocholate micelles may promote greater lipoprotein synthesis and secretion in Caco-2 cells.

Introduction to the DISRUPT postprandial database: subjects, studies and methodologies

Dysregulation of lipid and glucose metabolism in the postprandial state are recognised as important risk factors for the development of cardiovascular disease and type 2 diabetes. Our objective was to create a comprehensive, standardised database of postprandial studies to provide insights into the physiological factors that influence postprandial lipid and glucose responses. Data were collated from subjects (n = 467) taking part in single and sequential meal postprandial studies conducted by researchers at the University of Reading, to form the DISRUPT (DIetary Studies: Reading Unilever Postprandial Trials) database. Subject attributes including age, gender, genotype, menopausal status, body mass index, blood pressure and a fasting biochemical profile, together with postprandial measurements of triacylglycerol (TAG), non-esterified fatty acids, glucose, insulin and TAG-rich lipoprotein composition are recorded. A particular strength of the studies is the frequency of blood sampling, with on average 10-13 blood samples taken during each postprandial assessment, and the fact that identical test meal protocols were used in a number of studies, allowing pooling of data to increase statistical power. The DISRUPT database is the most comprehensive postprandial metabolism database that exists worldwide and preliminary analysis of the pooled sequential meal postprandial dataset has revealed both confirmatory and novel observations with respect to the impact of gender and age on the postprandial TAG response. Further analysis of the dataset using conventional statistical techniques along with integrated mathematical models and clustering analysis will provide a unique opportunity to greatly expand current knowledge of the aetiology of inter-individual variability in postprandial lipid and glucose responses.

Impact of age and menopausal status on the postprandial triacylglycerol response in healthy women

Objective To examine the impact of age and the natural menopause on the postprandial triacylglycerol (TAG) response in healthy women. Methods and results Thirty-seven premenopausal and sixty-one postmenopausal women underwent a sequential meal postprandial investigation, in which blood samples were taken at regular intervals after a test breakfast and lunch given at 0 and 330 min respectively. Lipids and glucose were measured in the fasting sample, with TAG analysed in the postprandial samples. Postmenopausal women were shown to have higher fasting total cholesterol, low density lipoprotein cholesterol (LDL-C) and glucose ( P < 0.02). Marked differences in the postprandial TAG response were evident between the groups, with a greater incremental area under the curve (IAUC) and maximum TAG concentration in the postmenopausal women ( P < 0.04). Multivariate regression analysis revealed both age and fasting TAG to be independently associated with the summary measures of the postprandial TAG response in the premenopausal women only. Interestingly, sub-division of the women into both younger and older pre- and postmenopausal subgroups, showed the most marked difference in TAG-IAUC to be between the younger and the older premenopausal women, whereas differences in fasting LDL-C were most evident between the older premenopausal and the younger postmenopausal women. Conclusions Our results suggest a divergence in the relationship of age and menopausal status with fasting LDL-C and postprandial TAG which may reflect differences in the metabolic effects of age and the menopause on these lipid risk markers or a greater impact of early oestrogen decline on pathways of TAG rather than LDL metabolism.

Association between glucokinase regulatory protein (GCKR) and apolipoprotein A5 (APOA5) gene polymorphisms and triacylglycerol concentrations in fasting, postprandial, and fenofibrate-treated states

BackgroundHypertriglyceridemia is a risk factor for cardiovascular disease. Variation in the apolipoprotein A5 (APOA5) and glucokinase regulatory protein (GCKR) genes has been associated with fasting plasma triacylglycerol. ObjectiveWe investigated the combined effects of the GCKR rs780094C→T, APOA5 −1131T→C, and APOA5 56C→G single nucleotide polymorphisms (SNPs) on fasting triacylglycerol in several independent populations and the response to a high-fat meal and fenofibrate interventions. DesignWe used a cross-sectional design to investigate the association with fasting triacylglycerol in 8 populations from America, Asia, and Europe (n = 7730 men and women) and 2 intervention studies in US whites (n = 1061) to examine postprandial triacylglycerol after a high-fat meal and the response to fenofibrate. We defined 3 combined genotype groups: 1) protective (homozygous for the wild-type allele for all 3 SNPs); 2) intermediate (any mixed genotype not included in groups 1 and 3); and 3) risk (carriers of the variant alleles at both genes). ResultsSubjects within the risk group had significantly higher fasting triacylglycerol and a higher prevalence of hypertriglyceridemia than did subjects in the protective group across all populations. Moreover, subjects in the risk group had a greater postprandial triacylglycerol response to a high-fat meal and greater fenofibrate-induced reduction of fasting triacylglycerol than did the other groups, especially among persons with hypertriglyceridemia. Subjects with the intermediate genotype had intermediate values (P for trend <0.001). ConclusionsSNPs in GCKR and APOA5 have an additive effect on both fasting and postprandial triacylglycerol and contribute to the interindividual variability in response to fenofibrate treatment.

Fasting triacylglycerol status, but not polyunsaturated/saturated fatty acid ratio, influences the postprandial response to a series of oral fat tolerance tests

Elevated postprandial lipemia is emerging as a risk factor for obesity-related chronic diseases, such as type 2 diabetes and cardiovascular disease, and is associated with alterations in several metabolic biomarkers of disease. Our goal was to examine the effects of specific polyunsaturated/saturated fatty acid (P/S) ratios on postprandial triacylglycerol (TAG) concentrations and metabolic biomarkers in men with different fasting TAG concentrations through a series of oral fat tolerance tests (OFTT) consisting solely of emulsified lipid. Otherwise healthy men with high (>1.69 mmol/L) fasting TAG (HTAG, n=8) and low fasting TAG (LTAG, n=8) underwent three OFTTs with specific P/S ratios of 0.2, 1.0 and 2.0, respectively, and a total lipid load of 1 g/kg subject body mass. All subjects received each treatment separated by at least 1 week. Postprandial plasma TAG fatty acid composition reflected fatty acids present in the OFTT. All other metabolic responses were independent of the P/S ratio ingested. An accelerated increase in postprandial TAGs was observed in HTAG compared to LTAG. Interleukin (IL)-6 and soluble intercellular adhesion molecule (sICAM)-1 were significantly elevated in HTAG at baseline ( P<.05). IL-6 increased significantly following each OFTT ( P<.05) in both groups. Postprandial glucose and CRP were significantly exaggerated ( P<.05) in HTAG. Overall, HTAG subjects had an accelerated postprandial TAG response and increased concentrations of several inflammatory markers following an OFTT, in the absence of an insulin response. However, P/S ratio had no influence on postprandial lipid and inflammatory parameters.

Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals

BackgroundWe have reported that, compared with glucose-sweetened beverages, consuming fructose-sweetened beverages with meals results in lower 24-h circulating glucose, insulin, and leptin concentrations and elevated triacylglycerol (TG). However, pure fructose and glucose are not commonly used as sweeteners. High-fructose corn syrup (HFCS) has replaced sucrose as the predominant sweetener in beverages in the United States. ObjectiveWe compared the metabolic/endocrine effects of HFCS with sucrose and, in a subset of subjects, with pure fructose and glucose. DesignThirty-four men and women consumed 3 isocaloric meals with either sucrose- or HFCS-sweetened beverages, and blood samples were collected over 24 h. Eight of the male subjects were also studied when fructose- or glucose-sweetened beverages were consumed. ResultsIn 34 subjects, 24-h glucose, insulin, leptin, ghrelin, and TG profiles were similar between days that sucrose or HFCS was consumed. Postprandial TG excursions after HFCS or sucrose were larger in men than in women. In the men in whom the effects of 4 sweeteners were compared, the 24-h glucose and insulin responses induced by HFCS and sucrose were intermediate between the lower responses during consumption of fructose and the higher responses during glucose. Unexpectedly, postprandial TG profiles after HFCS or sucrose were not intermediate but comparably high as after pure fructose. ConclusionsSucrose and HFCS do not have substantially different short-term endocrine/metabolic effects. In male subjects, short-term consumption of sucrose and HFCS resulted in postprandial TG responses comparable to those induced by fructose.

Postprandial serum triacylglycerols and oxidative stress in mice after consumption of fish oil, soy oil or olive oil: Possible role for paraoxonase-1 triacylglycerol lipase-like activity

Objective Postprandial triacylglycerols and oxidative stress responses are influenced by the type of fat consumed. We investigated the effect of individual unsaturated fatty acids or oils (fish, soy, or olive) on postprandial triglyceridemia response in association with serum resistance to oxidation and paraoxonase-1 (PON1) activity. Methods Balb/C mice were supplemented with phosphate buffered saline (control), docosahexaenoic acid (ω-3), linoleic acid (ω-6), or oleic acid (ω-9; 500 μg/300 μL of phosphate buffered saline) and with fish, soy, or olive oil (300 μL); blood samples were collected 2 h after feeding. Results Serum triacylglycerol and oxidative stress responses increased after intake of all unsaturated fatty acids and oil supplements. However, ingestion of fish oil or its major fatty acid, docosahexaenoic acid, induced the most remarkable increase in postprandial serum triacylglycerols and in the susceptibility of serum to in vitro oxidation. Serum PON1 activity was decreased by 24% after fish oil ingestion. The increase in postprandial serum susceptibility to oxidation was lower after soy oil supplementation to PON1-transgenic mice in comparison with Balb/C mice, showing that PON1 attenuates the postprandial serum oxidative response. In parallel, in PON1-transgenic mice, a decreased postprandial triacylglycerol response was noted, suggesting PON1 involvement in triacylglycerol metabolism. PON1 exhibited a triacylglycerol lipase-like activity on chylomicrons. Conclusion PON1 attenuates the postprandial oxidative stress response, and this could have resulted from PON1 lipase-like activity on chylomicron triacylglycerols.

Diacylglycerol Oil Does Not Affect Portal Vein Transport of Nonesterified Fatty Acids but Decreases the Postprandial Plasma Lipid Response in Catheterized Pigs

Studies have shown several beneficial effects of dietary diacylglycerol oil (DAG oil), but the mechanism behind these effects is still not clear. One hypothesis is that an increase in portal vein transport of nonesterified fatty acids (NEFA) with subsequent oxidation in the liver might be responsible for the positive effects. We examined the portal vein transport of NEFA and other lipid related variables, in response to DAG and triacylglycerol (TAG) bolus feeding and a bolus of standard pig feed in 4 portal vein and mesenteric artery catheterized pigs. Also, the effect of the boluses on postprandial lipid variables was examined. Portal vein transport of NEFA did not differ when pigs were administered the 2 oil bolus diets, consistent with the similar portal plasma concentrations of oleic and linolenic acids during h 1 after feeding. Glycerol, on the contrary, was transported by the portal vein to a much higher degree after intake of DAG oil (P < 0.001; 20, 40, and 60 min). The postprandial arterial TAG response at 5 and 6 h postprandially was significantly lower after the DAG bolus intake. Analysis of Delta AUC for the 6-h postprandial period of selected and total fatty acids showed a lower concentration of vaccenic acid (P = 0.002) after the DAG bolus diet. In conclusion, DAG bolus feeding did not increase the portal transport of NEFA, but it did increase the portal transport of glycerol and lower the postprandial lipid concentration in arterial plasma.

Butter and walnuts, but not olive oil, elicit postprandial activation of nuclear transcription factor κB in peripheral blood mononuclear cells from healthy men

Nuclear transcription factor kappaB (NF-kappaB) plays an important role in atherosclerosis by modulating gene expression. Postprandial lipemia has been correlated with an increase in NF-kappaB activation in vascular cells and it is associated with an increase in postprandial triacylglycerol-rich lipoproteins, which are involved in the development of atherosclerotic plaque. The objective of this study was to determine the effect of the intakes of 3 different foods with different fat compositions on the postprandial activation of monocyte NF-kappaB. Eight healthy men followed a 4-wk baseline diet and then consumed 3 fat-load meals consisting of 1 g fat/kg body wt (65% fat) according to a randomized crossover design. Each meal had a different fatty acid composition, and the consumption of each meal was separated by 1 wk. The compositions of the 3 test meals were as follows: olive oil meal [22% saturated fatty acids (SFAs), 38% monounsaturated fatty acids (MUFAs), 4% polyunsaturated fatty acids (PUFAs), and 0.7% alpha-linolenic acid], butter meal (38% SFAs, 22% MUFAs, 4% PUFAs, and 0.7% alpha-linolenic acid), and walnut meal (20% SFAs, 24% MUFAs, 16% PUFAs, and 4% alpha-linolenic acid). Ingestion of the olive oil meal did not elicit NF-kappaB activation compared with ingestion of either the butter meal at 3 h (P <0.05) or the walnut meal at 9 h (P <0.05). There was no significant difference in the postprandial triacylglycerol response between the 3 meals. Consumption of an olive oil-enriched meal does not activate NF-kappaB in monocytes as do butter and walnut-enriched meals. This effect could enhance the cardioprotective effect of olive oil-enriched diets.

Effects of diacylglycerol administration on serum triacylglycerol in a patient homozygous for complete lipoprotein lipase deletion

We investigated postprandial and long-term effects of dietary diacylglycerol (DAG) on serum triacylglycerol (TAG) levels in a 34-year-old man homozygous for complete lipoprotein lipase deletion (LPL deletion). In study 1, Three different oils (DAG, TAG, or medium-chain fatty acid TAG [MCT]) were ingested to examine differences in the postprandial serum TAG response. Postprandial serum TAG levels after DAG oil ingestion were lower than those after TAG oil ingestion and similar to those after MCT oil ingestion. In study 2, the patient was allowed to ingest ordinary cooking oil for 2 months and then DAG oil (containing 80% DAG; target, 20 g/d) for the next 3 months. During the test period, serum TAG levels were measured and dietary evaluations were performed every month. The patient was provided with dietary instruction and consultation at each clinical visit. Serum TAG levels were 1939 to 2525 mg/dL when he used ordinary cooking oil, 1926 to 1173 mg/dL when he used ordinary cooking oil together with DAG oil, and 749 mg/dL when he used DAG oil alone. The TAG intake decreased from 86.9 to 43.0 g and the DAG intake increased from 0.9 to 12.4 g during the study period. Subsequently, 45 g DAG oil (equivalent to 36 g DAG) per day was consumed, and the serum TAG level increased to 2195 mg/dL. Although there was a positive correlation between the TAG intake and serum TAG levels during the period of DAG oil use ( P < .01, y = 33.7 x − 583.1), there was no such correlation between DAG oil intake and serum TAG levels. These results suggested that substitution of 12.0 g/d DAG (equivalent to 15 g DAG oil) for TAG oil had the same effect as reducing TAG oil consumption for controlling the serum TAG levels in an LPL-depleted patient with hypertriglyceridemia. In conclusion, the results of study 1 and study 2 demonstrate that DAG oil might be replaced by MCT oil as cooking oil for those with LPL deletion.

Incremental area under response curve more accurately describes the triglyceride response to an oral fat load in both healthy and type 2 diabetic subjects

Elevation of postprandial triacylglycerol (TG)-rich plasma lipoproteins is considered potentially atherogenic. Type 2 diabetic patients have exaggerated postprandial TG compared with healthy subjects. Postprandial TG responses to oral fat loads are usually studied as the area under the TG curve. No consensus exists regarding the method of choice when calculating the TG response area. We evaluated the correlation between fasting TG and postprandial TG responses calculated by the trapezoid rule as total area under the curve (AUC) and incremental area under the curve (iAUC). Furthermore, we compared the AUC and iAUC to a 3-point calculation method. Ten healthy subjects and 47 type 2 diabetic patients ingested test meals consisting of an energy-free soup plus 80 g fat and 50 g carbohydrate. TG responses were measured in total plasma, in a chylomicron (CM)-rich fraction and in a CM-poor fraction. In healthy subjects the AUC, but not iAUC, correlated positively to fasting TG. In type 2 diabetic patients a strong correlation was found between fasting TG and AUC, whereas weak associations were found to the iAUCs. The iAUC was strongly correlated to the postprandial TG rise in both groups. The 3-point areas differed significantly from the trapezoid measurements in both healthy and type 2 diabetic subjects. In conclusion, in both healthy and type 2 diabetic subjects total AUC is highly correlated to fasting TG, whereas iAUC more accurately describes the TG response to an oral fat load. The 3-point test seems less suitable for the determination of postprandial response in both healthy and type 2 diabetic subjects.

Acute-on-chronic effects of fatty acids on intestinal triacylglycerol-rich lipoprotein metabolism.

Postprandial triacylglycerol (TAG) metabolism is an important metabolic state that has been associated with cardiovascular disease. The magnitude of the postprandial TAG response is determined by dietary fat composition, which alters intestinal and hepatic TAG-rich lipoprotein (TRL) metabolism. Caco-2 cell monolayers are morphologically and physiologically similar to the human intestinal enterocytes, hence they are a good model to study intestinal lipoprotein metabolism. To date only the acute effect of fatty acid composition on intestinal TRL metabolism in Caco-2 cells has been investigated. Little is known of the effect of habitual, or chronic, dietary fat composition on intestinal TRL metabolism. Using the Caco-2 cell model, the present study investigated the acute-on-chronic effect of fatty acid composition on TRL metabolism. Caco-2 cells were grown in the presence of 0.05 mm-palmitic acid (PA; 16 : 0), -oleic acid (OA; 18 : 1n-9),-eicosapentaenoic acid (EPA; 20 : 5n-3) or no fatty acid (control) for 19 d, then one of four acute treatments (control (bovine serum albumin (BSA; 5 g/l)) or BSA (5 g/l) plus 0.5 mm-PA, -OA or -EPA) were administered for 22 h. Significant acutexchronic interactions for the effect of fatty acid composition on cellular TAG:secreted de novo TAG, and cellular de novo TAG:de novo phospholipid were observed. Thus the effect of a fatty acid was determined by the duration of exposure to the fatty acid intervention. Acute PA treatment increased de novo TAG synthesis, but chronic PA supplementation did not. Acute and chronic OA treatments increased de novo TAG secretion. For EPA, chronic supplementation had the greatest effect on TAG synthesis and secretion. The acute-on-chronic effects of fatty acids on apolipoprotein B metabolism were relatively minor compared with the changes noted for TRL lipid composition. The present study shows that the Caco-2 cell model is valuable for studying intestinal TRL metabolism and that fatty acids modulate this process, the nature of which can be determined by the length of exposure of the cell to the fatty acid.

Timing of vagal stimulation affects postprandial lipid metabolism in humans , ,

Vagal stimulation combined with an oral fat load enhances postprandial lipemia in animals and humans. We assessed whether the observed postprandial increase in plasma lipids could be explained by changes in exogenous (chylomicron) or endogenous (VLDL) lipid metabolism and whether the timing of vagal stimulation in relation to fat intake was important. Vagal stimulation was achieved by using the modified sham feeding (MSF) technique, in which food is tasted and chewed but not swallowed. Seven healthy men consumed an oral fat load (50 g) on one occasion (control protocol). On 2 other occasions, they consumed an oral fat load combined with MSF of an appetizing meal. MSF was performed for either 1 h before or 1 h after the oral fat load. Blood was collected for 7 h and was analyzed for hormones and metabolites. The postprandial triacylglycerol response differed significantly (P < 0.001) between the 3 protocols. Both MSF studies resulted in significantly higher plasma pancreatic polypeptide concentrations compared with the control. Compared with MSF for 1 hour after fat intake, MSF for 1 h before fat intake resulted in significantly higher plasma insulin concentrations (P = 0.013), a more rapid rise in chylomicron triacylglycerol concentrations (P = 0.04), and higher VLDL triacylglycerol and apoliprotein B-100 concentrations. Vagal stimulation enhanced postprandial lipemia via effects on both chylomicron and VLDL metabolism. MSF before fat intake had more dramatic effects on postprandial lipemia than did MSF after fat intake, possibly because of increased parasympathetic activity at the time of ingestion.

Postprandial hormone and metabolic responses amongst shift workers in Antarctica.

The circadian rhythms of many night-shift workers are maladapted to their imposed behavioural schedule, and this factor may be implicated in the increased occurrence of cardiovascular disease (CVD) reported in shift workers. One way in which CVD risk could be mediated is through inappropriate hormonal and metabolic responses to meals. This study investigated the responses to standard meals at different circadian times in a group of night-shift workers on a British Antarctic Survey station at Halley Bay (75 degrees S) in Antarctica. Twelve healthy subjects (ten men and two women) were recruited. Their postprandial hormone and metabolic responses to an identical mixed test meal of 3330 kJ were measured on three occasions: (i) during daytime on a normal working day, (ii) during night-time at the beginning of a period of night-shift work, and (iii) during the daytime on return from night working to daytime working. Venous blood was taken for 9 h after the meal for the measurement of glucose, insulin, triacylglycerol (TAG) and non-esterified fatty acids. Urine was collected 4-hourly (longer during sleep) on each test day for assessment of the circadian phase via 6-sulphatoxymelatonin (aMT6s) assay. During normal daytime working, aMT6s acrophase was delayed (7.7+/-1.0 h (s.e.m.)) compared with that previously found in temperate zones in a comparable age-group. During the night shift a further delay was evident (11.8+/-1.9 h) and subjects' acrophases remained delayed 2 days after return to daytime working (12.4+/-1.8 h). Integrated postprandial glucose, insulin and TAG responses were significantly elevated during the night shift compared with normal daytime working. Two days after their return to daytime working, subjects' postprandial glucose and insulin responses had returned to pre-shift levels; however, integrated TAG levels remained significantly elevated. These results are very similar to those previously found in simulated night-shift conditions; it is the first time such changes have been reported in real shift workers in field conditions. They provide evidence that the abnormal metabolic responses to meals taken at night during unadapted night shifts are due, at least in part, to a relative insulin resistance, which could contribute to the documented cardiovascular morbidity associated with shift work. When applied to the 20% of the UK workforce currently employed on shift work, these findings have major significance from an occupational health perspective.

Postprandial Triacylglycerol Responses in Simulated Night and Day Shift: Gender Differences

Postprandial Triacylglycerol Responses in Simulated Night and Day Shift: Gender Differences

Postprandial triacylglycerol responses in simulated night and day shift: gender differences.

A number of reports suggest that shift workers have an increased risk of coronary heart disease (CHD). One contributing factor may be the consumption of meals at night with consequent altered postprandial responses. This study investigated circulating triacylglycerol (TAG), a possible risk factor for CHD, after meals during a simulated day and night shift. Twenty-five healthy participants (10 women and 15 men) were studied. They were given a pre-meal at 0800 h and a test meal at 1330 h on a simulated day shift and then an identical pre-meal at 2000 h and test meal at 0130 h, respectively, on a simulated night shift with maintained wakefulness. Blood was sampled for 9 h after the test meal for analysis of basal and postprandial plasma TAG levels. ANOVA for repeated measures indicated higher TAG in men compared with women (p < 0.0001) and higher responses at night in both genders (p = 0.027). Incremental area under the curve (IAUC) analysis indicated that men had significantly increased postprandial TAG levels at night compared with the day: (IAUC 0-540 min, mean +/- SEM) 253.29 +/- 28.73 versus 148.33 +/- 17.28 mmol/L x min, respectively, p = 0.025. In women, night and day responses (61.16 +/- 8.93 versus 34.09 +/- 7.87 mmol/L x min, respectively, p = 0.457) were not significantly different. Circulating TAG remained elevated for longer at night in the men compared with the women (p = 0.009). This study demonstrates the existence of gender and time-of-day differences in TAG responses to a meal. These raised TAG levels at night, for a prolonged time in men, may be relevant to the increased risk of CHD in shift workers.

Predictors of postprandial triacylglycerol response in children: the Columbia University Biomarkers Study

Predictors of postprandial lipemia have not been explored in children. Our objective was to determine whether the postprandial triacylglycerol response is associated with low HDL-cholesterol and high fasting triacylglycerol concentrations and family history of early-onset ischemic heart disease (IHD) in children. We administered a standardized fat load (52.5 g fat/m(2)) to 60 children (mean age: 14.0 y), 20 with and 40 without a family history of early-onset IHD, and to 29 mothers, all recruited from families enrolled in the Columbia University Biomarkers Study. Plasma lipid and retinyl palmitate concentrations were measured in the fasting state and 3, 6, and 8 h after the oral fat load. In children, postprandial lipemia, as indicated by the incremental area under the triacylglycerol response curve, was associated with elevated fasting triacylglycerol concentrations (>/=1.13 mmol/L; P: < 0.01), with low fasting HDL-cholesterol concentrations (</=0.91 mmol/L; P: < 0.01), and with the combination of low HDL-cholesterol and high triacylglycerol concentrations (P: < 0.05). Family history of IHD, baseline LDL-cholesterol concentration, and apolipoprotein E genotype were not associated with the postprandial triacylglycerol or retinyl palmitate response. The mothers had fasting triacylglycerol concentrations similar to those of their children but a more prolonged response with higher triacylglycerol concentrations at 6 and 8 h (P: < 0.01 and P: < 0.05, respectively). In children, a delayed postprandial triacylglycerol response to a fat load is associated with the combination of high fasting triacylglycerol and low HDL-cholesterol concentrations. Predictors of postprandial triacylglycerol concentrations may be similar in children and adults.

Fasting Lipoprotein and Postprandial Triacylglycerol Responses to a Low-Carbohydrate Diet Supplemented with n-3 Fatty Acids

Background: The effects of a prolonged low-carbohydrate diet rich in n-3 fatty acids on blood lipid profiles have not been addressed in the scientific literature.Objective: This study examined the effects of an eight-week ketogenic diet rich in n-3 fatty acids on fasting serum lipoproteins and postprandial triacylglycerol (TG) responses.Design: Ten men consumed a low-carbohydrate diet rich in monounsaturated fat (MUFA) and supplemented with n-3 fatty acids for eight weeks. Fasting blood samples were collected before and after one week of habitual diet and on two consecutive days after 2, 4, 6 and 8 weeks of the intervention diet. Postprandial TG responses to a fat-rich test meal were measured prior to and after the intervention diet.Results: Compared to the habitual diet, subjects consumed significantly (p ≤ 0.05) greater quantities of protein, fat, MUFA and n-3 fatty acids and significantly less total energy, carbohydrate and dietary fiber. Body weight significantly declined over the experimental period (−4.2 ± 2.7 kg). Compared to baseline, fasting total cholesterol, LDL cholesterol and HDL cholesterol were not significantly different after the intervention diet (+1.5%, +9.7% and +10.0%, respectively). Fasting TG were significantly reduced after the intervention diet (−55%). There was a significant reduction in peak postprandial TG (−42%) and TG area under the curve (−48%) after the intervention diet.Conclusions: A hypocaloric low-carbohydrate diet rich in MUFA and supplemented with n-3 fatty acids significantly reduced postabsorptive and postprandial TG in men that were not hypertriglyceridemic as a group before the diet. This may be viewed as a clinically significant positive adaptation in terms of cardiovascular risk status. However, transient increases in total cholesterol and LDL cholesterol were also evident and should be examined further in regard to which particular subfractions are elevated.

The effect of low and moderate fat intakes on the postprandial lipaemic and hormonal responses in healthy volunteers

Present literature indicates that whereas an acute fat intake of 5 g does not elicit a postprandial triacylglycerolaemic response, 20 g of fat does. Since 67% of fat intake occasions involve fat doses of less than 20 g, the present study examined the effect of a relatively low-fat (LF) meal (0.2 g/kg body weight; mean 14 g) on postprandial triacylglycerol (TAG) metabolism, compared with a high-fat (HF) meal (0.6 g/kg body weight; mean 43 g), a fat dose which is more typical of laboratory studies. Plasma- and chylomicron-TAG concentrations increased significantly (P < or = 0.001) following both meals, and the increase was significantly (P < or = 0.02) greater after the HF meal. The postprandial areas under the curves and maximal postprandial TAG concentrations for plasma- and chylomicron-TAG were significantly higher following the HF meal (P < or = 0.05). Postprandial plasma insulin and gastric inhibitory polypeptide concentrations increased significantly (P < or = 0.001) after each meal, but there was no difference between the two meals. These data show that modest amounts of fat in a meal will elicit a measurable postprandial TAG response. Since postprandial lipaemia affects the composition and concentration of the TAG- and cholesterol-rich lipoproteins, controlling dietary TAG supply may influence the metabolic fate of these lipoproteins.

Effect of long-term olive oil dietary intervention on postprandial triacylglycerol and factor VII metabolism

Although the beneficial effects of Mediterranean-type diets, which are rich in olive oil, a good source of monounsaturated fatty acids (MUFAs), are generally accepted, little is known about the effects of long-term dietary MUFA intake on postprandial lipoprotein metabolism and hemostasis. This study used a single-blind, randomized, crossover design to investigate the relative effects of a long-term dietary olive oil intervention and a control [saturated fatty acid (SFA)-enriched] diet on postprandial triacylglycerol metabolism and factor VII activity. The postprandial response to a standard test meal was investigated in 23 healthy men who adhered to both diets for 8 wk. cis-MUFAs were successfully substituted for SFAs in the MUFA diet without affecting total dietary fat or energy intakes. The long-term dietary MUFA intervention significantly reduced plasma and LDL-cholesterol concentrations (P = 0.01). Postprandial triacylglycerol concentrations were significantly greater in the early postprandial period after the MUFA diet (P = 0.003). Postprandial factor VII activation and the concentration of the factor VII antigen were significantly lower after the MUFA diet (P = 0.04 and P = 0.006, respectively). This study showed that isoenergetic substitution of MUFAs for SFAs reduces plasma cholesterol and reduces the degree of postprandial factor VII activation. The alterations in the postprandial triacylglycerol response suggest a greater rate of dietary fat absorption and postprandial triacylglycerol metabolism after a diet rich in MUFAs. This study presents new insights into the biochemical basis of the beneficial effects associated with long-term dietary MUFA consumption, which may explain the lower rates of coronary mortality in Mediterranean regions. Am J Clin Nutr 1998;68:552–60.