Postprandial Lipemic Response Research Articles

Epigenome-wide association study of triglyceride postprandial responses to a high-fat dietary challenge

Postprandial lipemia (PPL), the increased plasma TG concentration after consuming a high-fat meal, is an independent risk factor for CVD. Individual responses to a meal high in fat vary greatly, depending on genetic and lifestyle factors. However, only a few loci have been associated with TG-PPL response. Heritable epigenomic changes may be significant contributors to the unexplained inter-individual PPL variability. We conducted an epigenome-wide association study on 979 subjects with DNA methylation measured from CD4+ T cells, who were challenged with a high-fat meal as a part of the Genetics of Lipid Lowering Drugs and Diet Network study. Eight methylation sites encompassing five genes, LPP, CPT1A, APOA5, SREBF1, and ABCG1, were significantly associated with PPL response at an epigenome-wide level (P < 1.1 × 10−7), but no methylation site reached epigenome-wide significance after adjusting for baseline TG levels. Higher methylation at LPP, APOA5, SREBF1, and ABCG1, and lower methylation at CPT1A methylation were correlated with an increased TG-PPL response. These PPL-associated methylation sites, also correlated with fasting TG, account for a substantially greater amount of phenotypic variance (14.9%) in PPL and fasting TG (16.3%) when compared with the genetic contribution of loci identified by our previous genome-wide association study (4.5%). In summary, the epigenome is a large contributor to the variation in PPL, and this has the potential to be used to modulate PPL and reduce CVD.

Impaired postprandial lipemic response in chronic kidney disease

Dyslipidemia in chronic kidney disease (CKD) is usually characterized by hypertriglyceridemia. Here we studied postprandial lipemia in children and young adults to determine whether an increasing degree of CKD results inaproportional increase in triglyceride and chylomicron concentration. Secondary goals were to determine whether subnephrotic proteinuria, apolipoprotein (apo)C-III and insulin resistance modify the CKD effect. Eighteen fasting participants (mean age of 15 years, mean glomerular filtration rate (GFR) of 50 ml/min/1.73 m(2)) underwent apostprandial challenge with a high fat milkshake. Triglycerides, apoB-48, insulin, and other markers were measured before and 2, 4, 6, and 8 hours afterward. Response was assessed by the incremental area under thecurve of triglycerides and of apoB-48. The primary hypothesis was tested by correlation to estimated GFR. Significantly, for every 10 ml/min/1.73 m(2) lower estimated GFR, the incremental area under the curve of triglycerides was 17% greater while that of apoB-48 was 16% greater. Univariate analyses also showed that the incremental areaunder the curve of triglycerides and apoB-48 were significantly associated with subnephrotic proteinuria, apoC-III, and insulin resistance. In multivariate analysis, CKD and insulin resistance were independently associated with increased area under the curve and were each linkedto increased levels of apoC-III. Thus, postprandial triglyceride and chylomicron plasma excursions are increased in direct proportion to the degree of CKD. Independent effects are associated with subclinical insulin resistance and increased apoC-III is linked to both CKD andinsulin resistance.

Hepatic insulin resistance both in prediabetic and diabetic patients determines postprandial lipoprotein metabolism: from the CORDIOPREV study.

Background/aimsPrevious evidences have shown the presence of a prolonged and exaggerated postprandial response in type 2 diabetes mellitus (T2DM) and its relation with an increase of cardiovascular risk. However, the response in prediabetes population has not been established. The objective was to analyze the degree of postprandial lipemia response in the CORDIOPREV clinical trial (NCT00924937) according to the diabetic status.Methods1002 patients were submitted to an oral fat load test meal (OFTT) with 0.7 g fat/kg body weight [12 % saturated fatty acids (SFA), 10 % polyunsaturated fatty acids (PUFA), 43 % monounsaturated fatty acids (MUFA), 10 % protein and 25 % carbohydrates]. Serial blood test analyzing lipid fractions were drawn at 0, 1, 2, 3 and 4 h during postprandial state. Postprandial triglycerides (TG) concentration at any point >2.5 mmol/L (220 mg/dL) has been established as undesirable response. We explored the dynamic response in 57 non-diabetic, 364 prediabetic and 581 type 2 diabetic patients. Additionally, the postprandial response was evaluated according to basal insulin resistance subgroups in patients non-diabetic and diabetic without pharmacological treatment (N = 642).ResultsPrevalence of undesirable postprandial TG was 35 % in non-diabetic, 48 % in prediabetic and 59 % in diabetic subgroup, respectively (p < 0.001). Interestingly, prediabetic patients displayed higher plasma TG and large triacylglycerol-rich lipoproteins (TRLs-TG) postprandial response compared with those non-diabetic patients (p < 0.001 and p = 0.003 respectively). Moreover, the area under the curve (AUC) of TG and AUC of TRLs-TG was greater in the prediabetic group compared with non-diabetic patients (p < 0.001 and p < 0.005 respectively). Patients with liver insulin resistance (liver-IR) showed higher postprandial response of TG compared with those patients with muscle-IR or without any insulin-resistance respectively (p < 0.001).ConclusionsOur findings demonstrate that prediabetic patients show a lower phenotypic flexibility after external aggression, such as OFTT compared with nondiabetic patients. The postprandial response increases progressively according to non-diabetic, prediabetic and type 2 diabetic state and it is higher in patients with liver insulin-resistance. To identify this subgroup of patients is important to treat more intensively in order to avoid future cardiometabolic complications.

Does Moderate Intensity Exercise in the Postprandial Period Attenuate the Inflammatory Response to a High‐Fat Meal?

BackgroundConsuming a high‐fat meal (HFM) may lead to postprandial lipemia (PPL) and inflammation. Postprandial exercise has been shown to effectively attenuate PPL. However, little is known about the impact of postprandial exercise on systemic inflammation and whether PPL and inflammation are associated. The purpose of this study was to determine whether moderate intensity exercise, performed 60 minutes following a true‐to‐life HFM, would attenuate PPL and inflammation.MethodsThirty‐nine young adults (18–40yrs) with no known metabolic disease, were randomized to either a control group (CON) who remained sedentary during the postprandial period, or an exercise (EX) group who walked at 60% VO2peak to expend ≈5 kcal/kgbw one‐hour following the HFM. Participants consumed a HFM of 10 kcal/kgbw, and blood draws were performed immediately before, 2hrs and 4hrs post‐HFM for blood lipids and inflammatory markers.ResultsAt baseline, there were no differences between EX and CON groups for any metabolic or inflammatory markers (p&gt;0.05). Postprandial TRG increased from baseline to 4hr in the EX and CON groups (69.1±48.5 and 82.9±72.9 mg/dL respectively; p&lt;0.001), with no differences between groups (p=0.871). HDL‐C decreased in both groups across time (p&lt;0.001) with no differences between groups (p=0.338). In the EX group, IL‐6 changed as a quadratic function (baseline=0.76±0.51, 2hrs=0.52±0.37, 4hr=1.0±0.71 pg/ml, p=0.005), but did not change in the CON group. IL‐6 and TNF‐α were not different between EX and CON from baseline to 4hr (p&gt;0.05). In the EX group sVCAM‐1 increased 47.34±56.89 ng/ml, p=0.003, from baseline to 4hr, while the CON group did not. Changes in TRG were associated with changes in IL‐10 from 0–2hrs (r=0.467, p=0.007), but no other associations were found between change in TRG and change in IL‐6, IL‐8, IL‐10, TNF‐α, sICAM‐1 or sVCAM‐1 from baseline to 2hrs or 4hrs postprandially (p&gt;0.05).ConclusionsDespite significant increases in PPL following a HFM, there was no clear pro‐inflammatory response to the meal. Moderate intensity exercise in the postprandial period mitigated neither the PPL response to the meal, nor inflammation. These results indicate that in populations with low metabolic risk, PPL and inflammation following a HFM may not be directly related.

Resistance Exercise Attenuates High-Fructose, High-Fat-Induced Postprandial Lipemia.

INTRODUCTIONMeals rich in both fructose and fat are commonly consumed by many Americans, especially young men, which can produce a significant postprandial lipemic response. Increasing evidence suggests that aerobic exercise can attenuate the postprandial increase in plasma triacylglycerols (TAGs) in response to a high-fat or a high-fructose meal. However, it is unknown if resistance exercise can dampen the postprandial lipemic response to a meal rich in both fructose and fat.METHODSEight apparently healthy men (Mean ± SEM; age = 27 ± 2 years) participated in a crossover study to examine the effects of acute resistance exercise on next-day postprandial lipemia resulting from a high-fructose, high-fat meal. Participants completed three separate two-day conditions in a random order: (1) EX-COMP: a full-body weightlifting workout with the provision of additional kilocalories to compensate for the estimated net energy cost of exercise on day 1, followed by the consumption of a high-fructose, high-fat liquid test meal the next morning (day 2) (~600 kcal) and the determination of the plasma glucose, lactate, insulin, and TAG responses during a six-hour postprandial period; (2) EX-DEF: same condition as EX-COMP but without exercise energy compensation on day 1; and (3) CON: no exercise control.RESULTSThe six-hour postprandial plasma insulin and lactate responses did not differ between conditions. However, the postprandial plasma TAG concentrations were 16.5% and 24.4% lower for EX-COMP (551.0 ± 80.5 mg/dL × 360 minutes) and EX-DEF (499.4 ± 73.5 mg/dL × 360 minutes), respectively, compared to CON (660.2 ± 95.0 mg/dL × 360 minutes) (P < 0.05).CONCLUSIONSA single resistance exercise bout, performed ~15 hours prior to a high-fructose, high-fat meal, attenuated the postprandial TAG response, as compared to a no-exercise control condition, in healthy, resistance-trained men.

The relationship between the postprandial lipemic response and lipid composition in persons with spinal cord injury

ObjectiveTo determine the influence of lipid concentration, lipid particle size, and total abdominal fat (TAF) on postprandial lipemic response (PPLr) in persons with spinal cord injury (SCI).MethodsThirty-five persons with SCI (17 paraplegia, 18 tetraplegia) and 18 able-bodied (AB) individuals participated. Following a 10-hour fast, blood was drawn for lipids, apolipoprotein (apo) A1 and B concentrations, and low-density (LSP) and high-density (HSP) lipoprotein particle sizes. A high-fat milkshake was consumed (∼1.3 g fat/kg). Blood was drawn at 2, 4, and 6 hours to determine PPLr, (triglyceride (TG) area under the curve). TAF and visceral (VF) fat were measured by ultrasonography; total body fat (TBF) by dual-energy X-ray absorptiometry. Differences between the groups were determined by independent sample t-tests. Pearson correlation coefficients determined the relationship among PPLr and lipids, and TAF.ResultsThere were no significant differences in fasting TG, low-density lipoprotein (LDL), apoB, TAF, or PPLr values between the groups. In SCI, PPLr significantly correlated with: apoB (r = 0.63, P < 0.01, LSP (r = 0.57, P < 0.01), and TAF (r = 0.36, P < 0.01). After controlling for age and duration of injury, PPLr significantly correlated with apoB (r = 0.66, P = 0.001), TBF (r = 0.45, P = 0.03), VF (r = 0.66, P = 0.02), and TAF (r = 0.56, P = 0.007).ConclusionsAlthough concentrations of LDL cholesterol and apoB were not different between SCI and AB groups, LSP, apoB, and TAF correlated with PPLr in persons with SCI. ApoB was associated with a greater PPLr in those with motor complete SCI, after controlling for age and duration of injury.

Abstract 597: Nobiletin Reduces Intestinal Lipoprotein Production in LDL Receptor-Null Mice With Diet-Induced Insulin Resistance

Insulin resistant subjects display excessive postprandial lipemia (PPL), defined by overproduction of intestinal triglyceride (TG)-rich, apoB48-containing chylomicrons (CM), which contribute to atherogenesis. However, the regulation of intestinal lipoprotein secretion by insulin and the mechanisms underlying elevated CM production in insulin resistant states remain poorly understood. In mice, the citrus flavonoid nobiletin prevents diet-induced obesity, dyslipidemia, insulin resistance, hepatic steatosis and VLDL overproduction. In the present study, we sought to characterize the aberrant PPL response in mice with diet-induced insulin resistance and hypothesized that nobiletin treatment would correct this abnormal response by normalizing intestinal insulin signaling and TG metabolism. Ldlr-/- mice were fed a high-fat, cholesterol-containing (HFHC) diet (42% fat, 0.2% cholesterol), a HFHC diet plus 0.3% w/w nobiletin or chow for 8 weeks (n=8 per group). Compared to chow, HFHC-fed mice displayed elevated TG (3-fold) within intestinal tissue following a 6 hour fast, which was completely normalized by nobiletin. Fasting-refeeding studies revealed impaired FoxO1 phosphorylation, increased mTOR phosphorylation and elevated Srebp1c mRNA in the jejunum of HFHC-fed mice, indicating intestinal insulin resistance. These parameters were normalized by nobiletin. Measurement of plasma TG following an oral gavage of 150ul olive oil revealed a 3-fold elevation in the total TG area under the curve, which was prevented by nobiletin. Intestinal CM production was determined by injection of mice with poloxamer-407 to inhibit plasma TG-rich lipoprotein lipolysis followed by a gavage containing olive oil and 3H-triolein. Although plasma TG was higher at baseline in HFHC-fed mice, no difference in secretion rates of TG mass or TG radioactivity was observed compared to nobiletin-treated or chow-fed mice. However, secretion of apoB48 was elevated by 20% in HFHC-fed mice, whereas nobiletin decreased apoB48 secretion to levels observed in chow-fed mice. These results indicate that nobiletin prevents intestinal TG accumulation and apoB48 overproduction induced by a HFHC diet, in part, through correction of intestinal insulin resistance.

Genome-wide association studies identified novel loci for non-high-density lipoprotein cholesterol and its postprandial lipemic response

Non-high-density lipoprotein cholesterol(NHDL) is an independent and superior predictor of CVD risk as compared to low-density lipoprotein alone. It represents a spectrum of atherogenic lipid fractions with possibly a distinct genomic signature. We performed genome-wide association studies (GWAS) to identify loci influencing baseline NHDL and its postprandial lipemic (PPL) response. We carried out GWAS in 4,241 participants of European descent. Our discovery cohort included 928 subjects from the Genetics of Lipid-Lowering Drugs and Diet Network Study. Our replication cohorts included 3,313 subjects from the Heredity and Phenotype Intervention Heart Study and Family Heart Study. A linear mixed model using the kinship matrix was used for association tests. The best association signal was found in a tri-genic region at RHOQ-PIGF-CRIPT for baseline NHDL (lead SNP rs6544903, discovery p = 7e-7, MAF = 2 %; validation p = 6e-4 at 0.1 kb upstream neighboring SNP rs3768725, and 5e-4 at 0.7 kb downstream neighboring SNP rs6733143, MAF = 10 %). The lead and neighboring SNPs were not perfect surrogate proxies to each other (D' = 1, r (2) = 0.003) but they seemed to be partially dependent (likelihood ration test p = 0.04). Other suggestive loci (discovery p < 1e-6) included LOC100419812 and LOC100288337 for baseline NHDL, and LOC100420502 and CDH13 for NHDL PPL response that were not replicated (p > 0.01). The current and first GWAS of NHDL yielded an interesting common variant in RHOQ-PIGF-CRIPT influencing baseline NHDL levels. Another common variant in CDH13 for NHDL response to dietary high-fat intake challenge was also suggested. Further validations for both loci from large independent studies, especially interventional studies, are warranted.

Modulation of human postprandial lipemia by changing ratios of polyunsaturated to saturated (P/S) fatty acid content of blended dietary fats: a cross-over design with repeated measures.

BackgroundPostprandial lipemia (PL) contributes to coronary artery disease. The fatty acid composition of dietary fats is potentially a modifiable factor in modulating PL response.MethodsThis human postprandial study evaluated 3 edible fat blends with differing polyunsaturated to saturated fatty acids (P/S) ratios (POL = 0.27, AHA = 1.00, PCAN = 1.32). A cross-over design included mildly hypercholestrolemic subjects (9 men and 6 women) preconditioned on test diets fats at 31% energy for 7 days prior to the postprandial challenge on the 8th day with 50 g test fat. Plasma lipids and lipoproteins were monitored at 0, 1.5, 3.5, 5.5 and 7 hr.ResultsPlasma triacylglycerol (TAG) concentrations in response to POL, AHA or PCAN meals were not significant for time x test meal interactions (P > 0.05) despite an observed trend (POL > AHA > PCAN). TAG area-under-the-curve (AUC) increased by 22.58% after POL and 7.63% after PCAN compared to AHA treatments (P > 0.05). Plasma total cholesterol (TC) response was not significant between meals (P > 0.05). Varying P/S ratios of test meals significantly altered prandial high density lipoprotein-cholesterol (HDL-C) concentrations (P < 0.001) which increased with decreasing P/S ratio (POL > AHA > PCAN). Paired comparisons was significant between POL vs PCAN (P = 0.009) but not with AHA or between AHA vs PCAN (P > 0.05). A significantly higher HDL-C AUC for POL vs AHA (P = 0.015) and PCAN (P = 0.001) was observed. HDL-C AUC increased for POL by 25.38% and 16.0% compared to PCAN and AHA respectively. Plasma low density lipoprotein-cholesterol (LDL-C) concentrations was significant (P = 0.005) between meals and significantly lowest after POL meal compared to PCAN (P = 0.004) and AHA (P > 0.05) but not between AHA vs PCAN (P > 0.05). AUC for LDL-C was not significant between diets (P > 0.05). Palmitic (C16:0), oleic (C18:1), linoleic (C18:2) and linolenic (C18:3) acids in TAGs and cholesteryl esters were significantly modulated by meal source (P < 0.05).ConclusionsP/S ratio of dietary fats significantly affected prandial HDL-C levels without affecting lipemia.

Within-person variation in the postprandial lipemic response of healthy adults

The response to dietary fat plays a key role in metabolic health. Although this can vary widely between individuals, variation within an individual and the associated contribution of phenotypic and genotypic factors to this variation are less defined. The objectives were to quantify within-person variation in triacylglycerol response by means of a novel variation score (S(v)) and to explore the phenotypic and genotypic factors associated with this score. Two consecutive 5-h oral-lipid-tolerance tests (OLTTs) were conducted in 51 healthy adults aged 18-60 y with a BMI (in kg/m²) of 18.5 to 49.8. Detailed body composition, physical function, biochemistry, and genotype data were gathered. The postprandial triacylglycerol response profile did not differ (P = 0.64) across OLTTs for the group; nor did average concentrations of functional markers apolipoprotein C2 (P = 0.73) and apolipoprotein C3 (P = 0.74). S(v) was low in most (82%) of the adults and was significantly (P < 0.05) associated with age, fasting triacylglycerol, triacylglycerol AUC, and fasting nonessential fatty acids. Significant associations were also observed between S(v) and single nucleotide polymorphisms in 7 genes (APOA1, IL1α, IL1β, TLR4, TCF7L2, CCK1Rec, and STAT3) after correction for phenotypic differences. This work showed that the within-person variability in postprandial lipemic response is low in most healthy adults. It also showed that variability in this response is associated with a defined set of phenotypic and genotypic characteristics.

Scientific Opinion on the substantiation of a health claim related to Vichy Catalan carbonated natural mineral water and reduction of post‐prandial lipaemic response pursuant to Article 13(5) of Regulation (EC) No 1924/2006

Following an application from S.A. Vichy Catalan, submitted for authorisation of a health claim pursuant to Article 13(5) of Regulation (EC) No 1924/2006 via the Competent Authority of Spain, the Panel on Dietetic Products, Nutrition and Allergies (NDA) was asked to deliver an opinion on the scientific substantiation of a health claim related to Vichy Catalan carbonated natural mineral water and reduction of post-prandial lipaemic response. The food, Vichy Catalan carbonated natural mineral water, that is the subject of the health claim is sufficiently characterised. The claimed effect, reduction of post-prandial lipaemic response, is a beneficial physiological effect. In weighing the evidence, the Panel took into account that the results of the only study from which conclusions could be drawn for the scientific substantiation of the claim do not support an effect of Vichy Catalan carbonated natural mineral water on the reduction of post-prandial lipaemic response. A cause and effect relationship has not been established between the consumption of Vichy Catalan carbonated natural mineral water and reduction of post-prandial lipaemic response.

The fiber and/or polyphenols present in lingonberries null the glycemic effect of the sugars present in the berries when consumed together with added glucose in healthy human volunteers

This study was undertaken on the broad hypothesis that lingonberry (Vaccinium vitis-idaea L.) has potential to reduce postprandial glycemic and lipemic response. More specifically, 2 postprandial crossover studies with healthy normal-weight male subjects were conducted to study the influence of commercial lingonberry powder on postprandial glycemia and lipemia. The test meals contained fat-free yoghurt with either glucose (50 g) or triacylglycerols (35 g) with or without (control) the lingonberry powder. The lingonberry powder provided the meals with a known amount of fiber and a known amount and composition of sugars, and it was a rich source of polyphenols. Postprandial glucose, insulin, and triacylglycerol responses were analyzed. There were no significant differences in the postprandial glucose concentration between the meals in the glycemia trial despite the fact that the lingonberry meal contained more glucose and fructose. When the meal did not contain added sugar but, instead, added triacylglycerol, no glycemia or lipemia-lowering effect was detected. On the contrary, there were indications of higher glycemic and insulinemic effect after the lingonberry meal. The results of this study indicate that the fibers and/or polyphenols present in lingonberries null the glycemic effect of the sugars present in the berries when consumed together with added glucose. By contrast, the lingonberry powder did not affect the postprandial lipemic response.

Effect of Overweight and Obesity on Postprandial Lipemia among the Subjects with Type 2 Diabetes

Introduction: The prevalence of type 2 diabetes mellitus (DM) and obesity is actually mountingspeedily in Westernized and developing countries. Type 2 diabetes (T2D) is a complex pathology with several risk factors.It is recently known through several studies that postprandial hyperlipemia is a significant and independent risk factor for cardiovascular disease. In fact, numerous alterations in plasma lipid and lipoprotein concentrations are found in obese patients. Method: The study, which concerned 51 patients with type 2 diabetes, took place in Diabetic Center (Ex. Gambetta) and in the division of Diabetes and Endocrinology at University Hospital (Hassani Abdelkader, Sidi-Bel-Abbes). The aim was to evaluate the relationship between the postprandial lipemia response and overweight and obesity in the type 2 diabetes. The weight, height, waist and hip circumferences, Body Mass Index (BMI) and Waist to Hip Ratio (WHR) were measured. Blood samples were analyzed for total cholesterol, glucose, triglycerides, HDL-cholesterol and LDL-c 2h after meal, fasting glucose. Result: The obtained result determined a correlation between postprandial triglycerides concentration and the BMI especially in overweight and obese women with r 2 = 0.09 and correlation r 2 = 0.01 for men. PPHDL-c was highly elevated among women than men with a significant differences (60.44± 24.17 mg/dL vs. 43.30±18.27 mg/dL; p = 0.016).PPTG among women than men with significant differences (168.33±71.37 mg/ dL vs.121.87±60.84 mg/dL; p=003).It has been noticed that the PPHDL-c was inversely linked to fasting glucose levels (r 2 =0.07) and to the BMI values (r=0.12; p=0.34) among women. Conclusion: The management and loss of weight still indispensible for type 2 diabetic subjects especially overweight and obese women one to avoid postprandial hypertriglyceridemia and its complications mainly coronary heart disease.

Phenotypic and genotypic determinants of postprandial lipaemic response variation in healthy adults

Phenotypic and genotypic determinants of postprandial lipaemic response variation in healthy adults

Morning exercise appears to promote greater fat oxidation and reduce postprandial lipaemic response more than evening exercise

Morning exercise appears to promote greater fat oxidation and reduce postprandial lipaemic response more than evening exercise

Body mass interacts with fat quality to determine the postprandial lipoprotein response in healthy young adults

Background and aimsPostprandial lipemia predicts the evolution of cardiovascular disease. Obesity is associated with an increase in the magnitude of postprandial lipemia. Our objective was to evaluate the influence of body mass index (BMI) on the effects of acute ingestion of different types of fat on the postprandial lipemic response. Methods and resultsTwenty-one healthy men followed a 4-week baseline diet and then consumed three fat-loaded meals that included 1g fat/kg body wt (65%fat) according to a randomized crossover design. The compositions of the three meals were olive oil meal (22% saturated fatty acids (SFA), 38% monounsaturated fatty acids (MUFA), 4% polyunsaturated fatty acids (PUFA)); butter meal (35% SFA, 22% MUFA, 4% PUFA); walnuts meal (20% SFA, 24% MUFA, 16% PUFA, and 4% α-linolenic acid). Higher-weight (HW) subjects (BMI greater than the median 26.18kg/m2, n=11) presented higher incremental area under the curve (iAUC) for triglycerides (TG), both in large- and small-TG rich lipoproteins (TRL) than lower-weight (LW) subjects (BMI<26.18kg/m2, n=10) (p<0.05), and a similar trend for plasma TG (p=0.084). Moreover, HW subjects presented higher concentrations for small TRL-cholesterol and small TRL-TG in different timepoints of the postprandial lipemia after the intake of enriched walnuts or butter meals compared with the olive oil-enriched meal (p<0.05) No significant differences were observed between the three types of meals in the postprandial response of LW subjects. ConclusionHW subjects present a greater postprandial response than LW subjects, and they benefit from the consumption of monounsaturated fatty acids from olive oil, to lower their levels of TRL particles during the postprandial state.

The Influence of Visceral Fat on the Postprandial Lipemic Response in Men with Paraplegia

Background: Postprandial lipemia (PPL) is associated with vascular dysfunction and may be an etiologic factor in the progression of atherogenic cardiovascular disease.Objective: In 10 men with paraplegia and 10 able-bodied men, the magnitude of the PPL responses and the relationship of abdominal adiposity and the PPL responses were determined.Methods: Anthropometrics, dual energy x-ray absorptiometry, and abdominal ultrasonography were performed to determine visceral fat and total body fat. A fasting lipid profile was performed. A high-fat milkshake (1.3 g fat/kg body mass) was administered with serum collected at baseline and at 2, 4, and 6 hours after the test meal for subsequent measurement of triglyceride. The triglyceride response was determined by the area under the triglyceride curve.Results: No significant differences were noted between the groups in fasting lipid values or in measures of visceral fat. Total body fat tended to be higher in men with paraplegia than in able-bodied men (34.9 ± 10.0 vs. 27.3 ± 6.7%, p = 0.07). No significant difference between the groups was observed in triglyceride response. In men with paraplegia, visceral fat was strongly associated with the triglyceride (r = 0.8, p = 0.005), fasting low-density lipoprotein (r = 0.66, p = 0.04), and triglyceride responses (r = 0.80, p = 0.005); a significant relationship was not found between fasting high-density lipoprotein and any measure of adiposity. In men with paraplegia, triglyceride response was positively related to all measures of abdominal adiposity.Conclusion: Visceral abdominal fat was related to delayed triglyceride clearance after a fat load, which may contribute to coronary heart disease (CHD) risk and progression of vascular disease in men with paraplegia.

Postprandial lipemic response to alpha‐linolenic acid rich oil, butter, and olive oil

AbstractPostprandial lipemia varies with composition of dietary fat due to partitioning of fatty acids between β‐oxidation, incorporation into TAG, and tissue lipids. Effects of alpha‐linolenic acid (ALA) are poorly characterized. Lipase‐catalyzed transesterification was used to produce a novel ALA‐oil (35% ALA) from rapeseed and linseed oil. We hypothesized a lower postprandial lipemic response with ALA‐oil than with olive oil and butter due to higher β‐oxidation of ALA. A randomized crossover study with 26 healthy men compared the effects on plasma lipids 7 h after a breakfast containing 35 g ALA‐rich oil, butter fat, or olive oil. The incremental area under curve for plasma TAG was lower with butter than with olive oil (34%, p&lt;0.05) and ALA‐oil (25%, ns). After ALA‐oil percentage ALA increased, in TAG to a constant level of 7 mol% and in NEFA to 6% after 7 h. Since total NEFA increased with time the amount of exogenous ALA in NEFA also increased. Butter resulted in lower postprandial lipemia than the oils, the difference exceeding what is expected from the presence of short and medium chain fatty acids in butter. There was a considerable recirculation of ALA into the NEFA pool available for oxidation.Practical application: Enzymatic transesterification was used to produce a dietary oil rich in ALA. By randomizing the partitioning of ALA more evenly between the TAG molecules the risk of oxidation could be reduced. Analyses showed that the ALA‐oil was stable during storage for at least 3 months. Enzymatic transesterification could be used as an advantageous method to design an ALA rich dietary oil with new properties regarding fatty acid composition, susceptibility to oxidation, and effects on blood lipids.

Postprandial Lipemia and Fitness Status

Elevated postprandial triglycerides (postprandial lipemia; PPL) are a risk factor for the development of coronary artery disease. Chronic exercise training and the maintenance of high levels of aerobic fitness may lead to an attenuated PPL response. However, some research indicates this is due to the effects of recent exercise as acute bouts of exercise can attenuate the postprandial rise in triglycerides in active and sedentary individuals. Furthermore, to induce the PPL response, most research utilizes high-fat meal challenges which may not represent typical eating habits. PURPOSE: To investigate the role of aerobic fitness status on PPL after a 60-hr period of exercise avoidance and following the ingestion of a mixed-macronutrient nutritional beverage (360 kcal; 15% Protein, 50% Carbohyrdate, 35% Fat). METHODS: Sixteen healthy, young (22 ± 3 yrs) men participated in this IRB approved investigation. The men were categorized according to aerobic fitness (VO2max: 42.50 ± 4.0 ml/kg/min for the low group, n=8, and 58.0 ± 3.2 ml/kg/min for the high group, n=8). Plasma triglyceride levels were measured at baseline and hourly for four hours following ingestion of the meal. All data reported as mean ± standard deviation. Area under the curve (AUC) and subject characteristic data were analyzed with independent t-tests and group x time interactions of select variables were analyzed using a repeated-measures ANOVA model. Statistical significance was accepted at P < 0.05. RESULTS: Following ingestion of the meal, the four-hour incremental AUC was greater in the low aerobic fitness group than in the high aerobic fitness group (1608.37 ± 863.86 vs. 791.05 ± 234.38 mmol/l/480min; p = 0.022). CONCLUSION: In this sample of men, those with high aerobic fitness displayed an attenuated postprandial lipemic response as compared to those with low aerobic fitness after 60-hr of exercise avoidance. Funded in part by the Office of Research and Sponsored Programs at Ohio University

Predicting Postprandial Lipemia in Healthy Adults and in At‐Risk Individuals With Components of the Cardiometabolic Syndrome

To determine whether a single-point triglyceride (TG) concentration could estimate the 8-hour postprandial lipemic (PPL) response, men and women performed baseline PPL (n=188) and postexercise PPL (n=92) trials. Correlations were generated between TG concentrations at baseline and at various time points after a high-fat meal vs 8-hour area under the TG curve (TG-AUC) and peak TG level. Stepwise multiple regression and bootstrap simulations using TG level and additional predictor variables of sex, age, percentage of body fat, training status, and maximal oxygen consumption indicated that the 4-hour TG concentrations accounted for >90% of the variance in TG-AUC and peak TG responses during the PPL trials. Equations were confirmed by cross-validation in healthy as well as at-risk individuals with components of the cardiometabolic syndrome. Our data suggest that the 4-hour TG value is highly related to the total 8-hour PPL response and can be used for accurate estimation of PPL in a clinical or research setting.