Postprandial Lipemic Response Research Articles

Glucokinase regulatory protein gene polymorphism affects postprandial lipemic response in a dietary intervention study

Postprandial triglyceridemia is an emerging risk factor for cardiovascular disease. However, most of the genes that influence postprandial triglyceridemia are not known. We evaluated whether a common nonsynonymous SNP rs1260326/P446L in the glucokinase regulatory protein (GCKR) gene influenced variation in the postprandial lipid response after a high-fat challenge in seven hundred and seventy participants in the Amish HAPI Heart Study who underwent an oral high-fat challenge and had blood samples taken in the fasting state and during the postprandial phase at 1, 2, 3, 4, and 6 h. We found that the minor T allele at rs1260326 was associated with significantly higher fasting TG levels after adjusting for age, sex, and family structure (P (a) = 0.06 for additive model, and P (r) = 0.0003 for recessive model). During the fat challenge, the T allele was associated with significantly higher maximum TG level (P (a) = 0.006), incremental maximum TG level (P (a) = 0.006), TG area under the curve (P (a) = 0.02) and incremental TG area under the curve (P (a) = 0.03). Our data indicate that the rs1260326 T allele of GCKR is associated with both higher fasting levels of TG as well as the postprandial TG response, which may result in higher atherogenic risk.

Exaggerated Postprandial Triglyceride Response Identified In Individuals With Spinal Cord Injury With Cardiac Risk Factors

Able-bodied individuals who have a greater number of cardiac risk factors and greater abdominal adiposity have increased difficulty in metabolizing fat loads, resulting in prolonged elevation of postprandial triglyceride. The lipemic response to a high fat meal and its relationship to abdominal adiposity and coronary heart disease (CHD) is unknown in individuals with spinal cord injury (SCI). PURPOSE: To compare the postprandial lipemic (PPTG) responses, abdominal adiposity and CHD factors between able-bodied (AB) and individuals with SCI. METHODS: Twenty-five men with SCI (13 paraplegia, 12 tetraplegia) and 13 able-bodied (AB) men participated. The CHD risk factors were determined and subjects were stratified as having low risk (2 or less risk factors) or elevated risk (3+ risk factors). Following a 10-hour fast, a high-fat milkshake was consumed to deliver approximately 1.3 g fat, 1.2 g carbohydrate, and 0.2 g protein per kilogram body mass. Blood samples were drawn at baseline, 2, 4, and 6 hours to measure PPTG, determined as the area under the curve. Total abdominal fat (TAF) was measured by abdominal ultrasonography. RESULTS: SCI and AB subjects were similar in age, height, and weight. In AB and SCI subjects, TAF was significantly related to PPTG responses (R=0.49, P=0.02). TAF in low risk SCI was significantly less in AB with elevated risk (P=0.02) and SCI with elevated risk (P=0.01). SCI with elevated risk had the greatest PPTG response compared to low and elevated risk AB (2053±911 vs. 1356±633, and 1725±981 units, respectively), which was significantly greater than low risk SCI (1016±333 units, P=0.01). When controlling for TAF, the groups with SCI at low and elevated CHD risk had a PPTG response that was greater by 183±83 and 366±83 units, respectively, than the low risk AB group (P=0.001). CONCLUSIONS: Individuals with SCI appear to exhibit a greater postprandial response after a fat load than their able-bodied counterparts. An exaggerated postprandial response may be associated with greater overall cardiac risk in SCI. Supported by RR&D Center of Excellence on the Medical Consequences of Spinal Cord Injury # B2648C

Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects

An exaggerated postprandial lipemic response is associated with increased risk of coronary heart disease, due to acute effects on lipids, oxidative stress, hemostatic factors and vascular function. Lipid released slowly from a complex food matrix during digestion may attenuate postprandial lipemia1. The present study therefore investigates the effects of lipid release (lipid bioaccessibility (LB)) on postprandial changes (over 8h) in plasma triacylglycerol (TAG) concentration, oxidative stress (measured by 8‐isoprostane F2α) and vascular function (measured by peripheral augmentation index (PAIx)). Subjects (n = 20, aged 18–40y) were fed test meals containing 50g fat of low LB (intact whole almonds; WA), high LB (almond oil + defatted almond flour; AO) or as a control meal (CO) in a randomised cross‐over design, with 1‐wk washout. The postprandial increase in plasma TAG was significantly lower (74% & 58% lower incremental area under curve) following the WA vs. the AO and CO meals, respectively (P<0.001). The peak reduction in PAIx (by −9.5%, −10.1% & −12.6% at 2h following WA, AO and CO meals respectively, time effect; P<0.001) was not significantly different between meals. There were no changes in plasma 8‐isoprostane F2α concentrations. Reducing LB of almonds beneficially influences postprandial lipemia.This study was funded by the Almond Board of California

Effect of Prior Exercise on Postprandial Triglycerides in Overweight Young Women after Ingesting a High-Carbohydrate Meal

To examine the effect of prior exercise on the postprandial lipid response to a high-carbohydrate meal in normal-weight (NW=BMI <25) and overweight (OW=BMI >or= 25) women (age 18-25), 10 NW and 10 OW participants completed 2 conditions separated by 1 month. In the morning, the day after control (CT=no exercise) or exercise conditions (EX=60 min cycling at 60% VO(2peak)), participants consumed a high-carbohydrate meal (80% CHO, 15% protein, 5% fat; 75 kJ/kg BM) followed by 6 hr of hourly blood sampling. Blood was analyzed for triglycerides (TG), blood glucose (BG), and insulin (IN). TG levels over the 6-hr period were lower in NW than OW (p= .021) and lower in EX than in CT (p= .006). Area under the curve (AUC) for TG was lower in NW than OW (p= .016) and EX than CT (p= .003). There were nonsignificant tendencies for reduced BG over time (p= .053) and AUC (p= .083), and IN AUC was lower in EX than in CT (p= .040) for both groups and lower in NW than in OW (p= .039). Prior exercise improved TG levels after a high-carbohydrate meal in both groups, and OW women demonstrated a greater postprandial lipemic response than NW regardless of condition. There were tendencies for improved glucose removal with prior exercise in NW vs. OW. Acute exercise can improve postprandial TG responses and might also improve postprandial BG and IN after a large meal in NW and OW young women.

Reply by Zafeiridis and Mougios

We thank Drs Burns and Stensel for their interest in our work. We agree that the published articles on the delayed effect of resistance exercise (RE) on postprandial lipaemia (PL) provide controversial results. Three studies1–3 employed comparable methodologies in terms of exercise protocol and feeding plan of the subjects, that is, two to four sets of eight to eleven exercises at relatively similar intensities (about 10–12 repetitions maximum (RM)) with 1·5–2·0 min of rest between sets and a standardised meal on the night prior to the fat tolerance test. These studies reported a decrease1,3 or no change2 in the postprandial lipaemic response. A fourth study4 employed a similar RE protocol but focused on maintaining the subjects in a state of energy balance by increasing food intake up to two-fold after RE v. control on the night prior to the fat tolerance test. This study found no significant effect of RE on PL.

The solid fat content of stearic acid–rich fats determines their postprandial effects

Background:The process of randomization is used commercially to harden fats as an alternative to partial hydrogenation, but its effects on cardiovascular disease risk factors are uncertain.Objective:The objective was to compare the chronic and acute effects of randomization of a fat rich in 1,3-distearyl, 2-oleyl glycerol on fasting and postprandial lipids, glucose, insulin, and activated clotting factor VII (FVIIa) concentrations.Design:A crossover design study in 16 men compared fasting and postprandial lipid, glucose, insulin, and FVIIa concentrations at baseline and after a 3-wk diet providing 30 g unrandomized or randomized shea butter and sunflower oil blends (SSOBs), both of which contained ≈50% stearic acid. Fecal fat excretion was measured during each dietary period. Postprandial changes were assessed after the consumption of meals providing 50 g test fat. A subsequent study compared postprandial changes after the consumption of an oleic acid–rich sunflower oil meal and an unrandomized SSOB meal.Results:Both SSOBs were well digested and absorbed. Randomization did not affect fasting or postprandial lipid, glucose, insulin, or FVIIa concentrations. Compared with the oleic acid–rich meal, the unrandomized SSOB resulted in 53% lower postprandial lipemia, 23% higher hepatic lipase activity, and a 25% lower postprandial increase in FVIIa concentration. The solid fat contents at 37 °C were 22%, 41%, and 0% with the unrandomized SSOB, randomized SSOB, and oleic acid–rich meals, respectively.Conclusions:Stearic acid–rich triacylglycerol in both unrandomized and randomized forms does not adversely affect lipid risk factors for cardiovascular disease. The high proportion of solid fat at 37 °C may explain the decreased postprandial lipemic response.

Meal fatty acids and postprandial vascular reactivity

With increasing recognition of the pivotal role of vascular dysfunction in the progression of atherosclerosis, the vasculature has emerged as an important target for dietary therapies. Recent studies have indicated that chronic fatty acid manipulation alters vascular reactivity, when measured after an overnight fast. However, individuals spend a large proportion of the day in the postprandial (non-fasted) state. Several studies have shown that high fat meals can impair endothelial function within 3-4 h, a time period often associated with peak postprandial lipaemia. Although the impact of meal fatty acids on the magnitude and duration of the postprandial lipaemic response has been extensively studied, very little is known about their impact on vascular reactivity after a meal.

Estimating Postprandial Lipemia Using A Single Point TViglyceride Concentration

Traditionally, postprandial lipemia (PPL) has been measured through a time consuming process in which subjects are fed a high-fat meal and plasma triglyceride (TG) concentrations are measured at two hour time intervals for eight hours. PURPOSE: The purpose of this study was to determine whether a single point triglyceride (TG) concentration could be used to accurately estimate the 8h postprandial lipemic response with and without exercise. METHODS: Baseline PPL trials (N = 205; 111 males, 94 females) and exercise PPL trials (N = 105; 61 males, 44 females) were used to generate Pearson correlations between TG concentrations at 0h (baseline) and time points up to 8h after a high-fat meal vs. the PPL response quantified as area under the TG curve (TG-AUCtot and TG-AUCinc) and peak TG response (TG-peaktot and TG-peakinc). Stepwise multiple regression was used to create prediction equations for PPL measures using additional predictor variables: gender, age, percent body fat, training status, and VO2max. RESULTS: Except training status, all predictor variables significantly correlated with the PPL response, with 4htot TG concentration having the highest correlations with each quantification of PPL (r>0.93, p<0.001), with or without exercise. Multiple regression indicated the 4htot TG concentrations accounted for 94% of the variance in TG-AUCtot (p<0.001), with baseline TG values only adding a slight contribution to the model (R2adj=0.96, p<0.001). The4hinc TG concentration accountedfor 86% of thevariance in TG-AUCinc. Results were similar for 4h TG concentrations in predicting TG-peak responses. Other predictor variables did not significantly contribute to the models. Cross-validation on additional trials (n=119) indicated that predicted values were highly correlated with actual values, e.g., TG-AUCtot r=.98, p < 0.001. CONCLUSIONS: Our data suggest that the 4h TG concentration is highly related to the total 8h PPL response and can be used for accurate estimation of PPL. The abbreviated single point method could be useful in clinical risk factor assessment.

The −250G/A polymorphism in the hepatic lipase gene promoter influences the postprandial lipemic response in healthy men

Background and aim The −250G/A promoter polymorphism of the hepatic lipase gene has been associated with changes in the activity of the enzyme. We investigated whether this polymorphism modifies the postprandial response of triacylglycerol-rich lipoproteins (TRL) in young normolipemic males. Methods and results Fifty-one healthy apolipoprotein (apo) E3/E3 male volunteers (30 G/G and 21 carriers of the A allele) underwent a vitamin A fat-loading test and blood samples were drawn every hour until the 6th, and every 2 h and 30 min until the 11th. Total plasma cholesterol and triacylglycerols (TG), as well as cholesterol, TG and retinyl palmitate (RP) in TRL, isolated by ultracentrifugation, were determined. Carriers of the A allele showed a higher response ( P = 0.008), a higher area under the curve (AUC; P = 0.022) and a lower RP peak time ( P = 0.029) in small TRL during the postprandial response, as well as a lower peak time in total plasma TG levels ( P = 0.034) and large TRL-TG ( P = 0.033) than subjects who were homozygous for the G allele. Conclusion Our data indicate that the presence of the A allele in the −250G/A promoter polymorphism of the hepatic lipase gene is associated with a higher postprandial lipemic response.

Effects of low- and high-volume resistance exercise on postprandial lipaemia

Postprandial lipaemia (PL) is associated with the metabolic syndrome, CVD and endothelial dysfunction. Aerobic exercise has been shown to reduce PL. Although resistance exercise is recommended for the improvement of the quality of life, management of body weight and prevention of several disorders, its effect on PL has received little attention. The present study examined the effects of low-volume resistance exercise (LVRE) and high-volume resistance exercise (HVRE) on PL. Ten healthy young men performed three trials, each conducted over 2 d. On the afternoon of day 1, they either refrained from exercise (control), performed LVRE (two sets of eight exercises, twelve repetitions at twelve repetitions maximum (RM) in each set; energy expenditure 0 x 76 MJ), or performed HVRE (four sets of eight exercises, twelve repetitions at 12 RM in each set; energy expenditure 1 x 40 MJ). On the morning of day 2 they consumed a meal containing 67 kJ/kg body weight, of which 65 % energy was from fat. Blood samples were obtained in the fasted state and for 6 h postprandially. The total area under the TAG curve (AUC; mmol/l x h) was lower (P<0 x 05) in HVRE (8 x 76 (sd 3 x 20)) and LVRE (9 x 29 (sd 3 x 64)) compared with control (11 x 60 (sd 4 x 35)). The incremental AUC was lower in HVRE compared with control (3 x 07 (sd 2 x 53) v. 5 x 58 (sd 3 x 72)), but not different between LVRE (3 x 86 (sd 2 x 29)) and control. In conclusion, resistance exercise of 1 x 40 MJ (four sets - eight exercises - twelve RM) or 0 x 76 MJ (two sets - eight exercises - twelve RM) before a high-fat meal reduces the total postprandial lipaemic response.

Postprandial Lipemia is Modified by the Presence of the APOB‐516C/T Polymorphism in a Healthy Caucasian Population

Apolipoprotein (apoB) plays a fundamental role in the transport and metabolism of plasma triacylglycerols (TAGs) and cholesterol. Several apoB polymorphic sites have been studied for their potential use as markers for coronary heart disease in the population. In view of the importance of apoB in postprandial metabolism, our objective was to determine whether the presence of the -516C/T polymorphism in the APOB gene promoter could influence postprandial lipoprotein metabolism in healthy subjects. Forty-seven volunteers who were homozygous for the E3 allele at the APOE gene were selected (30 homozygous for the common genotype (C/C) and 17 heterozygotes for the -516T allele (C/T). They were given a fat-rich meal containing 1 g fat and 7 mg cholesterol per kg body weight and vitamin A 60,000 IU/m(2) body surface. Fat accounted for 60% of calories, and protein and carbohydrates for 15 and 25% of energy, respectively. Blood samples were taken at time 0, every 1 h until 6 h, and every 2.5 h until 11 h. Total cholesterol and TAGs in plasma, and cholesterol, TAGs and retinyl palmitate in triacylglycerol-rich lipoproteins (large and small triacylglycerol-rich lipoproteins) were determined by ultracentrifugation. Individuals carrying the C/T genotype presented greater postprandial concentrations of TAGs in small triacylglycerol-rich lipoproteins than did carriers of the C/C genotype (P = 0.022). Moreover, C/T individuals presented higher concentrations of plasma TAGs during the postprandial period than did C/C subjects (P = 0.039). No other statistically significant genotype-related differences for other parameters were observed. These results suggest that the presence of the genotype C/T is associated with a higher postprandial response. Thus, the allele variability in the -516C/T polymorphism in the APOB gene promoter may partly explain the interindividual differences in postprandial lipemic response in healthy subjects.

Comparison of Low-Fat Meal and High-Fat Meal on Postprandial Lipemic Response in Non-Obese Men according to the −1131T>C Polymorphism of the Apolipoprotein A5 (APOA5) Gene (Randomized Cross-Over Design)

Objective: The purpose of this study was to compare low-fat (LF) meal and high-fat (HF) meal on the postprandial lipemic responses according to the −1131T>C polymorphism of the APOA5 gene in a population usually consuming a LF diet and having a high frequency of the variant allele at the APOA5 −1131T>C SNP.Methods: This study was conducted using a cross-over design and 49 non-obese healthy men (42.8 ± 0.7 yrs, 23.9 ± 0.25 kg/m2) participated in the meal tolerance test. They were randomly assigned to consume one of two types of experimental enteral formulae (LF vs HF) with a seven-day interval. Blood samples were collected at 0, 2, 3, 4 and 6h after ingestion and analyzed for total and chylomicron TG, glucose, insulin and free fatty acid.Results: No differences were found in anthropometic parameter, calorie and macronutrient intakes and total energy expenditure between TT (n = 23) and TC + CC (n = 26) men. Fasting total TG were higher in TC + CC men than TT men, but fasting chylomicron TG were not significantly different between TT men and C carriers, TT subjects had no significant differences in postprandial responses of total TG and chylomicron TG and postprandial mean changes of chylomicron TG between LF and HF meal. On the other hand, C carriers had delayed peak time of total TG compared to TT subject and higher postprandial response and mean changes of chylomicron TG at HF meal compared to LF meal.Conclusion: The capacity to clear chylomicron-TG or hydrolyze TG might become a rate-limiting factor on HF diet in TC + CC men resulting in higher postprandial triglyceridemia. Therefore, HF diet for C carriers of the APOA5 gene may be one of important CVD risk factors.

Postprandial lipid metabolism

Atherogenic effects of postprandial lipoproteins are supported by many studies comparing patients with advanced clinical signs or early markers of cardiovascular disease with subjects without vascular disease. Postprandial lipoprotein abnormalities are more frequent in individuals with type 2 diabetes and other states of insulin resistance, which could be a major factor accounting for the higher rate of cardiovascular diseases observed in these conditions. In patients with type 2 diabetes multiple abnormalities of lipoproteins of both endogenous and exogenous origin are observed also in the presence of good blood glucose control and normal fasting triglyceridaemia, and a direct role of insulin resistance in the development of postprandial dyslipidaemia has been demonstrated. Clinical and experimental studies have demonstrated that a high fat consumption is associated with impaired insulin sensitivity and may worsen postprandial hypertriglyceridemia in individuals with type 2 diabetes and/or hyperlipidaemia. In addition to the amount of fat also the physical structure of the food in which fat is present is able to influence postprandial lipaemia. Data on the effects of dietary fatty acid (FA) modifications in humans are scarce. These studies have provided some evidence that dietary polyunsaturated FA, particularly those of the n-3 class, induce an attenuated postprandial lipaemic response as compared to saturated FA (SFA) and monounsaturated FA (MUFA); however, the data are often conflicting and their interpretation is, generally, controversial. Very little is known in patients with type 2 diabetes, in whom both insulin sensitivity and postprandial lipaemia are particularly relevant. In a medium term (3 weeks) study in type 2 diabetic patients, a MUFA rich diet did not modify insulin sensitivity as compared to the SFA rich diet. The MUFA diet induced a higher early peak of chylomicrons and a significantly lower postprandial response o f small VLDL after a standard test meal, rich in saturated fat. In conclusion, postprandial lipoprotein abnormalities are a frequent feature of type 2 diabetes and of other conditions clustering with insulin resistance. The total amount of fat, more than the specific type of fatty acid, seems to influence postprandial lipoproteins. Data are needed on long term interventions as well as on the interactions between dietary fat and other food components or physical structure. Keywords: postprandial lipoproteins; metabolism of dietary fat

Omega-3 Fatty Acid Supplementation and Exercise Training Attenuate Postprandial Lipemia in Sedentary Individuals

Omega-3 fatty acid (n-3fa) supplementation and exercise training each can attenuate postprandial lipemia (PPL), but the combination effect is not clear in sedentary individuals. PURPOSE: We examined the effects of four weeks of n-3fa supplementation alone or in combination with aerobic training on the PPL response and high density lipoprotein cholesterol (HDL-C) in previously sedentary individuals. METHODS: Previously sedentary subjects (N=20, 12 women, 8 men, mean age 33y, mean BMI 26 kg/m2) were randomly assigned to one of two treatment groups: n-3fa supplementation alone (FO, n=10) or n-3fa supplementation plus exercise training (FO + ExTr, n=10). Both groups consumed 4 g/d n-3fa, while exercise training consisted of 45 min/d, 5d/wk of walking and/or treadmill jogging at 60% VO2max. Before treatment subjects performed a baseline PPL (Pre-PPL) and an acute exercise PPL (Pre-ExPPL), after a 24h controlled diet including a 12h fast overnight. In Ex-PPL, an acute exercise session at 60% VO2max for 60 min was performed 12h prior to the PPL. Subjects were administered a high fat meal (standardized high fat shake, 1.3 g fat/kg), and blood samples were collected pre, 2h, 4h, 6h, and 8h after the high fat meal for triglyceride (TG) analyses. After treatment, the two PPL trials (Post-PPL and Post- ExPPL) were repeated. PPL response was quantified as total area under the TG curve (TG-AUCTol) and TG peak response. HDL-C and subfractions were analyzed in pre high fat meal samples. RESULTS: Acute exercise did not attenuate the PPL response. Together treatments significantly attenuated the PPL response measured as total TG-AUCTol; FO: Pre-PPL 1121.7 ± 84.1 mg/dl *; 8hr (means ± SE), and Post-PPL 1021.2 ± 57.7; FO + ExTr: Pre-PPL 1580.5 ± 184.3, and Post-PPL 1168.1 ± 115.0. There was no significant main effect for group or group by week interaction. Both groups had higher HDL-C and HDL2-C after treatment than before treatment. CONCLUSION: N-3fa supplementation or the combination of n-3fa with aerobic exercise training attenuates the PPL response and improves HDL-C in previously sedentary people. Combination treatment neither magnifies nor attenuates the effect of n-3fa alone on postprandial lipemia. Supported by Food for the 21st Century, MU HES Margaret Mangel Grant, and NIH T32 AR48523.

Hemostatic response to postprandial lipemia before and after exercise training

Chronic hypertriglyceridemia is thought to be atherogenic and is associated with an elevated thrombotic potential, both of which may be improved with aerobic exercise training. Eight subjects were tested for aerobic capacity, body composition, and postprandial lipemia (PPL), followed by 6 mo of exercise training and final testing. Blood samples were obtained for measurement of free fatty acid (FFA), triglycerides (TG), insulin (Ins), and glucose (Glu). Hemostatic variables including factor VII activity (FVIIa), tissue factor pathway inhibitor-factor Xa complex (TFPI/Xa), and plasminogen activator inhibitor-1 (PAI-1) antigen/activity as well as leukocyte tumor necrosis factor-alpha (TNF-alpha) gene expression were determined among four subjects. We found that the exercise training was of sufficient intensity to increase aerobic capacity (P < 0.0001) and improve body composition (P = 0.04). There were no differences between tests among PPL responses of FFA, TG, Ins, or Glu; however, the mean TG response and fat oxidation rate improved. PAI-1 antigen/activity, FVIIa, TFPI/Xa, and TNF-alpha gene expression were all improved after exercise training after adjusting for confounders. We conclude that aerobic exercise training reduces the potential for coagulation, improves fibrinolytic potential, and reduces leukocyte TNF-alpha gene expression after the ingestion of a high-fat meal.

Postprandial lipemic response and lipoprotein composition in subjects with low or high cholesterol absorption efficiency

Backgroud The purpose of this study was to investigate the effect of differences in cholesterol absorption efficiency on the postprandial lipemia and lipoprotein composition. Methods Fifteen healthy subjects were divided into low and high cholesterol absorbers on the basis of serum cholestanol to cholesterol ratio. A high-performance liquid chromatographic method with evaporative light scattering detection was developed for quantitation of free and esterified cholesterol, triglycerides and major phospholipids from the same lipid extract in two runs utilizing the same internal standard. Results The free cholesterol to phosphatidylcholine ratio of chylomicrons was higher in the high cholesterol absorption group. The total increase of cholesterol in combined chylomicron and very low density lipoprotein (VLDL) fraction was also higher in this group. Chylomicron free cholesterol and cholesterol ester responses correlated with fasting low density lipoprotein (LDL) cholesterol. VLDL and VLDL1 triglyceride responses correlated inversely with fasting insulin and homeostasis model assessment of insulin resistance. Conclusions High cholesterol absorption efficiency was seen in chylomicrons as higher cholesterol to phosphatidylcholine ratio during the postprandial peak. Chylomicron cholesterol response was linked to fasting LDL cholesterol and low VLDL triglyceride response to fasting insulin.

Effect of aerobic exercise on lipaemia and its fatty acid profile after a meal of moderate fat content in eumenorrhoeic women

Exercise prior to eating has repeatedly been shown to reduce postprandial lipaemia. The aim of the present study was to investigate whether this effect was manifest in the presence of two factors that independently mitigate postprandial lipaemia: eumenorrhoea and moderate fat intake. Eight healthy eumenorrhoeic rowers consumed a meal of moderate fat content (35 % total energy, 0.66 g/kg body mass) 14 h after having either rowed at 55 % of maximal aerobic power (81 % of maximal heart rate) for 80 min or rested. Both trials were performed during the luteal phase. Blood samples were drawn before the meal and for 8 h postprandially for the measurement of individual fatty acids in the triacylglycerol and NEFA fractions, as well as of glucose, insulin and oestradiol. Plasma oestradiol concentrations were not significantly different in the two trials. The postprandial lipaemic response, expressed as either plasma triacylglycerol concentration or area under the triacylglycerol-time curve, was 35 % lower (P<0.05) after exercise. The postprandial glycaemic and insulinaemic responses were also lower, indicating increased insulin sensitivity, whereas the NEFA response was higher, suggesting a lower entrapment of dietary fatty acids in adipose tissue after exercise. Finally, exercise increased the proportion of unsaturated:saturated NEFA during the postprandial period. In conclusion, aerobic exercise performed 14 h before a moderate-fat meal reduced postprandial lipaemia in women in the luteal phase. This effect shows the potential of exercise to mitigate even moderate lipaemic responses in eumenorrhoeic women.

Resistance exercise and postprandial lipemia: the dose effect of differing volumes of acute resistance exercise bouts

Introduction Resistance exercise has been shown to reduce postprandial lipemia, but no dose-response effect has been established. Purpose The purpose of this study was to determine whether prior resistance exercise exhibited a dose-response effect on postprandial lipemia, while controlling for energy balance. Methods Subjects were healthy resistance-trained men (n = 4) and women (n = 6) aged 23.4 ± 2.5 years. Subjects participated in 4 different treatment conditions consisting of control (no exercise), 1 set, 3 sets, and 5 sets of 8 resistance exercises in a repeated-measures design. On day 1, each exercise was performed at 75% of the subject's 1-repetition maximum for 10 repetitions. This was followed by consumption of a postexercise meal equal in caloric volume designed to maintain energy balance. On day 2, after a 12-hour overnight fast (approximately 13 hours postexercise) in the General Clinical Research Center, subjects consumed a high-fat meal consisting of 1.7 g fat, 1.65 g carbohydrate, 0.25 g-protein per kilogram of fat-free mass and equal to 95 kJ of energy per kilogram of fat-free mass. Blood collections occurred before meal, and at 0.5, 1, 2, 3, 4, 5, and 6 hours after meal consumption and were analyzed for triacylglycerol (TAG), glucose, and insulin concentrations. The lipemic response was evaluated as the area under curve (AUC) for TAG versus time. Glucose and insulin AUCs were also calculated. Results No significant differences were observed among treatments for postprandial lipemia (mmol/L per 6 hours) as measured by the TAG AUC (control 2.96 ± 0.79, 1 set 2.52 ± 0.60, 3 sets 2.61 ± 0.59, 5 sets 2.45 ± 0.58). Similarly, no differences were observed for insulin or glucose AUC or for insulin sensitivity between treatments. There was a sex effect with TAG AUC significantly lower in women for control, 1 set, and 3 sets. Conclusion The results of this investigation suggest no dose-response attenuation of the postprandial lipemic response to a high-fat meal after previous resistance exercise.

T03-P-010 Influence of the body mass INDEX on the postprandial lipemic response to a overload of fat in healthy young subjects

T03-P-010 Influence of the body mass INDEX on the postprandial lipemic response to a overload of fat in healthy young subjects

The −1131T→C polymorphism in the apolipoprotein A5 gene is associated with postprandial hypertriacylglycerolemia; elevated small, dense LDL concentrations; and oxidative stress in nonobese Korean men

Apolipoprotein A5 plays an important role in modulating triacylglycerol metabolism in experimental animal models. The objective was to determine associations of the common apolipoprotein A5 gene (APOA5) -1131T-->C polymorphism with postprandial lipemic response and other cardiovascular disease risk factors in humans. Healthy, nonobese subjects [n = 158; mean (+/-SEM) age: 33.8 +/- 1.2 y; body mass index (in kg/m(2)): 23.3 +/- 0.3] were subdivided into 3 genotype groups: TT (n = 85), TC (n = 56), and CC (n = 17). We measured fasting and postprandial lipid concentrations, lipid peroxidation, C-reactive protein concentrations, and DNA damage. Fasting triacylglycerol concentrations in carriers of the C allele were higher (P < 0.05) than in carriers of the TT genotype. No other significant genotype-related differences were observed for any of the other baseline measures. After consumption of a mixed meal, carriers of the C allele had significantly greater increases in total chylomicron and VLDL triacylglycerol than did subjects with the TT genotype. Moreover, carriers of the C allele had higher dense LDL, serum C-reactive protein, and urinary 8-epi-prostaglandin F(2alpha) concentrations and more lymphocyte DNA damage. Conversely, we did not find significant genotype-related differences in postprandial glucose, insulin, or free fatty acid measures. Our data confirm the genetic modulation of serum fasting triacylglycerol concentrations by the APOA5 gene polymorphism and extend this observation to postprandial triacylglycerol concentrations and to markers of oxidation and inflammation. The presence of the C allele in the APOA5 promoter region at position 1131 could be a significant factor contributing to higher cardiovascular disease risk in Koreans independently of common environmental factors.