Plasma protein N-glycome composition associates with postprandial lipaemic response.

BACKGROUND: A dysregulated postprandial metabolic response is a risk factor for chronic diseases, including type 2 diabetes mellitus (T2DM). The plasma protein N-glycome is implicated in both lipid metabolism and T2DM risk. Hence, we first investigate the relationship between the N-glycome and postprandial metabolism and then explore the mediatory role of the plasma N-glycome in the relationship between postprandial lipaemia and T2DM. METHODS: We included 995 individuals from the ZOE-PREDICT 1 study with plasma N-glycans measured by ultra-performance liquid chromatography at fasting and triglyceride, insulin, and glucose levels measured at fasting and following a mixed-meal challenge. Linear mixed models were used to investigate the associations between plasma protein N-glycosylation and metabolic response (fasting, postprandial (Cmax), or change from fasting). A mediation analysis was used to further explore the relationship of the N-glycome in the prediabetes (HbA1c = 39-47 mmol/mol (5.7-6.5%))-postprandial lipaemia association. RESULTS: We identified 36 out of 55 glycans significantly associated with postprandial triglycerides (Cmax ß ranging from -0.28 for low-branched glycans to 0.30 for GP26) after adjusting for covariates and multiple testing (padjusted < 0.05). N-glycome composition explained 12.6% of the variance in postprandial triglycerides not already explained by traditional risk factors. Twenty-seven glycans were also associated with postprandial glucose and 12 with postprandial insulin. Additionally, 3 of the postprandial triglyceride-associated glycans (GP9, GP11, and GP32) also correlate with prediabetes and partially mediate the relationship between prediabetes and postprandial triglycerides. CONCLUSIONS: This study provides a comprehensive overview of the interconnections between plasma protein N-glycosylation and postprandial responses, demonstrating the incremental predictive benefit of N-glycans. We also suggest a considerable proportion of the effect of prediabetes on postprandial triglycerides is mediated by some plasma N-glycans.

The Effect of GLP-1 Receptor Agonists on Postprandial Lipaemia.

PURPOSE OF REVIEW: To review the currently available data on the effect of Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) on postprandial lipaemia. RECENT FINDINGS: Out of the available studies that examined the respective lipid parameter, exenatide reduced postprandial triacyglycerol (TAG) in 4/6, apolipoprotein B-48 in 3/3, non-esterified fatty acids in 2/2, and apolipoprotein C-III and very low-density lipoprotein cholesterol (VLDL-C) in 1/1 studies. Liraglutide reduced postprandial TAG in 2/2, apolipoprotein B-48 in 3/3 and apolipoprotein C-III, chylomicron-TAG and VLDL1-TAG in 1/1 studies. Lixisenatide reduced postprandial chylomicron-TAG and apolipoprotein B-48 in 1 study. Semaglutide reduced postprandial TAG, apolipoprotein B-48 and VLDL in 1 study. Dulaglutide reduced postprandial apolipoprotein B-48 in 1 study. GLP-1 RAs have consistent beneficial effects on postprandial lipaemia with most of the data coming from studies with exenatide and liraglutide. Reduction of postprandial lipaemia might be one of the mechanisms behind the pleiotropic effects of GLP-1 RAs.

Acute exercise improves glucose and TAG metabolism in young and older adults following high-fat, high-carbohydrate meal intake.

A single high-fat, high-carbohydrate meal (HFHC) results in elevated postprandial glucose (GLU), triglycerides (TAG) and metabolic load index (MLI; TAG (mg/dl) + GLU (mg/dl)) that contributes to chronic disease risk. While disease risk is higher in older adults (OA) compared to younger adults (YA), the acute effects of exercise on these outcomes in OA is understudied. Twelve YA (age 23.3 ± 3.9 yrs, n = 5 M/7 F) and 12 OA (age 67·7 ± 6.0 yrs, n = 8 M/4 F) visited the laboratory in random order to complete a HFHC with no exercise (NE) or acute exercise (EX) condition. EX was performed 12 hours prior to HFHC at an intensity of 65 % of maximal heart rate to expend 75 % of the kcals consumed in HFHC (Marie Callender's Chocolate Satin Pie; 12 kcal/kgbw; 57 % fat, 37 % CHO). Blood samples were taken at 0, 30, 60, 90 minutes, and then every hour until 6 hours post-meal. TAG levels increased to a larger magnitude in OA (Δ∼61 ± 31 %) compared to YA (Δ∼37 ± 34 %, P < 0·001), which were attenuated in EX compared to NE (P < 0·05) independent of age. There was no difference in GLU between OA and YA after the HFM, however, EX had attenuated GLU independent of age (NE: Δ∼21 ± 26 %; EX: Δ∼12 ± 18 %, P = 0·027). MLI was significantly lower after EX compared to NE in OA and YA (P < 0·001). Pre-prandial EX reduced TAG, GLU and MLI post-HFHC independent of age.

Effects of statins and exercise on postprandial lipoproteins in metabolic syndrome vs metabolically healthy individuals.

AIMS: To determine if the combination of exercise and statin could normalize postprandial triglyceridaemia (PPTG) in hypercholesteraemic individuals. METHODS: Eight hypercholesteraemic (blood cholesterol 182 ± 38 mg dL-1 ; low-density lipoprotein-cholesterol [LDL-c] 102 ± 32 mg dL-1 ) overweight (body mass index 30 ± 4 kg m-2 ) individuals with metabolic syndrome (MetS) were compared to a group of 8 metabolically healthy (MetH) controls (blood cholesterol 149 ± 23 mg dL-1 ; LDL-c 77 ± 23 mg dL-1 , and body mass index 23 ± 2 kg m-2 ). Each group underwent 2 PPTG tests, either 14 hours after a bout of intense exercise or without previous exercise. Additionally, MetS individuals were tested 96 hours after withdrawal of their habitual statin medication to study medication effects. RESULTS: A bout of exercise before the test meal did not reduce PPTG in MetS (P = .347), but reduced PPTG by 46% in MetH (413 ± 267 to 224 ± 142 mg dL-1 for 5 h incremental area under the curve; P = .02). In both trials (i.e., either after a bout of intense exercise or without previous exercise), statin withdrawal in MetS greatly increased PPTG (average 65%; P < .01), mean LDL-c (average 25%; P < .01), total cholesterol (average 16%; P < .01) and apolipoprotein (Apo) B48 (24%; P < .01), without interference from exercise. However, Apo B100 was not affected by statin withdrawal. CONCLUSION: Hypercholesteraemic MetS individuals (compared to MetH controls) fail to show an effect of exercise on reducing PPTG. However, chronic statin medication blunts the elevations in triglyceride after a fat meal (i.e., incremental area under the curve of PPTG) reducing their cardiovascular risk associated with their atherogenic dyslipidaemia. Statin decreases PPTG by reducing the secretion or accelerating the catabolism of intestinal Apo B48.

Effects of statin therapy and exercise on postprandial triglycerides in overweight individuals with hypercholesterolaemia.

AIMS: To determine the effects of statins on postprandial lipaemia (PPL) and to study if exercise could enhance statin actions. METHODS: Ten hypercholesteraemic (blood cholesterol 204 ± 36 mg dL-1 ; low-density lipoprotein-cholesterol 129 ± 32 36 mg dL-1 ) overweight (body mass index 30 ± 4 kg m-2 ), metabolic syndrome individuals chronically medicated with statins (>6 months) underwent 5-hour PPL tests in 4 occasions in a randomized order: (i) substituting their habitual statin medication by placebo for 96 hours (PLAC trial); (ii) taking their habitual statin medicine (STA trial); (iii) placebo combined with a bout of intense aerobic exercise (EXER+PLAC trial); and (iv) combining exercise and statin medicine (EXER+STA trial). RESULTS: Before the fat meal, statin withdrawal (i.e. PLAC and EXER+PLAC) increased blood triglycerides (TG; 24%), low-density lipoprotein-cholesterol (31%) and total cholesterol (19%; all P < .05) evidencing treatment compliance. After the meal, statin withdrawal increased 5-hour postprandial TG (PPTG) compared to its matched trials (94% higher PLAC vs STA and 45% higher EXER+PLAC vs EXER+STA; P < .05). EXER+PLAC trial did not lower PPTG below PLAC (i.e. incremental AUC of 609 ± 152 vs 826 ± 190 mg dL-1 5 h; P = .09). Adding exercise to statin did not result in larger reductions in PPTG (i.e. EXER+STA vs STA incremental area under the curve of 421 ± 87 vs 421 ± 84 mg dL-1 5 h; P = .99). CONCLUSION: In hypercholesteraemic metabolic syndrome individuals, chronic statin therapy blunts the elevations in TG after a fat meal (i.e. incremental area under the curve of PPTG) reducing the cardiovascular risk associated to their atherogenic dyslipidaemia. However, a single bout of intense aerobic exercise before the high fat meal, does not reduce PPTG but also does not interfere with the effects of statin treatment.

Acute whole apple consumption did not influence postprandial lipaemia: a randomised crossover trial.

Whole apples are a source of pectin and polyphenols, both of which show potential to modulate postprandial lipaemia (PPL). The present study aimed to explore the effects of whole apple consumption on PPL, as a risk factor for CVD, in generally healthy but overweight and obese adults. A randomised, crossover acute meal trial was conducted with seventeen women and nine men (mean BMI of 34·1 (sem 0·2) kg/m2). Blood samples were collected for 6 h after participants consumed an oral fat tolerance test meal that provided 1 g fat/kg body weight and 1500 mg acetaminophen per meal for estimating gastric emptying, with and without three whole raw Gala apples (approximately 200 g). Plasma TAG (with peak postprandial concentration as the primary outcome), apoB48, chylomicron-rich fraction particle size and fatty acid composition, glucose, insulin and acetaminophen were analysed. Differences between with and without apples were identified by ANCOVA. Apple consumption did not alter postprandial TAG response, chylomicron properties, glucose or acetaminophen (P > 0·05), but did lead to a higher apoB48 peak concentration and exaggerated insulin between 20 and 180 min (P < 0·05). Overall, as a complex food matrix, apples did not modulate postprandial TAG when consumed with a high-fat meal in overweight and obese adults, but did stimulate insulin secretion, potentially contributing to an increased TAG-rich lipoprotein production.

Pre-meal and postprandial lipaemia in subjects with the metabolic syndrome: effects of timing and protein quality (randomised crossover trial).

Non-fasting TAG - postprandial lipaemia (PPL) - are to a higher degree associated with cardiovascular risk compared with fasting TAG. Dietary protein, especially whey proteins (WP), may lower PPL. We hypothesised that a WP pre-meal (17·6 g protein) consumed 15 v. 30 min before a fat-rich meal reduces the PPL response in subjects with the metabolic syndrome (MetS) and that a WP pre-meal has more potent effects than casein and gluten pre-meals. A total of sixteen subjects with the MetS completed an acute, randomised, crossover trial. WP pre-meals were consumed 15 and 30 min, and casein and gluten 15 min before a fat-rich meal. Blood samples were drawn 360 min postprandially to determine metabolite and hormone responses, S-paracetamol (for assessment of gastric emptying) and amino acids. Insulin and glucagon responses were affected by both timing and protein type (for all P <0·01), with significantly higher concentrations for WP given at -15 min than WP at -30 min and higher responses compared with gluten for the first 30 min after pre-meal consumption (for all P <0·05). The PPL responses changed neither by timing nor by protein type. Glucose-dependent insulinotropic peptide but not glucagon-like peptide 1 responses differed between the three protein types. S-paracetamol concentration was higher for WP (-30 min) than for WP (-15 min) 15 min after the main meal (P = 0·028), and higher for casein and gluten than for WP at time point 30 min (for all P <0·05). In conclusion, the PPL response was not changed by ingestion of a 17·6 g protein pre-meal, whereas both timing and protein quality affected hormone secretion (insulin and glucagon).

A pre-meal of whey proteins induces differential effects on glucose and lipid metabolism in subjects with the metabolic syndrome: a randomised cross-over trial.

PURPOSE: Postprandial lipaemia (PPL), an independent risk factor for cardiovascular disease, is affected by composition and timing of meals. We evaluated if whey proteins (WP) consumed as a pre-meal before a fat-rich meal reduce postprandial triglyceride (TG) and apolipoprotein B-48 (ApoB-48) responses in subjects with the metabolic syndrome (MeS). METHODS: An acute, randomised, cross-over trial was conducted. 20 subjects with MeS consumed a pre-meal of 0, 10 or 20 g WP 15 min prior to a fat-rich meal. The responses of TG and ApoB-48 were assessed. We also analysed postprandial responses of free fatty acids (FFA), glucose, insulin, glucagon, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) and paracetamol (reflecting gastric emptying rates). RESULTS: WP pre-meal did not alter the TG or ApoB-48 responses. In contrast, the insulin response was more pronounced after a pre-meal of 20 g WP than with 10 g WP (P = 0.0005) and placebo (P < 0.0001). Likewise, the postprandial glucagon response was greater with a pre-meal of 20 g WP than with 10 g WP (P < 0.0001) and 0 g WP (P < 0.0001). A pre-meal with 20 g of WP generated lower glucose (P = 0.0148) and S-paracetamol responses (P = 0.0003) and a higher GLP-1 response (P = 0.0086) than placebo. However, the pre-meal did not influence responses of GIP, FFA or appetite assessed by a Visual Analog Scale. CONCLUSIONS: Consumption of a WP pre-meal prior to a fat-rich meal did not affect TG and chylomicron responses. In contrast, the WP pre-meal stimulates insulin and glucagon secretion and reduces blood glucose as expected, and delays gastric emptying. Consequently, our study points to a differential impact of a WP pre-meal on lipid and glucose metabolism to a fat-rich meal in subjects with MeS.

Effects of fructose consumption on postprandial TAG: an update on systematic reviews with meta-analysis.

The aim of this study was to re-examine the chronic effect (>7 d) of fructose consumption on postprandial TAG, in adolescents and adults. The research was carried out in March 2017 and used different electronic databases, such as Medline ® (Pubmed®), Embase® and Cochrane. The review considered clinical trials (parallel or crossed) that evaluated the effect of fructose consumption for a period longer than 7 d, in humans. Two investigators independently performed data extraction. The outcome was the absolute delta of TAG concentration in a 4-h postprandial period. The results were presented with delta mean difference between treatments with 95 % CI. The calculations were made based on random-effect models. Statistical heterogeneity of treatment effects between studies was assessed by Cochrane's 'Q Test' and 'I 2' inconsistency test. The meta-analysis of the twelve selected interventions (n 318) showed that fructose generated larger variation (δ) of TAG concentrations during the postprandial period, compared with other carbohydrates (mean difference: 8·02 (95 % CI 0·46, 15·58) mg/dl (0·09 (95 % CI 0·01, 0·18) mmol/l); I 2: 74 %). High heterogeneity was generated almost exclusively by one study, and its withdrawal did not alter the result. We concluded that chronic consumption of fructose (>7 d) has a negative role on postprandial TAG in healthy adolescents and adults, as well as in overweight/obese individuals, but not in diabetics.

Impact of meal fatty acid composition on postprandial lipaemia, vascular function and blood pressure in postmenopausal women.

CVD are the leading cause of death in women globally, with ageing associated with progressive endothelial dysfunction and increased CVD risk. Natural menopause is characterised by raised non-fasting TAG concentrations and impairment of vascular function compared with premenopausal women. However, the mechanisms underlying the increased CVD risk after women have transitioned through the menopause are unclear. Dietary fat is an important modifiable risk factor relating to both postprandial lipaemia and vascular reactivity. Meals rich in SFA and MUFA are often associated with greater postprandial TAG responses compared with those containing n-6 PUFA, but studies comparing their effects on vascular function during the postprandial phase are limited, particularly in postmenopausal women. The present review aimed to evaluate the acute effects of test meals rich in SFA, MUFA and n-6 PUFA on postprandial lipaemia, vascular reactivity and other CVD risk factors in postmenopausal women. The systematic search of the literature identified 778 publications. The impact of fat-rich meals on postprandial lipaemia was reported in seven relevant studies, of which meal fat composition was compared in one study described in three papers. An additional study determined the impact of a high-fat meal on vascular reactivity. Although moderately consistent evidence suggests detrimental effects of high-fat meals on postprandial lipaemia in postmenopausal (than premenopausal) women, there is insufficient evidence to establish the impact of meals of differing fat composition. Furthermore, there is no robust evidence to conclude the effect of meal fatty acids on vascular function or blood pressure. In conclusion, there is an urgent requirement for suitably powered robust randomised controlled trials to investigate the impact of meal fat composition on postprandial novel and established CVD risk markers in postmenopausal women, an understudied population at increased cardiometabolic risk.

Dietary fat and physiological determinants of plasma chylomicron remnant homoeostasis in normolipidaemic subjects: insight into atherogenic risk.

TAG depleted remnants of postprandial chylomicrons are a risk factor for atherosclerosis. Recent studies have demonstrated that in the fasted state, the majority of chylomicrons are small enough for transcytosis to arterial subendothelial space and accelerate atherogenesis. However, the size distribution of chylomicrons in the absorptive state is unclear. This study explored in normolipidaemic subjects the postprandial distribution of the chylomicron marker, apoB-48, in a TAG-rich lipoprotein plasma fraction (Svedberg flotation rate (Sf>400), in partially hydrolysed remnants (Sf 20-400) and in a TAG-deplete fraction (Sf<20), following ingestion of isoenergetic meals with either palm oil (PO), rice bran or coconut oil. Results from this study show that the majority of fasting chylomicrons are within the potentially pro-atherogenic Sf<20 fraction (70-75 %). Following the ingestion of test meals, chylomicronaemia was also principally distributed within the Sf<20 fraction. However, approximately 40 % of subjects demonstrated exaggerated postprandial lipaemia specifically in response to the SFA-rich PO meal, with a transient shift to more buoyant chylomicron fractions. The latter demonstrates that heterogeneity in the magnitude and duration of hyper-remnantaemia is dependent on both the nature of the meal fatty acids ingested and possible metabolic determinants that influence chylomicron metabolism. The study findings reiterate that fasting plasma TAG is a poor indicator of atherogenic chylomicron remnant homoeostasis and emphasises the merits of considering specifically, chylomicron remnant abundance and kinetics in the context of atherogenic risk. Few studies address the latter, despite the majority of life being spent in the postprandial and absorptive state.

Modulation of postprandial lipaemia by a single meal containing a commonly consumed interesterified palmitic acid-rich fat blend compared to a non-interesterified equivalent.

PURPOSE: Interesterification of palm stearin and palm kernal (PSt/PK) is widely used by the food industry to create fats with desirable functional characteristics for applications in spreads and bakery products, negating the need for trans fatty acids. Previous studies have reported reduced postprandial lipaemia, an independent risk factor for CVD, following interesterified (IE) palmitic and stearic acid-rich fats that are not currently widely used by the food industry. The current study investigates the effect of the most commonly consumed PSt/PK IE blend on postprandial lipaemia. METHODS: A randomised, controlled, crossover (1 week washout) double-blind design study (n = 12 healthy males, 18-45 years), compared the postprandial (0-4 h) effects of meals containing 50 g fat [PSt/PK (80:20); IE vs. non-IE] on changes in plasma triacylglycerol (TAG), glucose, glucose-dependent insulinotropic polypeptide (GIP), peptide YY (PYY), insulin, gastric emptying (paracetamol concentrations) and satiety (visual analogue scales). RESULTS: The postprandial increase in plasma TAG was higher following the IE PSt/PK versus the non-IE PSt/PK, with a 51 % greater incremental area under the curve [mean difference with 95 % CI 41 (23, 58) mmol/L min P = 0.001]. The pattern of lipaemia was different between meals; at 4-h plasma TAG concentrations declined following the IE fat but continued to rise following the non-IE fat. Insulin, glucose, paracetamol, PYY and GIP concentrations increased significantly after the test meals (time effect; P < 0.001 for all), but did not differ between test meals. Feelings of fullness were higher following the non-IE PSt/PK meal (diet effect; P = 0.034). No other significant differences were noted. CONCLUSIONS: Interesterification of PSt/PK increases early phase postprandial lipaemia (0-4 h); however, further investigation during the late postprandial phase (4-8 h) is warranted to determine the rate of return to baseline values. TRIAL REGISTRATION NUMBER: Clinicaltrials.gov as NCT02365987.

Association of the tumor necrosis factor-alpha promoter polymorphism with change in triacylglycerol response to sequential meals.

BACKGROUND: Reported associations between Tumor Necrosis Factor-alpha (TNFA) and the postprandial triacylglycerol (TAG) response have been inconsistent, which could be due to variations in the TNFA gene, meal fat composition or participant's body weight. Hence, we investigated the association of TNFA polymorphism (-308G → A) with body mass index (BMI) and postprandial lipaemia and also determined the impact of BMI on the association of the polymorphism with postprandial lipaemia. METHODS: The study participants (n = 230) underwent a sequential meal postprandial study. Blood samples were taken at regular intervals after a test breakfast (t = 0, 49 g fat) and lunch (t =330 min, 29 g fat) to measure fasting and postprandial lipids, glucose and insulin. The Metabolic Challenge Study (MECHE) comprising 67 Irish participants who underwent a 54 g fat oral lipid tolerance test was used as a replication cohort. The impact of genotype on postprandial responses was determined using general linear model with adjustment for potential confounders. RESULTS: The -308G → A polymorphism showed a significant association with BMI (P = 0.03) and fasting glucose (P = 0.006), where the polymorphism explained 13 % of the variation in the fasting glucose. A 30 % higher incremental area under the curve (IAUC) was observed for the postprandial TAG response in the GG homozygotes than A-allele carriers (P = 0.004) and the genotype explained 19 % of the variation in the IAUC. There was a non-significant trend in the impact of BMI on the association of the genotype with TAG IAUC (P = 0.09). These results were not statistically significant in the MECHE cohort, which could be due to the differences in the sample size, meal composition, baseline lipid profile, allelic diversity and postprandial characterisation of participants across the two cohorts. CONCLUSIONS: Our findings suggest that TNFA -308G → A polymorphism may be an important candidate for BMI, fasting glucose and postprandial TAG response. Further studies are required to investigate the mechanistic effects of the polymorphism on glucose and TAG metabolism, and determine whether BMI is an important variable which should be considered in the design of future studies. TRIAL REGISTRATION: NCT01172951 .

The effect of prior walking on coronary heart disease risk markers in South Asian and European men.

PURPOSE: Heart disease risk is elevated in South Asians possibly due to impaired postprandial metabolism. Running has been shown to induce greater reductions in postprandial lipaemia in South Asian than European men, but the effect of walking in South Asians is unknown. METHODS: Fifteen South Asian and 14 white European men aged 19-30 years completed two, 2-day trials in a randomised crossover design. On day 1, participants rested (control) or walked for 60 min at approximately 50 % maximum oxygen uptake (exercise). On day 2, participants rested and consumed two high-fat meals over a 9-h period during which 14 venous blood samples were collected. RESULTS: South Asians exhibited higher postprandial triacylglycerol [geometric mean (95 % confidence interval) 2.29 (1.82 to 2.89) vs. 1.54 (1.21 to 1.96) mmol L(-1) h(-1)], glucose [5.49 (5.21 to 5.79) vs. 5.05 (4.78 to 5.33) mmol L(-1) h(-1)], insulin [32.9 (25.7 to 42.1) vs. 18.3 (14.2 to 23.7) µU mL(-1) h(-1)] and interleukin-6 [2.44 (1.61 to 3.67) vs. 1.04 (0.68 to 1.59) pg mL(-1) h(-1)] than Europeans (all ES ≥ 0.72, P ≤ 0.03). Between-group differences in triacylglycerol, glucose and insulin were not significant after controlling for age and percentage body fat. Walking reduced postprandial triacylglycerol [1.79 (1.52 to 2.12) vs. 1.97 (1.67 to 2.33) mmol L(-1) h(-1)] and insulin [21.0 (17.0 to 26.0) vs. 28.7 (23.2 to 35.4) µU mL(-1) h(-1)] (all ES ≥ 0.23. P ≤ 0.01), but group differences were not significant. CONCLUSIONS: Healthy South Asians exhibited impaired postprandial metabolism compared with white Europeans, but these differences were diminished after controlling for potential confounders. The small-moderate reduction in postprandial triacylglycerol and insulin after brisk walking was not different between the ethnicities.

Effect of repeated sprints on postprandial endothelial function and triacylglycerol concentrations in adolescent boys.

This study investigated whether repeated, very short duration sprints influenced endothelial function (indicated by flow-mediated dilation) and triacylglycerol concentrations following the ingestion of high-fat meals in adolescent boys. Nine adolescent boys completed two, 2-day main trials (control and exercise), in a counter-balanced, cross-over design. Participants were inactive on day 1 of the control trial but completed 40 × 6 s maximal cycle sprints on day 1 of the exercise trial. On day 2, capillary blood samples were collected and flow-mediated dilation measured prior to, and following, ingestion of a high-fat breakfast and lunch. Fasting flow-mediated dilation and plasma triacylglycerol concentration were similar in the control and exercise trial (P > 0.05). In the control trial, flow-mediated dilation was reduced by 20% and 27% following the high-fat breakfast and lunch; following exercise these reductions were negated (main effect trial, P < 0.05; interaction effect trial × time, P < 0.05). The total area under the plasma triacylglycerol concentration versus time curve was 13% lower on day 2 in the exercise trial compared to the control trial (8.65 (0.97) vs. 9.92 (1.16) mmol · l(-1) · 6.5 h, P < 0.05). These results demonstrate that repeated 6 s maximal cycle sprints can have beneficial effects on postprandial endothelial function and triacylglycerol concentrations in adolescent boys.

Metabolic phenotypes of obesity influence triglyceride and inflammation homoeostasis.

BACKGROUND: We examined the degree of postprandial triglyceride (TG) response over the day, representing a highly dynamic state, with continuous metabolic adaptations, among normal-weight, overweight and obese patients, according to their metabolically healthy or abnormal status. MATERIALS AND METHODS: A total of 1002 patients from the CORDIOPREV clinical trial (NCT00924937) were submitted to an oral fat load test meal 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 analysing lipid fractions and inflammation markers (high-sensitivity C-reactive protein (hs-CRP)) were drawn at 0, 1, 2, 3 and 4 h during postprandial state. We explored the dynamic response according to six body size phenotypes: (i) normal weight, metabolically healthy; (ii) normal weight, metabolically abnormal; (iii) overweight, metabolically healthy; (iv) overweight, metabolically abnormal; (v) obese, metabolically healthy; and (vi) obese, metabolically abnormal. RESULTS: Metabolically healthy patients displayed lower postprandial response of plasma TG and large triacylglycerol-rich lipoproteins (TRLs)-TG, compared with those metabolically abnormal, independently whether or not they were obese (P < 0·001 and P < 0·001, respectively). Moreover, the area under the curve (AUC) of TG and AUC of large TRLs-TG were greater in the group of metabolically abnormal compared with the group of metabolically healthy (P < 0·001 and P < 0·001, respectively). Interestingly, metabolically abnormal subjects displayed higher postprandial response of plasma hs-CRP than did the subgroup of normal, overweight and obese, metabolically healthy patients (P < 0·001). CONCLUSIONS: Our findings showed that certain types of the metabolic phenotypes of obesity are more favourable modulating phenotypic flexibility after a dynamic fat load test, through TG metabolism and inflammation homoeostasis. To identify, these phenotypes may be the best strategy for personalized treatment of obesity.

The effect of upper- and lower-body exercise on next-day postprandial triglycerides in healthy young men.

Aims: High non-fasting triglycerides (TG) concentration is linked to the development of atherosclerosis, and physical activity is commonly recommended to reduce postprandial TG concentration and cardiovascular diseases. Previous studies have demonstrated that acute whole-body (walking and running) or lower-body (leg cycling) aerobic exercise reduces postprandial TG. However, it is unclear whether upper-body exercise (i.e. arm-cranking) with sufficient energy expenditure lowers postprandial TG. Therefore, this study aimed to evaluate the effects of energy-matched upper- and lower-body exercises on postprandial TG concentrations the next day in healthy young men. Method and Materials: Fifteen healthy young men (age 22.5 ± 1.7 years, height 173.8 ± 5.7 cm, body mass 68.2 ± 8.5 kg, peak oxygen uptake 48.0 ± 5.5 mL/min/kg and physically active) participated in a three-arm crossover trials: 1) arm-cranking, 2) leg-cycling exercise at 70% of mode-specific peak oxygen uptake to induce a net energy expenditure of 1,255 kJ, or 3) rested between 16:00 and 17:00 h on day 1 and consumed two standardised meals for breakfast (10:00 h) and lunch (13:00 h) on day 2. The mean macronutrient content of the breakfast was 44.9 ± 5.6 g fat, 104.8 ± 13.0 g carbohydrate, and 29.4 ± 3.6 g protein, which provided 3.95 ± 0.49 MJ energy (43% fat, 45% carbohydrate, and 12% protein), and that of the lunch was 45.2 ± 5.6 g fat, 106.7 ± 13.2 g carbohydrate, and 33.9 ± 4.2 g protein, which provided 4.06 ± 0.50 MJ energy (42% fat, 44% carbohydrate, and 14% protein). Results: Time-averaged postprandial serum TG concentrations over 8 h differed among trials (main effect of trial p < 0.001) and were lower in the upper- and lower-body exercise trials than in the control trial (1.46 ± 0.54 vs. 1.50 ± 0.69 vs. 1.79 ± 0.83 mmol/L, respectively). The incremental TG area under the curve (AUC) (main effect of trial, p = 0.012) was 39% and 37% higher in the control trial than in the upper- and lower-body exercise trials (p = 0.025 and p = 0.033, respectively). There were no significant differences in incremental TG AUC between the upper- and lower-body exercise trials. Conclusion: An acute bout of energy-matched upper- and lower-body exercises similarly lowered postprandial TG concentrations the following day in healthy young men.Trial registration number: UMIN000045449.Date of registration: 10 September 2021.

Biophysical insights into modulating lipid digestion in food emulsions.

During the last decade, major scientific advances on understanding the mechanisms of lipid digestion and metabolism have been made, with a view to addressing health issues (such as obesity) associated with overconsumption of lipid-rich and sucrose-rich foods. As lipids in common foods exist in the form of emulsions, the structuring of emulsions has been one the main strategies for controlling the rate of lipid digestion and absorption, at least from a colloid science viewpoint. Modulating the kinetics of lipid digestion and absorption offers interesting possibilities for developing foods that can provide control of postprandial lipaemia and control the release of lipophilic compounds. Food emulsions can be designed to achieve considerable differences in the kinetics of lipid digestion but most research has been applied to relatively simple model systems and in in vitro digestion models. Further research to translate this knowledge into more complex food systems and to validate the results in human studies is required. One promising approach to delay/control lipid digestion is to alter the stomach emptying rate of lipids, which is largely affected by interactions of emulsion droplets with the food matrices. Food matrices with different responses to the gastric environment and with different interactions between oil droplets and the food matrix can be designed to influence lipid digestion. This review focuses on key scientific advances made during the last decade on understanding the physicochemical and structural modifications of emulsified lipids, mainly from a biophysical science perspective. The review specifically explores different approaches by which the structure and stability of emulsions may be altered to achieve specific lipid digestion kinetics.

Postprandial lipaemia following consumption of a meal enriched with medium chain saturated and/or long chain omega-3 polyunsaturated fatty acids. A randomised cross-over study.

BACKGROUND & AIMS: Postprandial lipaemic response has emerged as a risk factor for cardiovascular disease. Dietary fats such as medium-chain saturated fatty acids (MCSFA) and long-chain omega-3 polyunsaturated fatty acids (LCn-3PUFA) are known to reduce postprandial lipaemic responses. The combination of the two could potentially have complementary and/or synergistic effects for optimising cardiovascular health. This study aims to investigate the effects of MCSFA (coconut oil) with or without LCn-3PUFA (fish oil) inclusion in the test meal on postprandial blood lipids in healthy adults. METHODS: In a randomised, double-blinded, placebo-controlled, 2 × 2 factorial cross-over study, participants (n = 15) were randomised to receive four standardised isocaloric test meals. Test meals include: placebo [PL, containing no fish oil (0 g EPA & DHA) or coconut oil (0 g MCSFA)], fish oil [FO, 6 g fish oil (3.85 g EPA & DHA), containing no coconut oil (0 g MCSFA)], coconut oil [CO, 18.65 g coconut oil (15 g MCSFA), containing no fish oil (0 g EPA & DHA)] and coconut oil + fish oil [COFO, 18.65 g coconut oil (15 g MCSFA) + 6 g fish oil (3.85 g EPA & DHA)]; all providing a total fat content of 33.5 g. Participants received all four treatments on four separate test days with at least 3 days washout in between. Blood parameters were measured by finger pricks at 7 timepoints between 0 and 300min. The primary outcome of this study was the change in postprandial triglycerides (TG) concentrations with secondary outcomes as total cholesterol, high-density lipoprotein cholesterol and blood glucose concentrations. RESULTS: TG area under the curve (AUC) (mmol/L/min) was significantly lower for FO (383.67, p = 0.0125) and COFO (299.12, p = 0.0186) in comparison to PL (409.17) only. TG incremental area under the curve (iAUC) (mmol/L/min) was significantly lower with COFO (59.67) in comparison to CO (99.86), (p = 0.0480). Compared to PL, the change in absolute TG concentrations (mmol/L) from baseline to post TG peak time (180min) after FO were significantly less at 240min (0.39 vs 0.15), 270min (0.2 vs 0.1), and 300min (0.28 vs 0.06), and after COFO was significantly less at 300min (0.28 vs 0.16) (p < 0.05). No significant differences in postprandial AUC and iAUC for any other blood parameters were reported. CONCLUSIONS: Our study demonstrated that LCn-3PUFA with or without MCSFA but not MCSFA alone are effective in reducing postprandial TG in healthy individuals.

Effects of a single bout of walking on postprandial triglycerides in men of Chinese, European and Japanese descent: a multisite randomised crossover trial.

INTRODUCTION: Elevated non-fasting triglyceride (TG) concentrations are a risk factor for cardiovascular diseases but can be reduced after acute exercise. Ethnic-based differences in the magnitude of postprandial lipaemia and the extent that acute exercise reduces postprandial TG are poorly characterised across some ethnicities including those of East Asian origin. This paper describes the protocol of a multisite randomised crossover study comparing the effect of acute walking on postprandial TG in two groups of East Asian men with European men. METHODS AND ANALYSIS: Twenty Japanese, 20 Singaporean Chinese and 20 white British healthy men (21-39 years) recruited from Japan, Singapore and the UK, respectively, will complete two, 2-day trials. Fasted and postprandial venous blood samples and arterial blood pressure measurements will be taken over 6 hours the day after either: (1) 60-min treadmill walking; or (2) a rest day of normal living. The primary outcome is the difference in postprandial TG among ethnic groups after rest and walking. Secondary outcomes include cholesterol, glucose, insulin, ketone bodies, preheparin lipoprotein lipase, C-reactive protein and systolic/diastolic blood pressure. ETHICS AND DISSEMINATION: The study was approved by the Ethics Review Committee on Research with Human Subjects of Waseda University and the Nanyang Technological University Institutional Review Board. Relevant approval will be obtained from the UK site. Research findings will be disseminated through peer-reviewed journal publication and health conferences. TRIAL REGISTRATION NUMBER: UMIN000038625.