People of Chinese ethnicity develop type 2 diabetes mellitus (T2DM) at a younger age and lower body mass index (BMI) than their Caucasian counterparts. Furthermore, Chinese migrants to Westernised countries have an increased risk of metabolic diseases compared to those in their country of origin(1,2). We propose that this increased risk is due to a greater manifestation of metabolic abnormalities in response to altered diet and lifestyle behaviours. Although fasting lipaemia and glycaemia are commonly used to predict risk of CVD and T2DM, assessment of impaired postprandial metabolism has been found to be a more sensitive indicator of risk(3). We hypothesised that Chinese migrants, at risk of T2DM, exhibit impaired postprandial lipid and lipoprotein metabolism compared to Australian-born Caucasian counterparts. Chinese and Caucasian adults at risk of T2DM were recruited to the study in which postprandial lipaemia and glycaemia were monitored following consumption of a high fat and high carbohydrate breakfast meal followed by a mixed, lunch meal. In a nonrandomised acute crossover trial, 15 adults (n = 8 Chinese and n = 7 Caucasian) aged ≥ 18 and ≤ 65 years at risk of T2DM (AUSDRISK score > 12 (median = 14.0, IQR = 3.0)), attended two postprandial test days separated by ≥ 7-day washout period. Test breakfast meals were isocaloric (3.6 MJ), high fat (46% energy from fat, 46% energy from carbohydrates) or high carbohydrate (74% E carbohydrates, 17.5% E fat). Blood samples were collected at baseline (fasting), 180 min and 360 min after consumption of the breakfast meal. The lunch meal (3.7 MJ, 18% E fat, 76% E carbohydrates) was consumed 240 min after baseline. Samples were analysed for lipaemia and glycaemia. Additionally, chylomicron-rich, and VLDL-rich lipoprotein fractions were isolated by sequential ultracentrifugation and chylomicron particle number (apolipoprotein (apo) B48), triacylglycerol (TAG), and total cholesterol were assessed in these fractions. Data were analysed using a mixed between-within-subject analysis of variance. There were no differences in age, and baseline anthropometric measures between groups, apart from the Chinese group exhibiting significantly lower waist circumference and BMI compared to the Caucasian group. There were no differences between groups in blood measures, apart from a higher total- and LDL-cholesterol concentration in the Caucasian compared to the Chinese group (P<0.05). Despite identical fasting TAG concentrations, the Chinese group, compared with the Caucasian group exhibited significantly elevated serum TAG and chylomicron-apo-B48 concentrations at 360 min following both test meals (P<0.01). All other postprandial measures were not different between groups. These findings show that despite having identical or improved fasting glycaemia and lipid profile, the Chinese group exhibited impaired postprandial lipid metabolism which may contributes to their increased risk of metabolic diseases.

Berries rich in anthocyanins have beneficial effects on postprandial glycaemia. We investigated whether blackcurrant (75 g in a portion) independently and in a product with fermented quinoa induced similar effects on the sugar-induced postprandial glucose metabolism as observed before with 150 g of blackcurrant. Twenty-six healthy subjects (twenty-two females and four males) consumed four test products after fasting overnight in a randomised, controlled crossover design. Each test product portion contained 31 g of available carbohydrates and had similar composition of sugar components: 300 ml water with sucrose, glucose and fructose (SW; reference), blackcurrant purée with added sugars (BC), a product consisting of the blackcurrant purée and a product base with fermented quinoa (BCP) and the product base without blackcurrant (PB). Blood samples were collected at 0, 15, 30, 45, 60, 90, 120 and 180 min after eating each test product to analyse the concentrations of glucose, insulin and NEFA. In comparison with the SW, the intake of both the BC and BCP resulted in reduced glucose and insulin concentrations during the first 30 min, a more balanced decline during the first hour and improved glycaemic profile. The BCP induced more efficient effects than the BC due to the product base with fermented quinoa. A rebound of NEFA after the sugar-induced hypoglycaemic response was attenuated at the late postprandial phase by the BC and BCP. In conclusion, we showed that 75 g of blackcurrant and the product with fermented quinoa were able to lower postprandial glycaemia and insulinaemia.

Se, an essential biological trace element, is required for fish growth. However, the underlying mechanisms remain unclear. Protein deposition in muscle is an important determinant for fish growth. This study was conducted on juvenile rainbow trout (Oncorhynchus mykiss) to explore the nutritional effects of Se on protein deposition in fish muscle by analysing the postprandial dynamics of both protein synthesis and protein degradation. Trout were fed a basal diet supplemented with or without 4 mg/kg Se (as Se yeast), which has been previously demonstrated as the optimal supplemental level for rainbow trout growth. After 6 weeks of feeding, dietary Se supplementation exerted no influence on fish feed intake, whereas it increased fish growth rate, feed efficiency, protein retention rate and muscle protein content. Results of postprandial dynamics (within 24 h after feeding) of protein synthesis and degradation in trout muscle showed that dietary Se supplementation led to a persistently hyperactivated target of rapamycin complex 1 pathway and the suppressive expression of numerous genes related to the ubiquitin–proteasome system and the autophagy–lysosome system after the feeding. However, the ubiquitinated proteins and microtubule-associated light chain 3B (LC3)-II:LC3-I ratio, biomarkers for ubiquitination and autophagy activities, respectively, exhibited no significant differences among the fish fed different experimental diets throughout the whole postprandial period. Overall, this study demonstrated a promoting effect of nutritional level of dietary Se on protein deposition in fish muscle by accelerating postprandial protein synthesis. These results provide important insights about the regulatory role of dietary Se in fish growth.

Men have earlier first-time event of CHD and higher postprandial TAG response compared with women. The aim of this exploratory sub-study was to investigate if intake of meals with the same amount of fat from different dairy products affects postprandial lipoprotein subclasses differently in healthy women and men. A total of thirty-three women and fourteen men were recruited to a randomised controlled cross-over study with four dairy meals consisting of butter, cheese, whipped cream or sour cream, corresponding to 45 g of fat (approximately 60 energy percent). Blood samples were taken at 0, 2, 4 and 6 h postprandially. Lipoprotein subclasses were measured using NMR and analysed using a linear mixed model. Sex had a significant impact on the response in M-VLDL (P=0·04), S-LDL (P=0·05), XL-HDL (P=0·009) and L-HDL (P=0·001) particle concentration (P), with women having an overall smaller increase in M-VLDL-P, a larger decrease in S-LDL-P and a larger increase in XL- and L-HDL-P compared with men, independent of meal. Men showed a decrease in XS-VLDL-P compared with women after intake of sour cream (P<0·01). In men only, XS-VLDL-P decreased after intake of sour cream compared with all other meals (v. butter: P=0·001; v. cheese: P=0·04; v. whipped cream: P=0·006). Meals with the same amount of fat from different dairy products induce different postprandial effects on lipoprotein subclass concentrations in men and women.

EPA and DHA are important components of cell membranes. Since humans have limited ability for EPA and DHA synthesis, these must be obtained from the diet, primarily from oily fish. Dietary EPA and DHA intakes are constrained by the size of fish stocks and by food choice. Seed oil from transgenic plants that synthesise EPA and DHA represents a potential alternative source of these fatty acids, but this has not been tested in humans. We hypothesised that incorporation of EPA and DHA into blood lipids from transgenic Camelina sativa seed oil (CSO) is equivalent to that from fish oil. Healthy men and women (18–30 years or 50–65 years) consumed 450 mg EPA + DHA from either CSO or commercial blended fish oil (BFO) in test meals in a double-blind, postprandial cross-over trial. There were no significant differences between test oils or sexes in EPA and DHA incorporation into plasma TAG, phosphatidylcholine or NEFA over 8 h. There were no significant differences between test oils, age groups or sexes in postprandial VLDL, LDL or HDL sizes or concentrations. There were no significant differences between test oils in postprandial plasma TNFα, IL 6 or 10, or soluble intercellular cell adhesion molecule-1 concentrations in younger participants. These findings show that incorporation into blood lipids of EPA and DHA consumed as CSO was equivalent to BFO and that such transgenic plant oils are a suitable dietary source of EPA and DHA in humans.

Discrete episodes of overconsumption may induce a positive energy balance and impair metabolic control. However, the effects of an ecologically relevant, single day of balanced macronutrient overfeeding are unknown. Twelve healthy men (of age 22 (sd 2) years, BMI 26·1 (sd 4·2) kg/m2) completed two 28 h, single-blind experimental trials. In a counterbalanced repeated measures design, participants either consumed their calculated daily energy requirements (energy balance trial (EB): 10 755 (sd 593) kJ) or were overfed by 50 % (overfeed trial (OF): 16 132 (sd 889) kJ) under laboratory supervision. Participants returned to the laboratory the next day, after an overnight fast, to complete a mixed-meal tolerance test (MTT). Appetite was not different between trials during day 1 (P>0·211) or during the MTT in the fasted or postprandial state (P>0·507). Accordingly, plasma acylated ghrelin, total glucagon-like peptide-1 and total peptide YY concentrations did not differ between trials during the MTT (all P>0·335). Ad libitum energy intake, assessed upon completion of the MTT, did not differ between trials (EB 6081 (sd 2260) kJ; OF 6182 (sd 1960) kJ; P=0·781). Plasma glucose and insulin concentrations were not different between trials (P>0·715). Fasted NEFA concentrations were lower in OF compared with EB (P=0·005), and TAG concentrations increased to a greater extent on OF than on EB during the MTT (P=0·009). The absence of compensatory changes in appetite-related variables after 1 d of mixed macronutrient overfeeding highlights the limited physiological response to defend against excess energy intake. This supports the concept that repeated discrete episodes of overconsumption may promote weight gain, while elevations in postprandial lipaemia may increase CVD risk.

Postprandial hypertriacylglycerolaemia is associated with an increased risk of developing CVD. How fat quality influences postprandial lipid response is scarcely explored in subjects with familial hypercholesterolaemia (FH). The aim of this study was to investigate the postprandial response of TAG and lipid sub-classes after consumption of high-fat meals with different fat quality in subjects with FH compared with normolipidaemic controls. A randomised controlled double-blind cross-over study with two meals and two groups was performed. A total of thirteen hypercholesterolaemic subjects with FH who discontinued lipid-lowering treatment 4 weeks before and during the study, and fourteen normolipidaemic controls, were included. Subjects were aged 18–30 years and had a BMI of 18·5–30·0 kg/m2. Each meal consisted of a muffin containing 60 g (70 E%) of fat, either mainly SFA (40 E%) or PUFA (40 E%), eaten in a random order with a wash-out period of 3–5 weeks between the meals. Blood samples were collected at baseline (fasting) and 2, 4 and 6 h after intake of the meals. In both FH and control subjects, the level of TAG and the largest VLDL sub-classes peaked at 2 h after intake of PUFA and at 4 h after intake of SFA. No significant differences were found in TAG levels between meals or between groups (0·25≤P≤0·72). The distinct TAG peaks may reflect differences in the postprandial lipid metabolism after intake of fatty acids with different chain lengths and degrees of saturation. The clinical impact of these findings remains to be determined.

Epidemiological studies demonstrate that poor glycaemic control is an independent risk factor for CVD. Postprandial glycaemia has been demonstrated as a better predictor of glycated Hb, the gold standard of glycaemic control, when compared with fasting blood glucose. There is a need for more refined strategies to tightly control postprandial glycaemia, particularly in those with type 2 diabetes, and nutritional strategies around meal consumption may be effective in enhancing subsequent glycaemic control. Whey protein administration around meal times has been demonstrated to reduce postprandial glycaemia, mediated through various mechanisms including an enhancement of insulin secretion. Whey protein ingestion has also been shown to elicit an incretin effect, enhancing the secretion of glucose-dependent insulinotropic peptide and glucagon-like peptide-1, which may also influence appetite regulation. Acute intervention studies have shown some promising results however many have used large dosages (50–55 g) of whey protein alongside high-glycaemic index test meals, such as instant powdered potato mixed with glucose, which does not reflect realistic dietary strategies. Long-term intervention studies using realistic strategies around timing, format and amount of whey protein in relevant population groups are required.

Dietary recommendations suggest decreased consumption of SFA to minimise CVD risk; however, not all foods rich in SFA are equivalent. To evaluate the effects of SFA in a dairy food matrix, as Cheddar cheese, v. SFA from a vegan-alternative test meal on postprandial inflammatory markers, a randomised controlled cross-over trial was conducted in twenty overweight or obese adults with metabolic abnormalities. Individuals consumed two isoenergetic high-fat mixed meals separated by a 1- to 2-week washout period. Serum was collected at baseline, and at 1, 3 and 6 h postprandially and analysed for inflammatory markers (IL-6, IL-8, IL-10, IL-17, IL-18, TNFα, monocyte chemotactic protein-1 (MCP-1)), acute-phase proteins C-reactive protein (CRP) and serum amyloid-A (SAA), cellular adhesion molecules and blood lipids, glucose and insulin. Following both high-fat test meals, postprandial TAG concentrations rose steadily (P < 0·05) without a decrease by 6 h. The incremental AUC (iAUC) for CRP was significantly lower (P < 0·05) in response to the cheese compared with the vegan-alternative test meal. A treatment effect was not observed for any other inflammatory markers; however, for both test meals, multiple markers significantly changed from baseline over the 6 h postprandial period (IL-6, IL-8, IL-18, TNFα, MCP-1, SAA). Saturated fat in the form of a cheese matrix reduced the iAUC for CRP compared with a vegan-alternative test meal during the postprandial 6 h period. The study is registered at clinicaltrials.gov under NCT01803633.

Previous studies regarding the acute effects of coffee on glycaemic control have used a single large dose of coffee, typically containing the caffeine equivalent of 2–4 servings of coffee. This study investigates whether the acute effects of coffee are dose-dependent, starting with a single serving. A total of ten healthy overweight males participated in a two-part randomised double-blind cross-over study. In the first part, they ingested 2, 4 or 8 g instant decaffeinated coffee (DC) dissolved in 400 ml water with caffeine added in proportion to the DC (total 100, 200 or 400 mg caffeine) or control (400 ml water) all with 50 g glucose. In the second part, they ingested the same amounts of DC (2, 4, 8 g) or control, but with a standard 100 mg caffeine added to each. Capillary blood samples were taken every 15 min for 2 h after each drink and glucose and insulin levels were measured. Repeated measures ANOVA on glucose results found an effect when caffeine was varied in line with DC (P=0·008). Post hoc analysis revealed that both 2 and 4 g DC with varied caffeine content increased the glycaemic response v. control. There was no effect of escalating doses of DC when caffeine remained constant at 100 mg. These results demonstrate that one standard serving of coffee (2 g) is sufficient to affect glucose metabolism. Furthermore, the amount of caffeine found in one serving (100 mg) is sufficient to mask any potential beneficial effects of increasing other components. No dose-dependent effect was found.

Studies have suggested that two major milk constituents, casein and Ca, favourably affect postprandial responses. However, effects of milk on postprandial metabolism are unknown. We therefore investigated effects of using milk with a fat-containing meal on lipid and glucose responses in overweight men. To identify the constituent responsible for possible effects, we also studied responses to Ca and protein. A total of sixteen men (BMI >27 kg/m2) participated in four postprandial tests. They consumed a breakfast (44 g of fat) plus a drink: a control drink, low-fat milk or a protein and Ca drink (500 ml). Blood samples were taken before the meals and at regular time points during 6 h thereafter. Compared with control, the incremental AUC (iAUC) for serum TAG was increased by 44 % after the protein meal (P= 0·015). Although the iAUC were not different (P= 0·051), peak glucose concentrations were reduced by 24 % after protein intake, as compared with control (P= 0·021). The decrease of 18 % after milk intake did not reach statistical significance. Compared with the milk meal, the iAUC for insulin was 52 % lower after the control meal (P= 0·035) and 51 % after the protein meal (P= 0·005). The present results indicate that the intake of milk with a fat-containing meal enhances postprandial TAG and insulin responses and may blunt glucose increases. The protein fraction of milk seems to be the main determinant for the effects on TAG and glucose. Ca did not change any of the postprandial responses.

It is unclear how timing of exercise relative to meal ingestion influences substrate balance and metabolic responses. The present study aimed to compare the effects of exercise performed before or after breakfast on fat balance and postprandial metabolism. A total of ten sedentary overweight men (aged 28·1 (sem 10·7) years, BMI 29·0 (sem 2·8) kg/m2) underwent three trials in random order involving: (1) performing no exercise (CON), or walking for 60 min at 50 % maximal O2 uptake either (2) before (Ex-Meal) or (3) after (Meal-Ex) consuming a standardised breakfast meal. In each trial an ad libitum lunch was provided 3·5 h after breakfast. Substrate utilisation was assessed by indirect calorimetry and blood was taken at regular intervals over an 8·5 h observation period. At the end of the observation period, fat balances in the Ex-Meal ( − 1043 (sem 270) kJ) and Meal-Ex ( − 697 (sem 201) kJ) trials were both significantly lower than CON (204 (sem 165) kJ) and fat balance in the Ex-Meal trial was significantly lower than in the Meal-Ex trial (all P <0·0001). Compared with the CON trial, the 8·5 h postprandial TAG response was only significantly lowered in the Ex-Meal trial ( − 17 %, P =0·025) and not in the Meal-Ex trial ( − 11 %, P =0·20). Both the Ex-Meal and Meal-Ex trials showed significantly lowered insulin responses relative to the CON trial (by 19 and 24 %, respectively, P <0·01 for both). There were no differences in lunch energy intake between trials. The present findings suggest that there may be an advantage for body fat regulation and lipid metabolism in exercising before compared with after breakfast. However, further study is needed to determine whether the present findings extend over the long term under free-living conditions.

High postprandial levels of TAG may further induce endothelial dysfunction and inflammation in subjects with high fasting levels of TAG, an effect that seems to be related to oxidative stress. The present study investigated whether minor compounds of olive oil with antioxidant activity decrease postprandial levels of soluble isoforms of intercellular adhesion molecule 1 (sICAM-1) and vascular cell adhesion molecule 1 (sVCAM-1), as surrogate markers of vascular inflammation, after a high-fat meal. A randomized crossover and blind trial on fourteen healthy and fourteen hypertriacylglycerolaemic subjects was performed. The study involved a 1-week adaptation lead-in period on a National Cholesterol Education Program Step I diet supplemented with extra-virgin olive oil (EVOO) containing 1125 mg polyphenols/kg and 350 mg tocopherols/kg, or refined olive oil (ROO) with no polyphenols or tocopherols. After a 12 h fast, the participants ate a high-fat meal enriched in EVOO or ROO (50 g/m2 body surface area), which on average provided 3700 kJ energy with a macronutrient profile of 72 % fat, 22 % carbohydrate and 6 % protein. Blood samples drawn hourly over the following 8 h demonstrated a similar postprandial TAG response for both EVOO and ROO meals. However, in both healthy and hypertriacylglycerolaemic subjects the net incremental area under the curve for sICAM-1 and sVCAM-1 were significantly lower after the EVOO meal. In conclusion, the consumption of EVOO with a high content of minor antioxidant compounds may have postprandial anti-inflammatory protective effects.

Raised serum cholesterol does not adequately explain the increased risk of CHD within populations or the relationship between diet and CHD. Nevertheless, the principal transport vehicle of cholesterol in the circulation, LDL, must still be regarded as the most atherogenic lipoprotein species, but not because of its contribution to serum cholesterol. The atherogenic potential of LDL in the majority of individuals arises from an increase in the number of small dense LDL particles and not from its cholesterol content per se. There is now a wealth of evidence from cross-sectional and prospective studies to show that LDL particle size is significantly associated with CHD and predictive of increased coronary risk. Moreover, there are a number of credible mechanisms to link small dense LDL with the atherogenic process. The rate of influx of serum lipoproteins into the arterial wall is a function of particle size, and will thus be more rapid for small dense LDL. Components of the extracellular tissue matrix in the intima, most notably proteoglycans, selectively bind small dense LDL with high affinity, sequestering this lipoprotein in a pro-oxidative environment. The oxidation of LDL promotes the final deposition of cholesterol in the arterial wall, and numerous studies have shown small dense LDL to be more susceptible to oxidative modification than its larger and lighter counterparts. An increase in the number of small dense LDL particles may originate from a defect in the metabolism of triacylglycerol-rich lipoproteins. One mechanism may involve the overproduction and increased residence time of large triacylglycerol-rich VLDL in the postprandial phase, a situation thought to arise through pathways of insulin resistance.

Postprandial plasma insulin concentrations after a single high-fat meal may be modified by the presence of specific fatty acids although the effects of sequential meal ingestion are unknown. The aim of the present study was to examine the effects of altering the fatty acid composition in a single mixed fat–carbohydrate meal on glucose metabolism and insulin sensitivity of a second meal eaten 5 h later. Insulin sensitivity was assessed using a minimal model approach. Ten healthy post-menopausal women underwent four two-meal studies in random order. A high-fat breakfast (40 g fat) where the fatty acid composition was predominantly saturated fatty acids (SFA), n-6 polyunsaturated fatty acids (PUFA), long-chain n-3 PUFA or monounsaturated fatty acids (MUFA) was followed 5 h later by a low-fat, high-carbohydrate lunch (5·7 g fat), which was identical in all four studies. The plasma insulin response was significantly higher following the SFA meal than the other meals after both breakfast and lunch (P<0·006) although there was no effect of breakfast fatty acid composition on plasma glucose concentrations. Postprandial insulin sensitivity (SI(Oral)) was assessed for 180 min after each meal. SI(Oral) was significantly lower after lunch than after breakfast for all four test meals (P=0·019) following the same rank order (SFA < n-6 PUFA < n-3 PUFA < MUFA) for each meal. The present study demonstrates that a single meal rich in SFA reduces postprandial insulin sensitivity with ‘carry-over’ effects for the next meal.

The effect of carbohydrate, protein and fat ingestion on simple as well as complex cognitive functions and the relationship between the respective postprandial metabolic changes and changes in cognitive performance were studied in fifteen healthy male students. Subjects were tested in three sessions, separated by 1 week, for short-term changes in blood variables, indirect calorimetry, subjective performance and different objective performance tasks using a repeated-measures counterbalanced cross-over design. Measurements were made after an overnight fast before and hourly during 3 h after test meal ingestion. Test meals consisted of either pure carbohydrates, protein or fat and were served as isoenergetic (1670 kJ) spoonable creams with similar sensory properties. Most aspects of subjective performance did not differ between test meals. For all objective tasks, however, postprandial cognitive performance was best after fat ingestion concomitant with an almost constant glucose metabolism and constant metabolic activation state measured by glucagon:insulin (G:I). In contrast, carbohydrate as well as protein ingestion resulted in lower overall cognitive performance, both together with partly marked changes (P<0.001) in glucose metabolism and metabolic activation. They also differently affected specific cognitive functions (P<0.05) in relation to their specific effect on metabolism. Carbohydrate ingestion resulted in relatively better short-term memory and accuracy of tasks concomitant with low metabolic activation, whereas protein ingestion resulted in better attention and efficiency of tasks concomitant with higher metabolic activation. Our findings support the concept that good and stable cognitive performance is related to a balanced glucose metabolism and metabolic activation state.

Previous studies in this laboratory have elicited a monophasic response in postprandial plasma triacylglycerol (TAG) level with fat intakes of 0.5 g fat/kg body weight accompanied by about 17 g carbohydrate as lactose. Recent studies involving the same level of fat with a higher level of carbohydrate, 136 g of which 60 g was sucrose, appeared to elicit a biphasic response. The present study compared these two test meals and showed a significant meal × time interaction for plasma total TAG (P = 0.0228) reflecting a monophasic response with the lower-carbohydrate test meal. The higher-carbohydrate meal induced significantly higher insulin and glucose-dependent insulinotropic polypeptide responses (P = 0.0009 and P = 0.0041 respectively). A significant meal × time interaction was seen for plasma non-esterified fatty acids (P = 0.0437). The biphasic plasma TAG response seen with the high-carbohydrate meal largely reflected the TAG-rich lipoprotein (TRL) or chylomicron fraction, which would tend to suggest a biphasic pattern of absorption. This was borne out by TRL-TAG fatty acid compositions. Both peaks in the biphasic response showed active incorporation of the main dietary fatty acids, 18:1n−9, 18:2n−6 and 18:3n−3 into TRL-TAG. These results indicate that under the specific test-meal conditions used in the present study, a biphasic pattern of fat absorption was seen.

The physiological importance and mechanism of the postprandial fall in plasma Zn concentration is not well understood. In order to gain further information on this apparent redistribution of plasma Zn, a stable isotope, 70Zn, was used to study the effect of a breakfast meal on plasma Zn kinetics. Nine women participated in two trials, a fasting trial and a breakfast-meal trial; five of the women participated in a third trial in which the energy content of the breakfast meal was doubled. At each trial, 0.1mg of 70Zn was infused intravenously, and the plasma disappearance of the isotope was analysed using a two-compartment model of Zn kinetics. Plasma Zn concentration fell significantly following the two trials in which the subjects were given meals, reaching low points that were 13 and 19 %, respectively, below concentrations at comparable times during the fasting trial. Kinetic analysis revealed that after the doubled breakfast meal there was a significant fall (P < 0.007) in the size of the most rapidly turning over Zn pool (pool (a)) from 2.90 (se 0.13)mg in the fasting state to 2.47 (se 0.14) mg postprandially. The fractional turnover rate of pool (a) to other extravascular Zn pools, i.e. outside the two-compartment system, was also significantly elevated after the doubled breakfast meal (P < 0.05). These results suggest that the decline in plasma Zn concentration following a meal is due to a redistribution of Zn from the plasma to other more slowly turning over extravascular pools that may be involved in the assimilation and metabolism of fuels following food intake.

The present study examined the influence of training, followed by a short period of detraining, on postprandial lipaemia. Fourteen normolipidaemic, recreationally active young adults aged 18–31 years participated, in two self-selected groups: three men and five women (BMI 21·7–27·6 kg/m2) completed 13 weeks of running training, after which they refrained from exercise for 9 d; three men and three women (BMI 21·5–25·6 kg/m2) maintained their usual lifestyle. Oral fat tolerance tests were conducted at baseline and again 15 h, 60 h and 9 d after the runners' last training session. Blood samples were drawn after an overnight fast and at intervals for 6 h after consumption of a high-fat meal (1·2 g fat, 1·4 g carbohydrate, 70·6 kJ energy/kg body mass). Heparin was then administered (100 IU/kg) and a further blood sample was drawn for measurement of plasma lipoprotein lipase (EC 3.1.1.34; LPL) activity. Endurance fitness improved in runners, relative to controls (maximal O2 uptake +3·2 (SE 1·1) ml/kg per min v. − 1·3 (SE 1·2) ml/kg per min; P < 0·05). In the absence of the acute effect of exercise, i.e. 60 h after the last training session, there was no effect of training on either postprandial lipaemia or on post-heparin LPL activity. However, changes during 9 d of detraining in both these variables differed significantly between groups; after 2 d without exercise (60 h test), the runners' lipaemic response was 37% higher than it was the morning after their last training session (15 h test; runners v. controls P < 0·05), with a reciprocal decrease in post-heparin LPL activity (P < 0·01). These findings suggest that improved fitness does not necessarily confer an effect on postprandial lipaemia above that attributable to a single session of exercise.

Previous studies have noted the presence of an early postprandial peak in plasma triacylglycerol concentrations following successive fat-rich meals. An earlier study has shown that the triacylglycerol in this early peak originates from a previous meal. The present study was performed to investigate the effects of different second meals on the plasma triacylglycerol response. Six healthy subjects were studied on four occasions each. At 5 h following a fat-rich breakfast they ingested one of the following in a balanced design: a fat-rich meal, a low-fat meal, water or nothing by mouth. Blood samples were taken for 2.5 h following the second meal. An early peak in chylomicron and plasma triacylglycerol concentrations was seen following both low-fat and fat-rich second meals but not following water. During studies investigating postprandial lipaemia, further meals must be avoided, even if they contain no fat, although water may be allowed.