The long-term cholesterol-lowering effect of replacing intake of SFA with PUFA is well established, but has not been fully explained mechanistically. We examined the postprandial response of meals with different fat quality on expression of lipid genes in peripheral blood mononuclear cells (PBMC) in subjects with and without familial hypercholesterolaemia (FH). Thirteen subjects with FH (who had discontinued lipid-lowering treatment ≥4 weeks prior to both test days) and fourteen normolipidaemic controls were included in a randomised controlled double-blind crossover study with two meals, each with 60 g of fat either mainly SFA (about 40% energy) or n-6 PUFA (about 40% energy). PBMC were isolated in fasting, and 4 and 6 h postprandial blood samples. Expression of thirty-three lipid genes was analysed by reverse transcription quantitative PCR. A linear mixed model was used to assess postprandial effects between meals and groups. There was a significant interaction between meal and group for MSR1 (P = 0·03), where intake of SFA compared with n-6 PUFA induced a larger reduction in gene expression in controls only (P = 0·01). Intake of SFA compared with n-6 PUFA induced larger reductions in gene expression levels of LDLR and FADS1/2, smaller increases of INSIG1 and FASN, and larger increases of ABCA1 and ABCG1 (P = 0·01 for all, no group interaction). Intake of SFA compared with n-6 PUFA induced changes in gene expression of cholesterol influx and efflux mediators in PBMC including lower LDLR and higher ABCA1/G1, potentially explaining the long-term cholesterol-raising effect of a high SFA intake.

Although polyphenols inhibit glucose absorption and transport in vitro, it is uncertain whether this activity is sufficient to attenuate glycaemic response in vivo. We examined this using orange juice, which contains high levels of hesperidin. We first used a combination of in vitro assays to evaluate the potential effect of hesperidin and other orange juice components on intestinal sugar absorption and then tested whether this translated to an effect in healthy volunteers. Hesperidin attenuated transfer of 14C-labelled glucose across differentiated Caco-2/TC7 cell monolayers. The involvement of the sugar transporter GLUT2 was demonstrated by experiments carried out in the absence of Na to exclude the contribution of sodium-glucose linked transporter 1 and further explored by the use of Xenopus laevis oocytes expressing human GLUT2 or GLUT5. Fructose transport was also affected by hesperidin partly by inhibition of GLUT5, while hesperidin, even at high concentration, did not inhibit rat intestinal sucrase activity. We conducted three separate crossover interventions, each on ten healthy volunteers using orange juice with different amounts of added hesperidin and water. The biggest difference in postprandial blood glucose between orange juice and control, containing equivalent amounts of glucose, fructose, sucrose, citric acid and ascorbate, was when the juice was diluted (ΔCmax=–0·5 mm, P=0·0146). The effect was less pronounced when the juice was given at regular strength. Our data indicate that hesperidin can modulate postprandial glycaemic response of orange juice by partial inhibition of intestinal GLUT, but this depends on sugar and hesperidin concentrations.

Postprandial inflammation is an important factor for human health since chronic low-grade inflammation is associated with chronic diseases. Dairy products have a weak but significant anti-inflammatory effect on postprandial inflammation. The objective of the present study was to compare the effect of a high-fat dairy meal (HFD meal), a high-fat non-dairy meal supplemented with milk (HFM meal) and a high-fat non-dairy control meal (HFC meal) on postprandial inflammatory and metabolic responses in healthy men. A cross-over study was conducted in nineteen male subjects. Blood samples were collected before and 1, 2, 4 and 6 h after consumption of the test meals. Plasma concentrations of insulin, glucose, total cholesterol, LDL-cholesterol, HDL-cholesterol, TAG and C-reactive protein (CRP) were measured at each time point. IL-6, TNF-α and endotoxin concentrations were assessed at baseline and endpoint (6 h). Time-dependent curves of these metabolic parameters were plotted, and the net incremental AUC were found to be significantly higher for TAG and lower for CRP after consumption of the HFM meal compared with the HFD meal; however, the HFM and HFD meals were not different from the HFC meal. Alterations in IL-6, TNF-α and endotoxin concentrations were not significantly different between the test meals. The results suggest that full-fat milk and dairy products (cheese and butter) have no significant impact on the inflammatory response to a high-fat meal.

The co-ingestion of protein, fat and fibre with carbohydrate reportedly affects postprandial glucose, insulin and incretin (glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1)) responses. However, the effects of combination dishes with carbohydrate-rich foods at typically eaten amounts remain unclear. The objective of the present study was to evaluate the effects of consuming recommended amounts of side dishes with boiled white rice in the same meal on postprandial plasma glucose, insulin and incretin hormone responses. A total of nine healthy male volunteers consumed four different meals in a random order on separate days. The test meals were as follows: S, white rice; SM, addition of protein-rich main dishes to the S meal; SMF, addition of a fat-rich food item to the SM meal; SMFV, addition of vegetables to the SMF meal. Plasma glucose, GIP and GLP-1 and serum insulin concentrations were determined during a 3 h period after consumption of these meals. Postprandial glucose responses were lower after SMFV meal consumption than after consumption of the other meals. The incremental AUC for GIP (0–180 min) were largest after consumption of the SMF and SMFV meals, followed by that after SM meal consumption, and was smallest after S meal consumption (P< 0·05). Furthermore, we found GIP concentrations to be dose dependently increased by the fat content of meals of ordinary size, despite the amount of additional fat being small. In conclusion, the combination of recommended amounts of main and vegetable side dishes with boiled white rice is beneficial for lowering postprandial glucose concentrations, with an increased incretin response, when compared with white rice alone.

Milk consumption decreases inflammatory stress in overweight and obese subjects. Casein is the major protein in milk and enhances the secretion of insulin that has anti-inflammatory activity. The aim of the present study was to compare the acute effect of meals rich in casein and carbohydrate and a combination of both nutrients on postprandial plasma concentrations of IL-6, a marker of inflammation, in obese women. A total of twenty-five obese women aged 38–68 years consumed isoenergetic meals rich in potato (POT) or casein (CA) or a combination of both these meals (POT + CA), in random order in a cross-over trial. After an overnight fast, blood samples were collected before and at 1 and 4 h after the meals and circulating concentrations of IL-6, glucose, insulin and NEFA were measured. Plasma IL-6 concentrations increased significantly (P < 0·001) during 4 h after the meals. The AUC of postprandial IL-6 concentrations was not significantly (P = 0·77) different among the meals. Postprandial serum insulin concentration AUC was significantly higher during the POT + CA meal compared with the POT meal (P = 0·001) and the CA meal (P < 0·05), which in turn was significantly higher than the POT meal (P < 0·05). These data show that while ingestion of CA alone or combined with POT acutely increases circulating insulin concentrations, it does not appreciably alter the postprandial increase in plasma IL-6 concentrations in obese women.

Prior studies assessing the metabolic effects of different types of carbohydrates have focused on their glycaemic response. However, the response of postprandial cardiometabolic risk indicators has not been considered in these studies. The present study assessed postprandial lipid responses to two forms of carbohydrates used as reference foods for glycaemic index determinations, white bread (50 g available carbohydrate) and glucose (50 g), under controlled conditions and with intra-individual replicate determinations. A total of twenty adults (20–70 years) underwent two cycles of challenges with each pair of reference foods (four challenges/person), administered in a random order on separate days under standard conditions. Serum lipids (total cholesterol, LDL-cholesterol, HDL-cholesterol, TAG and NEFA), glucose and insulin were monitored for 5 h post-ingestion. Oral glucose resulted in greater glycaemic and insulinaemic responses than white bread for the first 90 min and a greater subsequent decline after 120 min (P =0·0001). The initial decline in serum NEFA concentrations was greater after the oral glucose than after the white bread challenge, as was the rebound after 150 min (P =0·001). Nevertheless, the type of carbohydrate had no significant effect on postprandial total cholesterol, LDL-cholesterol and HDL-cholesterol concentrations. Following an initial modest rise in TAG concentrations in response to both challenges, the values dropped below the fasting values for oral glucose but not for the white bread challenge. These data suggest that the type of carbohydrate used to determine the glycaemic index, bread or glucose, has little or modest effects on postprandial plasma cholesterol concentrations. Differences in TAG and NEFA concentrations over the 5 h time period were modest, and their clinical relevance is unclear.

Strong epidemiological evidence suggests that slow prenatal or postnatal growth is associated with an increased risk of CVD and other metabolic diseases. However, little is known whether early growth affects postprandial metabolism and, especially, the appetite regulatory hormone system. Therefore, we investigated the impact of early growth on postprandial appetite regulatory hormone responses to two high-protein and two high-fat content meals. Healthy, 65–75-year-old volunteers from the Helsinki Birth Cohort Study were recruited; twelve with a slow increase in BMI during the first year of life (SGI group) and twelve controls. Subjects ate a test meal (whey meal, casein meal, SFA meal and PUFA meal) once in a random order. Plasma glucose, insulin, TAG, NEFA, ghrelin, peptide tyrosine-tyrosine (PYY), glucose-dependent insulinotropic peptide, glucagon-like peptide-1 and a satiety profile were measured in the fasting state and for 4 h after each test meal. Compared with the controls, the SGI group had about 1·5-fold higher insulin responses after the whey meal (P= 0·037), casein meal (P= 0·023) and PUFA meal (P= 0·002). TAG responses were 34–69 % higher for the SGI group, but only the PUFA-meal responses differed significantly between the groups. The PYY response of the SGI group was 44 % higher after the whey meal (P= 0·046) and 115 % higher after the casein meal (P= 0·025) compared with the controls. No other statistically significant differences were seen between the groups. In conclusion, early growth may have a role in programming appetite regulatory hormone secretion in later life. Slow early growth is also associated with higher postprandial insulin and TAG responses but not with incretin levels.

Different dietary proteins vary in their ability to influence satiety and reduce food intake. The present study compared the effects of four protein meals, whey, tuna, turkey and egg albumin, on postprandial glucose and insulin concentrations as well as on appetite measures and energy intake in twenty-two lean, healthy men. This was a randomised, cross-over design study where participants consumed four liquid test meals on separate occasions followed by the collection of regular blood samples (fasting, +30, 60, 90, 120, 180 and 240 min). They were then offered a buffet meal 4 h later. The blood glucose response after the consumption of the test meal, as an incremental area under the curve (AUC), was significantly lower with the whey meal than with the turkey (P < 0·023) and egg (P < 0·001) meals, but it was not lower than with the tuna meal (P < 0·34). The AUC blood insulin after the consumption of the test meal was significantly higher with the whey meal than with the tuna, turkey and egg meals (all P < 0·001). The AUC rating of hunger was significantly lower with the whey meal than with the tuna (P < 0·033), turkey (P < 0·001) and egg (P < 0·001) meals. Mean energy intake at the ad libitum meal was significantly lower (P < 0·001) with the whey meal than with the tuna, egg and turkey meals. There was a strong relationship between self-rated appetite, postprandial insulin response and energy intake at lunch. Whey protein meal produced a greater insulin response, reduced appetite and decreased ad libitum energy intake at a subsequent meal compared with the other protein meals, indicating a potential for appetite suppression and weight loss in overweight or obese individuals.

Healthy male volunteers consumed hot lunches consisting of cooked white rice, fried chicken fillet, raisins, bigarreaus (sweet cherries) and curry sauce with carbohydrate: fat ratios of either 0·77 or 2·04, and polysaccharide: (mono+di)saccharide ratios (P: MD) varying between 5·3 and 0·95. Before and at various time intervals after the start of the meal, blood samples were analysed for glucose, insulin, triacylglycerol (TG), free glycerol (FG), free fatty acids (FFA) and cholesterol. Elevated postprandial glucose and insulin peaks were induced by the meals containing a larger amount of carbohydrate. The type of carbohydrate in the meal appeared to have little or no effect on the peak maximum. A small second glucose peak was seen at 2 h after the meals with P: MD > 3·1. The TG concentration in the blood showed a similar and rapid rise. After the meal containing the largest amount of simple sugars, the TG curve levelled off 1 h after the start of the meal and then remained at a nearly constant level (1·5 mM). In contrast, a larger amount of complex carbohydrates induced a TG concentration which rapidly rose to a maximum of 1·75 mM, and subsequently decreased slowly to somewhat below that of the simple sugar-rich meal at 4 h. The postprandial curves after the fat-rich meals showed a continuous rise of TG up to a maximum of about 2 mM at 2 h, and a subsequent slow decrease. FG and FFA all showed a rapid drop immediately after the start of the consumption of the meals, followed by a rebound at 1 h. The postprandial curves of total cholesterol, as well as the areas below the curve of both total cholesterol and free, unesterified cholesterol were lower after the carbohydrate-rich meals than after the fat-rich meals. This is attributed to the larger amount of cholesterol in the fat-rich meals.