The present study investigated the potential of a wild blueberry (WB)-enriched diet to improve blood lipid profile and modulate the expression of genes related to lipid homeostasis in obese Zucker rats (OZR), a model of the metabolic syndrome with severe dyslipidaemia. For this purpose, twenty OZR and twenty lean Zucker rats (LZR; controls) were placed either on a control (C) or an 8 % WB diet for 8 weeks. Plasma total cholesterol (TC), HDL-cholesterol and TAG concentrations were determined. The relative expression of six genes involved in lipid metabolism was also determined in both the liver and the abdominal adipose tissue (AAT). Plasma TAG and TC concentrations were significantly lower in the OZR following WB consumption (4228 (sem 471) and 2287 (sem 125) mg/l, respectively) than in those on the C diet (5475 (sem 315) and 2631 (sem 129) mg/l, P< 0·05), while there was no change in HDL-cholesterol concentration. No significant effects were observed for plasma lipids in the LZR. Following WB consumption, the expression of the transcription factors PPARα and PPARγ in the OZR was increased in the AAT, while that of sterol regulatory element-binding protein 1 (SREBP-1) was decreased in the liver and AAT. The expression of fatty acid synthase was significantly decreased in both the liver and AAT and that of ATP-binding cassette transporter 1 was increased in the AAT following WB consumption. In conclusion, WB consumption appears to improve lipid profiles and modulate the expression of key enzymes and transcription factors of lipid metabolism in severely dyslipidaemic rats.

The present study aimed to investigate the responses of broilers with different hatching weights (HW) to dietary methionine (Met). A total of 192 1-d-old Arbor Acres broiler chicks with different HW (heavy: 48·3 (sem 0·1) g and light: 41·7 (sem 0·1) g) were allocated to a 2 (HW) × 2 (Met) factorial arrangement with six replicates of eight chicks. Control starter (1–21 d) and finisher (22–42 d) diets contained 0·50 and 0·43 % Met, respectively. Corresponding values for a high-Met treatment were 0·60 and 0·53 %. Light chicks had poorer (P< 0·05) growth performance and breast muscle weight and lower (P< 0·05) insulin-like growth factor-I (IGF-I) concentration and mRNA level in breast muscle than heavy chicks when both were fed the control diets. High-Met diets improved performance and promoted breast muscle growth and IGF-I concentration in light chicks (P< 0·05). Increased IGF-I and target of rapamycin (TOR) mRNA levels as well as decreased eIF4E-binding protein 1 (4EBP1), atrogin-1 and forkhead box O 4 (FOXO4) mRNA levels were induced by high-Met diets in light chicks (P< 0·05). In conclusion, the Met requirement of broilers might depend on their HW and Met levels used in the control diets in the present study were adequate for heavy chicks but inadequate for light chicks, resulting in poorer performance and breast muscle growth, which were improved by increasing dietary Met supply presumably through alterations in IGF-I synthesis and gene expression of the TOR/4EBP1 and FOXO4/atrogin-1 pathway.

The metabolic syndrome (MetS) is associated with an increased risk of cardiac mortality, as it is characterised by the clustering of multiple cardiovascular risk factors. Studies have shown that capsaicin (red pepper) may be useful as a nutraceutical, ameliorating metabolic profile and cardiovascular function. The aim of the present study was to investigate the cardiovascular and metabolic effects of orally administered capsaicin in rats with the MetS. Neonate spontaneously hypertensive rats were injected with monosodium glutamate and subjected to one of the following three treatments by oral administration for 14 d, between 27 and 30 weeks: low-dose capsaicin (CAP05, n 18, synthetic capsaicin powder diluted in a vehicle (10 % ethyl alcohol) plus 0·5 mg/kg body weight (BW) of capsaicin); high-dose capsaicin (CAP1, n 19, synthetic capsaicin powder diluted in a vehicle (10 % ethyl alcohol) plus 1 mg/kg BW of capsaicin); control (C, n 18, vehicle). Lee's index, lipid/metabolic profile, and cardiovascular parameters with the rats being conscious, including arterial pressure (AP) and heart rate (HR) variability, as well as aortic wall thickness (haematoxylin and eosin staining) and CD68 (cluster of differentiation 68) antibody levels (monocyte/macrophage immunostaining) were evaluated. Weight, Lee's index, and lipid and metabolic parameters, as well as AP and HR and aortic wall thickness, were similar between the groups. Capsaicin determined HR variability improvement (16·0 (sem 9·0), 31·0 (sem 28·2) and 31·3 (sem 19·0) ms2 for the C, CAP05 and CAP1 groups, respectively, P= 0·003), increased vascular sympathetic drive (low-frequency component of systolic AP variability: 3·3 (sem 2·8), 8·2 (sem 7·7) and 12·1 (sem 8·8) mmHg2 for the C, CAP05 and CAP1 groups, respectively, P< 0·001) and increased α-index (spontaneous baroreflex sensitivity). The present data show that capsaicin did not improve lipid and glucose abnormalities in rats with the MetS. However, beneficial cardiovascular effects were observed with this nutraceutical.

Obese individuals have more (hyperplastic) and larger (hypertrophic) adipocytes in their white adipose tissue (WAT) than normal-weight individuals. The difference in cell number emerges early in childhood, suggesting that this is a critical period for being susceptible to obesity. Breast-feeding has been shown to be protective against obesity, and we have previously shown in mice that the physical structure of lipids in human milk may contribute to this protective effect. In the present study, we investigated how differences in the physical structure of lipids in the early diet may modulate adipose tissue development. Male mice were fed a diet containing control infant milk formula (Control IMF; Danone Research) or Nuturis® (Concept IMF with large phospholipid-coated lipid droplets; Danone Research) from postnatal day (PN)16 to 42. Subsequently, mice were challenged with a moderate Western-style diet (WSD) until PN98, and body composition was monitored by dual-energy X-ray absorptiometry. Epididymal WAT was analysed for adipocyte size, number and gene expression of metabolic transcription factors. Early Concept IMF exposure reduced fat accumulation during the WSD challenge by 30 % compared with the Control IMF. It reduced adipocyte size without affecting adipocyte number in adult mice. The Concept IMF decreased the expression of PPARγ, CCAAT/enhancer-binding protein and retinoid X receptor α in WAT in adulthood, key regulators of metabolic activity. In conclusion, Concept IMF exposure in early life reduced susceptibility to obesity in adult life, by preventing adipocyte hypertrophia upon adult dietary challenge without affecting adipogenesis. These data emphasise the importance of the physical properties of dietary lipids in early life in obesity risk later in life.

Impaired pancreatic β-cell function, as observed in the cases of early nutrition disturbance, is a major hallmark of metabolic diseases arising in adulthood. In the present study, we aimed to investigate the function/composition of the muscarinic acetylcholine receptor (mAChR) subtypes, M2 and M3, in the pancreatic islets of adult offspring of rats that were protein malnourished during lactation. Neonates were nursed by mothers that were fed either a low-protein (4 %, LP) or a normal-protein (23 %, NP) diet. Adult rats were pre-treated with anti-muscarinic drugs and subjected to the glucose tolerance test; the function and protein expression levels of M2mAChR and M3mAChR were determined. The LP rats were lean and hypoinsulinaemic. The selective M2mAChR antagonist methoctramine increased insulinaemia by 31 % in the NP rats and 155 % in the LP rats, and insulin secretion was increased by 32 % in the islets of the NP rats and 88 % in those of the LP rats. The selective M3mAChR antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide decreased insulinaemia by 63 % in the NP rats and 40 % in the LP rats and reduced insulin release by 41 % in the islets of the NP rats and 28 % in those of the LP rats. The protein expression levels of M2mAChR and M3mAChR were 57 % higher and 53 % lower, respectively, in the islets of the LP rats than in those of the NP rats. The expression and functional compositions of M2mAChR and M3mAChR were altered in the islets of the LP rats, as a result of metabolic programming caused by the protein-restricted diet, which might be another possible effect involved in the weak insulin secretion ability of the islets of the programmed adult rats.

The aim of the present study was to assess the effect of dietary macronutrients on postprandial incretin responses and satiety and hunger sensation in obese and normal-weight women. A total of eleven obese and nine normal-weight women were recruited for the assessment of plasma concentrations of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and insulin and the sensation of satiety and hunger using a visual analogue scale before and during a 6 h period after administration of three different macronutrient test meals. The AUCtotalGLP-1 and AUCtotalGIP values were decreased in obese women after the consumption of a fatty meal and all the test meals, respectively. However, the AUCtotal insulin value after a carbohydrate meal was greater in the obese group. The AUCtotal satiety value was decreased only after the intake of the protein meal in obese women when compared with normal-weight women. After the consumption of the fatty meal, a significant positive correlation between maximum satiety sensation and the AUCtotal GLP-1 value in the obese group and that between minimum hunger sensation and the AUCtotal GLP-1 value in the normal-weight group were observed. In conclusion, the findings of the present study suggest that: (1) satiety sensation after consumption of carbohydrate and protein meals in the obese group is related to the postprandial insulin response, while after consumption of a fatty meal, it is related to the postprandial GLP-1 release; (2) the postprandial GIP response does not influence the sensation of satiety and hunger; (3) the reduced GLP-1 release after the intake of a fatty meal in obese individuals may explain impaired satiety sensation; (4) the impaired postprandial GIP response is not related to the consumption of macronutrients and may be the early indicator of incretin axis dysfunction in obese women.

An adequate immune system is required to prevent diarrhoea in neonates, and IgA provides protection against microbial antigens on mucosal surfaces. Although β-carotene supplementation has been expected to enhance the retinoic acid (RA)-mediated immune response in neonates, the exact mechanism of the enhancement of mucosal IgA production in the small intestine by β-carotene is still unclear. In the present study, we investigated the effect of supplemental β-carotene on the concentrations of IgA, the numbers of IgA antibody-secreting cells (ASC) and the mRNA expressions of IgA C-region, CCL25, retinoid X receptor (RXR) α, retinoic acid receptor (RAR) α and RARγ in the jejunum and ileum of weanling mice. Weanling mice were fed rodent feed or 50 mg/kg β-carotene-supplemented rodent feed for 7, 14 or 21 d. The concentrations of IgA and the numbers of IgA ASC in the jejunum and ileum of mice increased markedly with age, and supplemental β-carotene increased the concentrations of IgA, the numbers of IgA ASC and the mRNA expressions of IgA C-region, CCL25 and RARγ in the jejunum after 14 and 21 d of treatment. Supplemental β-carotene increased the numbers of IgA ASC in the ileum after 14 and 21 d of treatment, but the concentrations of IgA in the ileum were not affected by β-carotene supplementation. The mRNA expressions of RXRα and RARα in the jejunum and those of RXRα and RARγ in the ileum after 21 d of treatment were enhanced by β-carotene supplementation. These results indicate that β-carotene supplementation in weanling mice is effective to enhance mucosal IgA induction in the jejunum or ileum and that the effects are mainly due to the RA-mediated immune response.

We have demonstrated previously that n-3 PUFA endogenously produced by fat-1 transgenic mice regulate CD4+ T-cell function by affecting the formation of lipid rafts, liquid-ordered mesodomains in the plasma membrane. In the present study, we tested the effects of dietary sources of n-3 PUFA, i.e. fish oil (FO) or purified DHA, when compared with an n-6 PUFA-enriched maize oil control diet in DO11.10 T-cell receptor transgenic mice. Dietary n-3 PUFA were enriched in CD4+ T-cells, resulting in the increase of the n-3:n-6 ratio. Following antigen-specific CD4+ T-cell activation by B-lymphoma cells pulsed with the ovalbumin 323–339 peptide, the formation of liquid-ordered mesodomains at the immunological synapse relative to the whole CD4+ T-cell, as assessed by Laurdan labelling, was increased (P< 0·05) in the FO-fed group. The FO diet also suppressed (P< 0·05) the co-localisation of PKCθ with ganglioside GM1 (monosialotetrahexosylganglioside), a marker for lipid rafts, which is consistent with previous observations. In contrast, the DHA diet down-regulated (P< 0·05) PKCθ signalling by moderately affecting the membrane liquid order at the immunological synapse, suggesting the potential contribution of the other major n-3 PUFA components of FO, including EPA.

Dissimilatory reduction of sulphate by sulphate-reducing bacteria in the rumen produces sulphide, which can lead to a build-up of the toxic gas hydrogen sulphide (H2S) in the rumen when increased concentrations of sulphate are consumed by ruminants. We hypothesised that adding ferric Fe would competitively inhibit ruminal sulphate reduction. The effects of five concentrations and two sources (ferric citrate or ferric ammonium citrate) of ferric Fe were examined in vitro (n 6 per treatment). Rumen fluid was collected from a steer that was adapted to a high-concentrate, high-sulphate diet (0·51 % S). The addition of either source of ferric Fe decreased (P< 0·01) H2S concentrations without affecting gas production (P= 0·38), fluid pH (P= 0·80) or in vitro DM digestibility (P= 0·38) after a 24 h incubation. An in vivo experiment was conducted using eight ruminally fistulated steers (543 (sem 12) kg) in a replicated Latin square with four periods and four treatments. The treatments included a high-concentrate, high-sulphate control diet (0·46 % S) or the control diet plus ferric ammonium citrate at concentrations of 200, 300 or 400 mg Fe/kg diet DM. The inclusion of ferric Fe did not affect DM intake (P= 0·21). There was a linear (P< 0·01) decrease in the concentration of ruminal H2S as the addition of ferric Fe concentrations increased. Ferric citrate appears to be an effective way to decrease ruminal H2S concentrations, which could allow producers to safely increase the inclusion of ethanol co-products.

Characterisation of long-term adherence to EPA and DHA intakes through biomarkers and dietary assessments has implications for interpreting the findings of long-term intervention studies. Adherence to dietary advice targeting an EPA+DHA intake of 1 g/d was examined over 1 year. Men and women (n 45) received dietary advice to increase EPA and DHA intakes from seafood, nutraceutical (fish oil) or functional food sources, while a fourth group received combined advice. Blood biomarkers and dietary intakes of EPA and DHA were evaluated at baseline and post-intervention at weeks 4, 8, 12, 24 and 52. Assessment by 3 d diet records indicated that EPA+DHA intakes increased relative to baseline in weeks 4–52 following the seafood, nutraceutical and combined advice (advice group × time effect, P= 0·03). The percentage of DHA in plasma and whole blood and the percentage of EPA in erythrocytes, plasma and whole blood were higher in weeks 4–52 when compared with the corresponding baseline measurement. In contrast, the percentage of DHA in erythrocytes increased to a maximum at week 12 and returned to baseline levels in weeks 24 and 52 (time effect, P< 0·01). Measurement of the percentage of DHA in erythrocytes indicates that adherence was sustained during the first 12 weeks following the dietary advice, while other blood measurements of the percentage of EPA and DHA and dietary assessment suggest short-term increases in EPA+DHA intakes immediately before weeks 24 and 52. The percentage of DHA in erythrocytes characterises adherence to EPA and DHA intakes in long-term interventions.

The present study investigated the effect of Bifidobacterium animalis ssp. lactis Bf-6 (LMG 24 384) (Bf-6)-supplemented yogurt on colonic transit time (CTT). A triple-blinded, randomised, placebo-controlled, two-period cross-over trial was conducted with sixty-eight women with a self-reported history of straining during bowel movements or hard or lumpy stools in the past 2 years. As per regulatory requirements for probiotic studies, eligible women were generally healthy and not actively constipated at the time of enrolment. Participants consumed both Bf-6 and placebo yogurts for 14 d each in a randomised order, with a 6-week washout period between the treatments. The primary outcome, CTT, was assessed via Sitz marker X-rays. The average CTT was 42·1 h for the active period and 43·3 h for the control period (mean difference 1·2 h, 95 % CI − 4·9, 7·4). Since the statistical tests for the cross-over study implied that the mean CTT for the active and control periods in period 2 were biased, the standard protocol suggests examining the results of only period 1 as a traditional randomised controlled trial. This showed that the mean CTT was 35·2 h for the active period v. 52·9 h for the control period (P= 0·015). Bootstrapping demonstrated that both the mean and median differences remained significant (P= 0·016 and P= 0·045, respectively). Few adverse events were noted, with no differences among the active and control periods. The paired analysis showed no differences between the active and control periods during the cross-over trial. Further trials should be conducted in populations with underlying problems associated with disordered transit to determine the potential value of probiotic supplementation more accurately.

Gastrointestinal hormones and Ca are associated with bone metabolism. The objective of the present human study was to determine the effect of calcium phosphate on the postprandial circulation of gastrointestinal hormones. A total of ten men participated in the present double-blind, placebo-controlled, cross-over study. The participants were divided into two groups. Of these, one group consumed bread enriched with 1 g Ca (pentacalcium hydroxy-triphosphate, CaP) daily for 3 weeks. The other group consumed placebo bread. After 2 weeks of washout, the intervention was changed between the groups for another 3 weeks. The subjects consumed a defined diet at the beginning (single administration) and at the end (repeated administration) of the intervention periods, and blood samples were drawn at 0, 30, 60, 120, 180 and 240 min. Between 0 and 30 min, the participants consumed a test meal, with or without CaP. The concentrations of gastrointestinal hormones (glucose-dependent insulinotropic polypeptide, glucagon-like peptide (GLP) 1 and GLP2), insulin and glucose were determined. The AUC of GLP1 (total and active) and GLP2 increased significantly after the repeated CaP administrations compared with that after placebo administration. The AUC of insulin and glucose showed no differences between the CaP and placebo administrations. CaP affects the postprandial plasma concentrations of gastrointestinal hormones through the modulation of the intestinal environment, e.g. bile acids and microbiota.

High-fat meals (HFM) induce metabolic stress, leading to the activation of protective mechanisms, including inflammation and endogenous antioxidant defences. In the present study, we investigated the effects of antioxidant-rich fruit juice drinks on the endogenous antioxidant response induced by HFM. In a double-blind, cross-over design (10 d washout), fourteen overweight volunteers were randomly assigned to one of the following interventions: HFM+500 ml placebo beverage (HFM-PB, free from fruit); HFM+500 ml antioxidant beverage 1 (HFM-AB1; apple, grape, blueberry and pomegranate juices and grape skin, grape seed and green tea extracts); HFM+500 ml antioxidant beverage 2 (HFM-AB2; pineapple, black currant and plum juices). HFM-PB consumption increased the plasma levels of thiols (SH) (4 h, P< 0·001) and uric acid (UA) (2 h, P< 0·01) and total radical-trapping antioxidant parameter (TRAP) (4 h, P< 0·01). Following the consumption of drinks, UA production was significantly reduced with respect to placebo beverage consumption 8 h after HFM-AB2 consumption (P< 0·05). SH levels were reduced 0·5 (P< 0·05), 1 (P< 0·05) and 2 h (P< 0·01) after HFM-AB1 consumption and 2, 4 and 8 h (P< 0·05) after HFM-AB2 consumption. Plasma TRAP (2 h, P< 0·001) and urinary ferric reducing antioxidant power (0–8 h, P< 0·01) were increased by HFM-AB1 consumption, the drink with the highest in vitro antioxidant capacity, but not by HFM-AB2 consumption. In urine, UA levels were significantly increased from basal levels after the consumption of HFM-PB and HFM-AB2. However, neither of the beverages increased the urinary excretion of UA with respect to the placebo beverage. In conclusion, the increase in UA and SH levels induced by HFM as part of an endogenous antioxidant response to postprandial stress can be prevented by the concomitant ingestion of antioxidant-rich fruit juice drinks.

The aims of the present study were to assess the possible differences in faecal microbiota between men with a low serum enterolactone concentration and those with a high concentration, and to investigate the impact of a synbiotic mixture on serum enterolactone concentration in men with a low concentration. We compared faecal microbiota between ten men with the lowest serum enterolactone concentration and ten men with the highest concentration at recruitment (n 84). Furthermore, we carried out a randomised, double-blind, placebo-controlled, cross-over intervention study (6-week intervention periods and 4-week washout period) to investigate the impact of a synbiotic mixture (two Lactobacillus strains, one Bifidobacterium strain, one Propionibacterium strain and galacto-oligosaccharides (32 g/l)) on serum enterolactone concentration in fifty-two men who had a concentration < 20 nmol/l. Serum sensitive C-reactive protein (CRP) concentration was measured at the end of the first intervention period. Men with a low serum enterolactone concentration when compared with those with a high concentration had less faecal bacteria, especially those belonging to the Lactobacillus–Enterococcus group (median 8·2 (interquartile range 7·8–8·4) log10 colony-forming units/g v. median 8·8 (interquartile range 8·5–8·9) log10 colony-forming units/g, P= 0·009). The synbiotic mixture that was used did not have a significant effect on serum enterolactone (synbiotic v. placebo ratio 0·96 (95 % CI 0·76, 1·22), P= 0·724) or serum sensitive CRP (synbiotic v. placebo ratio 0·99 (95 % CI 0·74, 1·33), P= 0·954) concentration. Men with a low serum enterolactone concentration harbour less colonic bacteria, especially those belonging to the Lactobacillus–Enterococcus group. A synbiotic mixture does not increase serum enterolactone concentration.

Brown rice (BR) and white rice (WR) produce different glycaemic responses and their consumption may affect the dietary management of obesity. In the present study, the effects of BR and WR on abdominal fat distribution, metabolic parameters and endothelial function were evaluated in subjects with the metabolic syndrome in a randomised cross-over fashion. In study 1, acute postprandial metabolic parameters and flow- and nitroglycerine-mediated dilation (FMD and NMD) of the brachial artery were determined in male volunteers with or without the metabolic syndrome after ingestion of either BR or WR. The increases in glucose and insulin AUC were lower after ingestion of BR than after ingestion of WR (P= 0·041 and P= 0·045, respectively). FMD values were decreased 60 min after ingestion of WR (P= 0·037 v. baseline), but the decrease was protected after ingestion of BR. In study 2, a separate cohort of male volunteers (n 27) with the metabolic syndrome was randomised into two groups with different BR and WR consumption patterns. The values of weight-based parameters were decreased after consumption of BR for 8 weeks, but returned to baseline values after a WR consumption period. Insulin resistance and total cholesterol and LDL-cholesterol levels were reduced after consumption of BR. In conclusion, consumption of BR may be beneficial, partly owing to the lowering of glycaemic response, and may protect postprandial endothelial function in subjects with the metabolic syndrome. Long-term beneficial effects of BR on metabolic parameters and endothelial function were also observed.

Bioactive milk proteins may be important in protecting preterm infants from developing inflammation and necrotising enterocolitis (NEC). A preterm pig model was used to investigate the protective effects of enteral bovine lactoferrin (bLF) against NEC development and inflammation. Caesarean-delivered preterm pigs were fed parenteral and minimal enteral nutrition for the first 2 d followed by 2 d of total enteral nutrition before euthanasia. Pigs were stratified into two groups and fed with either a control formula (CON, n 15) or a 10 g/l of bLF-enriched formula (LF, n 13). NEC incidence, gut functions and inflammatory cytokines were analysed. NEC incidence and nutrient absorption were similar between the two groups. In pigs that developed NEC, disease outcome was more severe in the colon accompanied by increased intestinal permeability in LF pigs. In contrary, the LF pigs had a lowered IL-1β level in the proximal small intestine. Dose-dependent effects of bLF on cell proliferation, intracellular signalling and cytokine secretion were tested in porcine intestinal epithelial cells (PsIc1) in vitro. Low doses (0·1–1 g/l) increased cell proliferation via extracellular signal-regulated kinase (ERK), limited IL-8 secretion and prevented NF-κB and hypoxia-inducible factor-1α (HIF-1α) activation, suggesting anti-inflammatory effects. In contrast, at a higher dose (10 g/l), bLF exerted adverse effects by reducing cell proliferation, stimulating IL-8 release, inhibiting ERK activation and up-regulating NF-κB and HIF-1α activation. Overall, at a dose of 10 g/l, bLF exacerbated disease severity in pigs that developed NEC, while the in vitro studies indicated the positive effects of bLF at low doses (0·1–1 g/l). Supplementation of infant formulas with bLF should therefore be optimised carefully.

Red meat and dairy products contain high sialic acid (Sia) levels, but the metabolic fate and health impact in children remain unknown. The aims of the present study were to quantify the levels of urinary Sia N-acetylneuraminic acid (Neu5Ac), N-glycolylneuraminic acid (Neu5Gc) and ketodeoxynonulosonic acid (KDN) and to determine their relationship with dietary Sia intake. Spot urine samples were collected from 386 healthy children aged 3 (n 108), 4 (n 144) and 5 (n 134) years at 06.30–07.00, 11.30–12.00 and 16.30–17.00 hours. Food intake levels were recorded on the day of urine sample collection. Sia levels were quantified using LC–MS/MS with [13C3]Sia as an internal standard. We found that (1) total urinary Sia levels in healthy pre-school children ranged from 40 to 79 mmol Sia/mol creatinine; (2) urinary Sia levels were independent of age and consisted of conjugated Neu5Ac (approximately 70·8 %), free Neu5Ac (approximately 21·3 %), conjugated KDN (approximately 4·2 %) and free KDN (approximately 3·7 %); Neu5Gc was detected in the urine of only one 4-year-old girl; (3) total urinary Sia levels were highest in the morning and declined over time in 4- and 5-year-old children (P< 0·05), but not in 3-year-old children; (4) Sia intake levels at breakfast and lunch were approximately 2·5 and 0·16 mg Sia/kg body weight; and (5) there was no significant correlation between dietary Sia intake levels and urinary Sia levels. Urinary Sia levels varied with age and time of day, but did not correlate with Sia intake in 3- to 5-year-old children. The difference in urinary Sia levels in children of different age groups suggests that the metabolism and utilisation rates of dietary Sia are age dependent.

In the present study, we investigated the association between dietary intake of carbohydrates and the risk of type 2 diabetes. Incident cases of diabetes (n 749) were identified and compared with a randomly selected subcohort of 3496 participants aged 40–79 years. For dietary assessment, we used 7 d food diaries administered at baseline. We carried out modified Cox proportional hazards regression analyses and compared results obtained from the different methods of adjustment for total energy intake. Dietary intakes of total carbohydrates, starch, sucrose, lactose or maltose were not significantly related to diabetes risk after adjustment for confounders. However, in the residual method for energy adjustment, intakes of fructose and glucose were inversely related to diabetes risk. The multivariable-adjusted hazard ratios (HR) of diabetes comparing the extreme quintiles of intake were 0·79 (95 % CI 0·59, 1·07; P for trend = 0·03) for glucose and 0·62 (95 % CI 0·46, 0·83; P for trend = 0·01) for fructose. In the nutrient density method, only fructose was inversely related to diabetes risk (HR 0·65, 95 % CI 0·48, 0·88). The replacement of 5 % energy intake from SFA with an isoenergetic amount of fructose was associated with a 30 % lower diabetes risk (HR 0·69, 95 % CI 0·50, 0·96). Results of the standard and energy partition methods were similar to those of the residual method. These prospective findings suggest that the intakes of starch and sucrose are not associated, but that those of fructose and glucose are inversely associated with diabetes risk. Whether the inverse associations with fructose and glucose reflect the effect of substitution of these carbohydrate subtypes with other nutrients (i.e. SFA), their net higher intake or other nutrients associated with their intake remains to be established through further investigation.

The protective effects of fruits and vegetables against CHD have been suggested by many epidemiological studies among Western populations. However, prospective data are lacking for Asian populations. In the present study, we examined the associations of fruit and vegetable intake with CHD incidence among 67 211 women (aged 40–70 years) and 55 474 men (aged 40–74 years) living in Shanghai, China. Food intake was assessed using validated FFQ through in-person interviews. Coronary events (non-fatal myocardial infarction or fatal CHD) were identified by biennial home visits and further confirmed by medical record review. During a mean follow-up period of 9·8 and 5·4 years, 148 events in women and 217 events in men were documented and verified. After adjustment for potential confounders, women in the highest quartile of total fruit and vegetable intake (median 814 g/d) had a hazard ratio (HR) of 0·62 (95 % CI 0·38, 1·02) for CHD (P for trend = 0·04) compared with those in the lowest quartile (median 274 g/d). This association was primarily driven by fruits (HR for the highest v. the lowest intake in women: 0·62, 95 % CI 0·37, 1·03). The strength of the association was attenuated after further controlling for history of diabetes or hypertension. For men, no significant association was found for fruit and vegetable intake when analysed either in combination or individually. The present findings suggest that a high consumption of fruits may reduce CHD risk in Chinese women.