High-fat diet is a major causative factor of overweight and obesity, which are associated with an increased risk of neuropsychiatric diseases, such as anxiety and depression. In the present study, we investigated the protective effects of bamboo extract (BEX) on anxiety- and depression-like neurobehaviours in mice treated with a high-fat diet. Male mice with CD-1 genetic background were treated for 2 months with either a standard or a high-fat diet (10 or 45 % energy from fat, respectively), with or without the BEX supplement (11 g dry mass per 17 MJ). The anxiety levels of mice were evaluated using open-field and hole-board tests, and depression was measured using the force-swimming test. The anxiety responses of the animals were found significantly increased after the high-fat diet treatment, and this elevation was effectively abolished by the BEX supplement. The high-fat diet seemed to have an anti-depressive effect in mice at the tested time point, but the effect of the BEX supplement on the depression level of the animals was not conclusive. The high-fat diet significantly decreased total glutathione content in the blood while the BEX supplement increased glutathione oxidation. In summary, the present study shows that decreased total glutathione concentration in the blood co-occurred with a high-fat treatment, high anxiety level and low depression level in mice, and when supplemented in a high-fat diet, BEX had an anxiolytic effect in mice.

As gut immaturity precludes full enteral feeding, very low birth weight (VLBW) preterm infants receive parenteral nutrition (PN) during the first few weeks of life. Weaning VLBW infants off PN, however, is a top priority since PN is associated with a high risk of complications. The decision making is purely empirical, as there is currently no suitable index of gastrointestinal (GI) maturity. Plasma citrulline concentration is considered an index of GI function in conditions such as short-bowel syndrome and coeliac disease in adults. To identify the factors determining urinary citrulline excretion, and determine whether urinary citrulline excretion could be used as a non-invasive index of GI tolerance to enteral feeding, nutritional intake and urinary citrulline were monitored bi-weekly in forty-seven preterm infants < 1500 g (interquartiles 880–1320 g), during their stay in the Neonatology unit. Median urinary citrulline was 24·7 μmol/mmol creatinine (14·5–38·6 μmol/mmol creatinine). No relationship was observed with the percentage of energy tolerated enterally. In multivariate regression analysis, weak correlations were found with post-conceptional age (P = 0·001), parenteral amino acid supply (P = 0·001) and the daily volume of enteral mixture administered (P = 0·043). A significant correlation was found with urinary nitrite+nitrate excretion (r 0·47; P < 0·001). We conclude that in preterm infants: (1) one of the major determinants of urinary citrulline may be the biosynthesis of citrulline from arginine by NO-synthase; (2) urinary citrulline cannot be used to predict GI tolerance. This is consistent with the observations that, in neonatal gut, citrulline is converted to arginine in situ rather than exported towards the kidneys as observed in adults.

The aim of the present study was to determine the effects of a cafeteria diet on the function and apoptosis of the pancreas, and the activity and expression of the insulin-degrading enzyme (IDE). Female Wistar rats were fed either with a cafeteria diet or a control diet for 17 weeks, and blood and tissues were then collected for analysis. The cafeteria diet-treated rats had higher plasma insulin and C-peptide levels (P < 0·05), showing increased insulin secretion by the pancreas. Insulin protein and gene expression levels were higher in the pancreas of obese rats, as was its transcriptional controller, pancreatic duodenal homeobox 1 (P < 0·05). Feeding a cafeteria diet down-regulated the gene expression of the anti-apoptotic marker B-cell/lymphoma 2 (BCL2), and up-regulated the protein levels of BCL2-associated X protein, a pro-apoptotic marker (P < 0·05). The cafeteria diet caused lipid accumulation in the pancreas and modified the expression of key genes that control lipid metabolism. To assay whether insulin clearance was also modified, we checked the activity of the IDE, one of the enzymes responsible for insulin clearance. We found increased liver IDE activity (P < 0·05) in the cafeteria diet-fed animals, which could, in part, be due to an up-regulation of its gene expression. Conversely, IDE gene expression was unmodified in the kidney and adipose tissue; although when the adipose tissue weight was considered, the insulin clearance potential was higher in the cafeteria diet-treated rats. In conclusion, treatment with a cafeteria diet for 17 weeks in rats mimicked a pre-diabetic state, with ectopic lipid accumulation in the pancreas, and increased the IDE-mediated insulin clearance capability.

Pancreatic β-cell death or dysfunction mediated by oxidative stress underlies the development and progression of diabetes mellitus. In the present study, we tested extracts from the edible mushroom Lactarius deterrimus and the chestnut Castanea sativa, as well as their mixture (MIX Ld/Cs), for potential beneficial effects on streptozotocin (STZ)-induced pancreatic β-cell death. Analysis of chelating effects, reducing power and radical-scavenging assays revealed strong antioxidant effects of the C. sativa extract and MIX Ld/Cs, while the L. deterrimus extract displayed a weak to moderate effect. The antioxidative effect of the chestnut extract corresponds with the high content of phenolics and flavonoids identified by HPLC analysis. In contrast, the mushroom extract contains relatively small amounts of phenols and flavonoids. However, both extracts, and especially their combination MIX Ld/Cs, increased cell viability after the STZ treatment as a result of a significant reduction of DNA damage and improved redox status. The chestnut extract and MIX Ld/Cs significantly lowered the STZ-induced increases in superoxide dismutase and catalase activities, while the mushroom extract had no impact on the activities of these antioxidant enzymes. However, the L. deterrimus extract exhibited good NO-scavenging activity. Different mechanisms that underlie antioxidant effects of the mushroom and chestnut extracts were discussed. When combined as in the MIX Ld/Cs, the extracts exhibited diverse but synergistic actions that ultimately exerted beneficial and protective effects against STZ-induced pancreatic β-cell death.

It is proven that nuts contain essential macro- and micronutrients, e.g. fatty acids, vitamins and dietary fibre (DF). Fermentation of DF by the gut microflora results in the formation of SCFA which are recognised for their chemopreventive potential, especially by influencing cell growth. However, little is known about cellular response to complex fermentation samples of nuts. Therefore, we prepared and analysed (pH, SCFA, bile acids, tocopherol, antioxidant capacity) fermentation supernatant (fs) fractions of nuts (almonds, macadamias, hazelnuts, pistachios, walnuts) after in vitro fermentation and determined their effects on growth of HT29 cells as well as their genotoxic/anti-genotoxic potential. The fermented nut samples contained 2- to 3-fold higher amounts of SCFA than the faeces control, but considerable reduced levels of bile acids. While most of the investigated native nuts comprised relatively high amounts of tocopherol (α-tocopherol in almonds and hazelnuts and γ- and δ-tocopherol in pistachios and walnuts), rather low concentrations were found in the fs. All nut extracts and nut fs showed a strong antioxidant potential. Furthermore, all fs, except the fs pistachio, reduced growth of HT29 cells significantly. DNA damage induced by H2O2 was significantly reduced by the fs of walnuts after 15 min co-incubation of HT29 cells. In conclusion, this is the first study which presents the chemopreventive effects (reduction of tumour-promoting desoxycholic acid, rise in chemopreventive SCFA, protection against oxidative stress) of different nuts after in vitro digestion and fermentation, and shows the potential importance of nuts in the prevention of colon cancer.

S-Equol is a metabolite resulting from the conversion of daidzein, a soya phyto-oestrogen, by the gut microflora. The potential protective effects of equol in breast cancer are still under debate. Consequently, we investigated the effects of equol on DNA methylation of breast cancer susceptibility genes (BRCA1 and BRCA2) and oncosuppressors in breast cancer cell lines (MDA-MB-231 and MCF-7) and in a dystrophic breast cell line (MCF-10a) following exposure to S-equol (2 μm) for 3 weeks. We demonstrated by quantitative analysis of methylated alleles a significant decrease in the methylation of the cytosine phosphate guanine (CpG) islands in the promoters of BRCA1 and BRCA2 after the S-equol treatment in MCF-7 and MDA-MB-231 cells and a trend in MCF-10a cells. We also showed that S-equol increases BRCA1 and BRCA2 protein expression in the nuclei and the cytoplasm in MCF-7, MDA-MB-231 and MCF-10a cell lines by immunohistochemistry. The increase in BRCA1 and BRCA2 proteins was also found after Western blotting in the studied cell lines. In summary, we demonstrated the demethylating effect of S-equol on the CpG islands inside the promoters of BRCA1 and BRCA2 genes, resulting in an increase in the level of expressed oncosuppressors in breast cancer cell lines.

Zingiber officinale (ZO), commonly known as ginger, has been traditionally used in the treatment of diabetes mellitus. Several studies have reported the hypoglycaemic properties of ginger in animal models. The present study evaluated the antihyperglycaemic effect of its aqueous extract administered orally (daily) in three different doses (100, 300, 500 mg/kg body weight) for a period of 30 d to streptozotocin (STZ)-induced diabetic rats. A dose-dependent antihyperglycaemic effect revealed a decrease of plasma glucose levels by 38 and 68 % on the 15th and 30th day, respectively, after the rats were given 500 mg/kg. The 500 mg/kg ZO significantly (P < 0·05) decreased kidney weight (% body weight) in ZO-treated diabetic rats v. control rats, although the decrease in liver weight (% body weight) was not statistically significant. Kidney glycogen content increased significantly (P < 0·05) while liver and skeletal muscle glycogen content decreased significantly (P < 0·05) in diabetic controls v. normal controls. ZO (500 mg/kg) also significantly decreased kidney glycogen (P < 0·05) and increased liver and skeletal muscle glycogen in STZ-diabetic rats when compared to diabetic controls. Activities of glucokinase, phosphofructokinase and pyruvate kinase in diabetic controls were decreased by 94, 53 and 61 %, respectively, when compared to normal controls; and ZO significantly increased (P < 0·05) those enzymes' activities in STZ-diabetic rats. Therefore, the present study showed that ginger is a potential phytomedicine for the treatment of diabetes through its effects on the activities of glycolytic enzymes.

Free radicals are continuously generated during an organism's lifetime. In order to understand the involvement in the oxidative status of fish, methionine and white tea were assayed as antioxidant supplements in diets for gilthead sea bream (Sparus aurata). For the purpose of this study, four isonitrogenous and isolipidic diets were formulated to contain 45 % of protein and 18 % lipid and 0·3 % methionine (Met diet), 2·9 % white tea dry leaves (Tea diet) and 2·9 % of white tea dry leaves+0·3 % methionine (Tea+Met diet). An unsupplemented diet was used as the control. Key enzymatic antioxidant defences, superoxide dismutase (SOD) isoenzyme profile, total, reduced and oxidised glutathione and oxidative damage markers were determined. The results showed that dietary methionine supplementation increased liver SOD activity, while white tea induced higher hepatic catalase activity. Dietary white tea induced a notable increase in Mn-SOD isoenzyme. This is the first study to provide evidence that dietary tea inclusion in fish feeding could be an important source of Mn with metabolic repercussions on antioxidant mechanisms.

The impact of slowly digestible sugars in reducing the risk of developing obesity and related metabolic disorders remains unclear. We hypothesised that such carbohydrates (CHO), resulting in a lower glycaemic and insulinaemic response, may lead to greater postprandial fat oxidation rates in subjects with impaired glucose tolerance (IGT). The present study intends to compare the postprandial metabolic responses to the ingestion of glucose (GLUC) v. trehalose (TRE) and sucrose (SUC) v. isomaltulose (IMU). In a randomised, single-blind, cross-over design, ten overweight IGT subjects were studied four times, following ingestion of different CHO drinks either at breakfast or in combination with a mixed meal at lunch. Before and 3 h after CHO ingestion, energy expenditure, substrate utilisation and circulating metabolite concentrations were determined. Ingestion of CHO drinks with a meal resulted in an attenuated rise in GLUC ( − 33 %) and insulin ( − 14 %) concentrations following TRE when compared with GLUC and following IMU, an attenuation of 43 and 34 % when compared with SUC ingestion, respectively. Additionally, there was less inhibition of the rise in NEFA concentrations and less decline in postprandial fat oxidation (22 %) after IMU when compared with SUC, whereas TRE did not differ from GLUC. The attenuated rise in GLUC and insulin concentrations following IMU ingestion attenuated the postprandial inhibition of fat oxidation compared with SUC when co-ingested with a meal. This suggests that exchange of SUC in the diet for IMU may result in a more favourable metabolic response and may help to reduce the risks associated with obesity and type 2 diabetes.

We previously demonstrated that intra-uterine growth-restricted (IUGR) Yucatan miniature pigs develop modestly elevated blood pressure (BP) as young adults. The present study evaluated the effects of a post-weaning Western-style, high-salt-fat-sugar (HSFS) diet on early programming of BP. IUGR piglets (3 d old, 0·77 (sem 0·04) kg, n 6) were paired with normal weight (NW) same-sex littermates (1·14 (sem 0·03) kg, n 6) and fed milk replacer for 4 weeks. A third littermate was left with the sow (SF; 1·01 (sem 0·05) kg, n 6). When 4 weeks old, all pigs were placed on a HSFS diet ad libitum for 5 h/d. When 11 months old, telemeters were implanted to measure BP in pigs before (4·5 % NaCl) and after (0·5 % NaCl) a 7 d reduced salt challenge. At necropsy, nephron numbers were determined. Before sexual maturity, IUGR pigs had greater relative feed intake (P < 0·05), and experienced catch-up growth with greater adiposity, with correlations between adiposity and BP (P < 0·05). Adult IUGR pigs had 26–34 % fewer nephrons and higher diastolic BP (107·7 (sem 4·9) mmHg, P = 0·044) than NW (97·2 (sem 1·8) mmHg) and SF (98·9 (sem 5·3) mmHg) pigs. Systolic BP was similar among the three groups, but was significantly elevated compared with levels previously reported for a control diet. Salt restriction reduced BP in all groups (P < 0·05), but with no differences (P>0·05) in the degree of salt sensitivity among groups. In conclusion, a post-weaning Western-style diet exacerbates early programming of diastolic BP in Yucatan miniature swine, whereas systolic BP is more sensitive to postnatal diet.

β-Glucans have been identified as natural biomolecules with immunomodulatory activity. The first objective of the present study was to compare the effects of purified β-glucans derived from Laminariadigitata, L. hyperborea and Saccharomyces cerevisiae on piglet performance, selected bacterial populations and intestinal volatile fatty acid (VFA) production. The second aim was to compare the gene expression profiles of the markers of pro- and anti-inflammation in both unchallenged and lipopolysaccharide (LPS)-challenged ileal and colonic tissues. β-Glucans were included at 250 mg/kg in the diets. The β-glucans derived from L. hyperborea, L. digitata and S. cerevisiae all reduced the Enterobacteriaceae population (P < 0·05) without influencing the lactobacilli and bifidobacteria populations (P>0·05) in the ileum and colon. There was a significant interaction between gastrointestinal region and β-glucan source in the expression of cytokine markers, IL-1α (P < 0·001), IL-10 (P < 0·05), TNF-α (P < 0·05) and IL-17A (P < 0·001). β-Glucans did not stimulate any pro- or anti-inflammatory cytokine markers in the ileal epithelial cells. In contrast, the expression of a panel of pro- and anti-inflammatory cytokines (IL-1α, IL-10, TNF-α and IL-17A) was down-regulated in the colon following exposure to β-glucans from all the three sources. However, the data suggest that the soluble β-glucans derived from L. digitata may be acting via a different mechanism from the insoluble β-glucans derived from L. hyperborea and S. cerevisiae, as the VFA profile was different in the L. digitata-treated animals. There was an increase in IL-8 gene expression (P < 0·05) in the gastrointestinal tract from the animals exposed to L. digitata following an LPS ex vivo challenge that was not evident in the other two treatment groups. In conclusion, β-glucans from both seaweed and yeast sources reduce Enterobacteriaceae counts and pro-inflammatory markers in the colon, though the mechanisms of action may be different between the soluble and insoluble fibre sources.

In the elderly, immunosenescence and malnourishment can contribute to increased risk and severity of upper respiratory tract infections (URTI). Gold kiwifruit (Actinidia chinensis ‘Hort16A’) contains nutrients important for immune function and mitigation of symptoms of infection, including vitamins C and E, folate, polyphenols and carotenoids. The objective of the present study was to evaluate whether regular consumption of gold kiwifruit reduces symptoms of URTI in older people, and determine the effect it has on plasma antioxidants, and markers of oxidative stress, inflammation and immune function. A total of thirty-two community-dwelling people ( ≥ 65 years) participated in a randomised crossover study, consuming the equivalent of four kiwifruit or two bananas daily for 4 weeks, with treatments separated by a 4-week washout period. Participants completed the Wisconsin Upper Respiratory Symptom Survey-21 daily, and blood samples were collected at baseline and at the end of each treatment and washout period. Gold kiwifruit did not significantly reduce the overall incidence of URTI compared with banana, but significantly reduced the severity and duration of head congestion, and the duration of sore throat. Gold kiwifruit significantly increased plasma vitamin C, α-tocopherol and lutein/zeaxanthin concentrations, and erythrocyte folate concentrations, and significantly reduced plasma lipid peroxidation. No changes to innate immune function (natural killer cell activity, phagocytosis) or inflammation markers (high-sensitivity C-reactive protein, homocysteine) were detected. Consumption of gold kiwifruit enhanced the concentrations of several dietary plasma analytes, which may contribute to reduced duration and severity of selected URTI symptoms, offering a novel tool for reducing the burden of URTI in older individuals.

The objective of the present study was to test the hypothesis that fatty acids are the circulating mediators acting in a pro-inflammatory manner towards activated circulating ovine monocyte/macrophages and neutrophils. Furthermore, whether soya protein hydrolysates (SPH) inhibit the fatty acid-induced increase in the production of pro-inflammatory responses by ovine phagocytes was tested in vitro. All the fatty acids tested (myristic, palmitic, palmitoleic, stearic and oleic) increased (P < 0·01; C18>C16>C14) membrane-bound urokinase plasminogen activator (u-PA) and u-PA free binding sites in cell membranes of activated ovine blood monocytes/macrophages, but only the C18 fatty acids (stearic, oleic) were effective towards blood neutrophils. The C18 fatty acids up-regulated (P < 0·05) the gene expression of u-PA, u-PA receptor, intercellular adhesion molecule 1 and inducible NO synthase (in monocytes) but not that of cyclo-oxygenase-2, integrin α X and plasminogen activator inhibitor types 1 and 2 by ovine phagocytes. SPH blocked completely or partially all C18 fatty acid-induced changes in the expression of various pro-inflammatory genes. In conclusion, fatty acids selectively ‘activate’ ovine phagocytes, suggesting that these cells ‘sense’ metabolic signals derived from adipocytes. Soya protein peptides inhibit all changes in gene expression induced by fatty acids in ovine phagocytes in vitro. This constitutes a novel mechanism of action.

Sida cordifolia Linn. (Malvaceae) is a plant used in folk medicine for the treatment of the inflammation of oral mucosa, asthmatic bronchitis, nasal congestion and rheumatism. We studied the hepatoprotective activity of 50 % ethanolic extract of S. cordifolia Linn. against alcohol intoxication. The duration of the experiment was 90 d. The substantially elevated levels of toxicity markers such as alanine aminotransferase, aspartate aminotransferase and γ-glutamyl transferase due to the alcohol treatment were significantly lowered in the extract-treated groups. The activity of antioxidant enzymes and glutathione content, which was lowered due to alcohol toxicity, was increased to a near-normal level in the co-administered group. Lipid peroxidation products, protein carbonyls, total collagen and hydroxyproline, which were increased in the alcohol-treated group, were reduced in the co-administered group. The mRNA levels of cytochrome P450 2E1, NF-κB, TNF-α and transforming growth factor-β1 were found to be increased in the alcohol-treated rats, and their expressions were found to be decreased in the co-administered group. These observations were reinforced by histopathological analysis. Thus, the present study clearly indicates that 50 % ethanolic extract of the roots of S. cordifolia Linn. has a potent hepatoprotective action against alcohol-induced toxicity, which was mediated by lowering oxidative stress and by down-regulating the transcription factors.

Choline is an essential nutrient and can also be obtained by de novo synthesis via an oestrogen responsive pathway. Choline can be oxidised to the methyl donor betaine, with short-term supplementation reported to lower plasma total homocysteine (tHcy); however, the effects of longer-term choline supplementation are less clear. We investigated the effect of choline supplementation on plasma concentrations of free choline, betaine and tHcy and B-vitamin status in postmenopausal women, a group more susceptible to low choline status. We also assessed whether supplementation altered plasma lipid profiles. In this randomised, double-blinded, placebo-controlled study, forty-two healthy postmenopausal women received 1 g choline per d (as choline bitartrate), or an identical placebo supplement with their habitual diet. Fasting blood samples were collected at baseline, week 6 and week 12. Administration of choline increased median choline and betaine concentrations in plasma, with significant effects evident after 6 weeks of supplementation (P < 0·001) and remaining significant at 12 weeks (P < 0·001); no effect was observed on folate status or on plasma lipids. Choline supplementation induced a median (25th, 75th percentile) change in plasma tHcy concentration at week 6 of − 0·9 ( − 1·6, 0·2) μmol, a change which, when compared to that observed in the placebo group 0·6 ( − 0·4, 1·9) μmol, approached statistical significance (P = 0·058). Choline supplementation at a dose of 1 g/d significantly increases the circulating concentration of free choline, and can also significantly increase the concentration of the methyl donor, betaine, thereby potentially enhancing the betaine–homocysteine methyltransferase-mediated remethylation of tHcy. This trial was registered at http://www.controlled-trials.com/ISRCTN82708510.

Skin is among the first and most heavily damaged organs upon sulphur mustard (SM) exposure. Pruritus is the most common chronic skin complication of SM, which adversely affects the quality of life (QoL). However, current therapies for the management of SM-induced pruritus are very limited and associated with side effects. The present trial investigated the efficacy of curcumin in the alleviation of SM-induced chronic pruritic symptoms. A total of ninety-six male Iranian veterans (age 37–59 years) were randomised to receive either curcumin (1 g/d, n 46) or placebo (n 50) for 4 weeks. Serum concentrations of substance P and activities of antioxidant enzymes were measured at baseline and at the end of the trial. Assessment of pruritus severity was performed using the pruritus score, visual analogue scale (VAS) and scoring atopic dermatitis (SCORAD) index. QoL was evaluated using the Dermatology Life Quality Index (DLQI) questionnaire. Serum concentrations of substance P (P < 0·001) as well as activities of superoxide dismutase (P = 0·02), glutathione peroxidase (P = 0·006) and catalase (P < 0·001) were significantly reduced in the curcumin group, while no significant change was observed in the placebo group. Curcumin supplementation was also associated with significant reductions in measures of pruritus severity including the pruritus score (P < 0·001), VAS score (P < 0·001), overall (P < 0·001) and objective SCORAD (P = 0·009), and DLQI's first question (P < 0·001). None of these measures was significantly changed in the placebo group. As for the QoL, although DLQI scores decreased in both groups (P < 0·001 and P = 0·003 in the curcumin and placebo groups, respectively), the magnitude of reduction was significantly greater in the curcumin group (P < 0·001). In conclusion, curcumin may be regarded as a natural, safe, widely available and inexpensive treatment for the management of SM-induced chronic pruritus.

Increasing dietary n-3 PUFA decreases the risk of CHD. Since n-6 PUFA compete with n-3 PUFA for common metabolic enzymes, the n-6:n-3 ratio intake rather than the n-3 PUFA intake levels per se may be critical. We aimed to examine whether altering the n-6:n-3 ratio affects cardiovascular risk factors in hypercholesterolaemic patients on lipid management with statins. Adhering to a randomised, crossover study design, patients on statins (n 11) were placed on one of two dietary interventions (Diet high-ratio (HR) – n-6:n-3 = 30:1 or Diet low-ratio (LR) – n-6:n-3 = 1·7:1) for 4 weeks followed after an 8-week washout period by the alternate diet. Foods enriched with n-3 or n-6 PUFA were delivered to each patient, who were given clear guidance on consumption expectations for the study. Measures of lipid profile, blood pressure and vascular function were determined. Diet LR significantly reduced body weight, LDL-cholesterol, high-sensitivity C-reactive protein, blood pressure and the apoA-1:apoB ratio. While Diet HR trended towards a similar cardioprotective profile, most of the parameters examined did not reach statistical significance. A direct comparison between diets demonstrated no significant superiority of Diet LR over Diet HR. These results suggest that a dietary intervention focused on n-6 and n-3 fatty acids may improve cardiovascular risk factors in patients over and above standard lipid management, but there is no significant advantage of a low n-6:n-3 ratio diet when compared to a high-ratio diet.

Shiftworkers have a higher risk of CHD and type 2 diabetes. They consume a large proportion of their daily energy and carbohydrate intake in the late evening or night-time, a factor which could be linked to their increase in disease risk. We compared the metabolic effects of varying both dietary glycaemic index (GI) and the time at which most daily energy intake was consumed. We hypothesised that glucose control would be optimal with a low-GI diet, consumed predominantly early in the day. A total of six healthy lean volunteers consumed isoenergetic meals on four occasions, comprising either high- or low-GI foods, with 60 % energy consumed predominantly early (breakfast) or late (supper). Interstitial glucose was measured continuously for 20 h. Insulin, TAG and non-esterified fatty acids were measured for 2 h following every meal. Highest glucose values were observed when large 5021 kJ (1200 kcal) high-GI suppers were consumed. Glucose levels were also significantly higher in predominantly late high- v. low-GI meals (P < 0·01). Using an estimate of postprandial insulin sensitivity throughout the day, we demonstrate that this follows the same trend, with insulin sensitivity being significantly worse in high energy consumed in the evening meal pattern. Both meal timing and GI affected glucose tolerance and insulin secretion. Avoidance of large, high-GI meals in the evening may be particularly beneficial in improving postprandial glucose profiles and may play a role in reducing the risk of type 2 diabetes; however, longer-term studies are needed to confirm this.

Few studies have examined nutrition transition in children in China. Our aim, in the present study, was to examine temporal trends in dietary energy, fat, carbohydrate and protein intake in Chinese children aged 7–17 years. The analysis used individual level, consecutive 3 d dietary recall data from seven rounds of the China Health and Nutrition Surveys in 1991 (n 2714), 1993 (n 2542), 1997 (n 2516), 2000 (n 2142), 2004 (n 1341), 2006 (n 1072) and 2009 (n 996). Mixed-effect models were constructed to obtain adjusted means and to examine trends after adjusting for intra-class correlation within clusters and for covariates including age, sex, urban/rural residence and income. From 1991 to 2009, daily energy intake steadily declined from 9511·0 to 7658·2 kJ (P < 0·0001). There was a steady decline in daily carbohydrate intake from 382·5 to 254·1 g (P < 0·0001), and in the proportion of energy from carbohydrate from 66·7 to 56·8 % (P < 0·0001). In contrast, daily fat intake steadily increased from 54·8 to 66·0 g (P < 0·0001), as did the proportion of energy from fat from 21·5 to 30·0 % (P < 0·0001). The proportion of children who consumed a diet with more than 30 % of energy from fat increased from 20·1 to 49·4 % (P < 0·0001). The proportion of energy from protein increased from 11·8 to 13·1 % (P < 0·0001), although daily protein intake dropped from 66·2 to 58·0 g (P < 0·0001). Our data suggest that Chinese children have been undergoing a rapid nutrition transition to a high-fat diet.

α-Linolenic acid (18 : 3n-3) intake and linoleic acid (18 : 2n-6) intake have been associated with lower rates of CHD, though results have not been consistent. The relationship of these fatty acids with incident heart failure (HF) is not well established. We examined the hypothesis that women with higher intakes of 18 : 3n-3 and 18 : 2n-6 would have lower rates of HF hospitalisation and mortality. We measured 18 : 3n-3 and 18 : 2n-6 intake in 36 234 Swedish Mammography Cohort participants aged 48–83 years using FFQ and followed participants through Swedish inpatient and cause-of-death registers from 1 January 1998 until 31 December 2006. Cox models were used to calculate incidence rate ratios (RR) and 95 % CI. Because of multicollinearity, 18 : 3n-3 and 18 : 2n-6 were examined separately. Over 9 years, 596 women were hospitalised and fifty-five died due to HF. In models accounting for age and other covariates, the RR for HF comparing the top quintile of 18 : 3n-3 (median 1·50 g/d) with the bottom quintile (median 0·88 g/d) was 0·91 (95 % CI 0·71, 1·17, Ptrend = 0·41). The RR comparing the top quintile of 18 : 2n-6 (median 7·8 g/d) with the bottom quintile (median 4·6 g/d) was 1·14 (95 % CI 0·88, 1·46, Ptrend = 0·36). We did not find evidence for the interaction of 18 : 3n-3 and 18 : 2n-6 with each other or with long-chain n-3 fatty acids. In conclusion, these data do not support our hypothesis that 18 : 3n-3 and 18 : 2n-6 are associated with HF. However, these results may not be generalisable to populations with higher intakes of 18 : 3n-3.