The bioavailability of α-linolenic acid (ALA) from flaxseed oil in an emulsified form v. a non-emulsified form was investigated by using two complementary approaches: the first one dealt with the characterisation of the flaxseed oil emulsion in in vitro gastrointestinal-like conditions; the second one compared the intestinal absorption of ALA in rats fed the two forms of the oil. The in vitro study on emulsified flaxseed oil showed that decreasing the pH from 7·3 to 1·5 at the physiological temperature (37°C) induced instantaneous oil globule coalescence. Some phase separation was observed under acidic conditions that vanished after further neutralisation. The lecithin used to stabilise the emulsions inhibited TAG hydrolysis by pancreatic lipase. In contrast, lipid solubilisation by bile salts (after lipase and phospholipase hydrolysis) was favoured by preliminary oil emulsification. The in vivo absorption of ALA in thoracic lymph duct-cannulated rats fed flaxseed oil, emulsified or non-emulsified, was quantified. Oil emulsification significantly favoured the rate and extent of ALA recovery as measured by the maximum ALA concentration in the lymph (Cmax = 14 mg/ml at 3 h in the emulsion group v. 9 mg/ml at 5 h in the oil group; P < 0·05). Likewise, the area under the curve of the kinetics was significantly higher in the emulsion group (48 mg × h/ml for rats fed emulsion v. 26 mg × h/ml for rats fed oil; P < 0·05). On the whole, ALA bioavailability was improved with flaxseed oil ingested in an emulsified state. Data obtained from the in vitro studies helped to partly interpret the physiological results.

Before the menopause, women are relatively protected against CVD compared with men. The reasons for this sex difference are not completely understood, but hepatic fatty acid metabolism may play a role. The present study aimed to investigate the utilisation of plasma NEFA by the liver and to determine whether they are partitioned differently into ketone bodies and VLDL-TAG in healthy, lean young men and women. Volunteers were studied during a prolonged overnight fast (12–19 h) using an intravenous infusion of [U-13C]palmitate. After 12 h fasting, the women had a more advantageous metabolic profile with lower plasma glucose (P < 0·05) and TAG (P < 0·05) but higher plasma NEFA (P < 0·05) concentrations. Plasma 3-hydroxybutyrate (3-OHB) concentrations rose more in women than in men, and the transfer of 13C from [U-13C]palmitate to plasma [13C]3-OHB reached a plateau 6–7 h after the start of the infusion in women but was still increasing at 6 h in men. This implies a slower 3-OHB production rate and/or dilution by other precursor pools in men. In women, the high isotopic enrichment of plasma 3-OHB suggested that systemic plasma fatty acids were the major source of 3-OHB production. However, in men, this was not observed during the course of the study (P < 0·01). There were no sex differences for the incorporation of 13C into VLDL1- or VLDL2-TAG. The ability of young women to partition fatty acids towards ketone body production rather than VLDL-TAG may contribute to their more advantageous metabolic profile compared with young men.

Oral administration of l-arginine has been reported to prevent gut disease in human infants. However, little is known about the effects of dietary arginine supplementation on intestinal development of weaned piglets. In the present study, twenty 21-d-old castrated piglets with 5·3 (sem 0·13) kg body weight (BW) were weaned from sows, individually housed and randomly assigned to one of the two maize- and soyabean meal-based diets supplemented with 0 or 1 % l-arginine. After consuming the diets for 7 d, six pigs were randomly selected from each group to obtain various tissues. Compared with control pigs, dietary supplementation with 1 % l-arginine did not affect feed intake but enhanced (P < 0·05) the relative weight of the small intestine (+33 %), daily BW gain (+38 %) and feed efficiency (+28 %). The villus height of the duodenum, jejunum and ileum in arginine-supplemented piglets was 21, 28 and 25 % greater (P < 0·05) than in the non-supplemented control group. Arginine supplementation increased (P < 0·05) protein levels for vascular endothelial growth factor (VEGF) in duodenal, jejunal and ileal mucosae by 14, 39 and 35 %, respectively. Compared with the control group, dietary supplementation with 1 % l-arginine increased (P < 0·05) plasma concentrations of arginine and insulin (+36 %), and decreased (P < 0·05) plasma concentrations of cortisol ( − 33 %), NH3 ( − 21 %) and urea ( − 19 %). These results indicate that arginine supplementation enhances intestinal growth, development and expression of VEGF in early-weaned pigs fed a maize- and soyabean meal-based diet. The findings may have important implications for neonatal pigs under stressful or diseased conditions.

We examined the effect of dietary nicotinic acid (NA) variations before and after oxidative stress (OS) treatment on the antioxidant defence system, function and morphology of the liver along with Zn status in rats. OS was generated by three intraperitoneal injections of tert-butyl hydroperoxide in the first week for the pre-exposure group and in the third week for the post-exposure group, respectively. These groups were further divided into subgroups and fed on a diet with marginally deficient Zn (10 mg Zn/kg diet) and NA variations as NA deficient, normal and excess with 10, 30 and 1000 mg NA/kg diet, respectively. Aspartate aminotransferase and alanine aminotransferase levels were elevated in rats with OS coupled with the Zn- and NA-deficient diet, which decreased towards normal with excess dietary NA. Excess NA supplementation in the OS pre-exposure group resulted in nearly preserved hepatic architecture with normal hepatocytes, whereas maximum tissue destruction was evident in the post-exposure group with NA deficiency. Dose-dependent improvement in the antioxidant defence system, enhanced reduced glutathione levels, lowered lipid peroxidation and higher hepatic Zn levels were observed with NA supplementation. The effect was more prominent in the pre-exposure group. In conclusion, dietary NA supplementation improves hepatic Zn uptake and results in hepatoprotection against OS-induced damage in rats.

The beneficial effects of a low-glycaemic index (GI) meal on postprandial glucose and insulin levels have been demonstrated. However, limited data are available on the impact of overweight and glucose tolerance on postprandial responses to different GI meals. Our aim was to study the effects of physiological characteristics on postprandial glucose, insulin and lipid responses and the relative glycaemic response (RGR) of a low-GI (LGI) and a high-GI (HGI) meal. We recruited twenty-four normal-weight and twenty-four overweight subjects, twelve with normal glucose tolerance (NGT) and twelve with impaired glucose tolerance (IGT) in each group. Both test meals were consumed once and the glucose reference twice. Blood glucose and insulin were measured in the fasting state and over a 2 h period after each study meal, and TAG and NEFA were measured in the fasting state and over a 5 h period. The glucose responses of subjects with IGT differed significantly from those of subjects with NGT. The highest insulin responses to both meals were observed in overweight subjects with IGT. Physiological characteristics did not influence TAG or NEFA responses or the RGR of the meals. The LGI meal resulted in lower glucose (P < 0·001) and insulin (P < 0·001) responses, but higher TAG responses (P < 0·001), compared with the HGI meal. The GI of the meals did not affect the NEFA responses. In conclusion, the LGI meal causes lower glucose and insulin responses, but higher TAG responses, than the HGI meal. The RGR of the meals does not differ between normal-weight and overweight subjects with NGT or IGT.

The present study examined the effects of milk protein on rehydration after exercise in the heat, via the comparison of energy- and electrolyte content-matched carbohydrate and carbohydrate–milk protein solutions. Eight male subjects lost 1·9 (sd 0·2) % of their body mass by intermittent exercise in the heat and rehydrated with 150 % of their body mass loss with either a 65 g/l carbohydrate solution (trial C) or a 40 g/l carbohydrate, 25 g/l milk protein solution (trial CP). Urine samples were collected before and after exercise and for 4 h after rehydration. Total cumulative urine output after rehydration was greater for trial C (1212 (sd 310) ml) than for trial CP (931 (sd 254) ml) (P < 0·05), and total fluid retention over the study was greater after ingestion of drink CP (55 (sd 12) %) than that after ingestion of drink C (43 (sd 15) %) (P < 0·05). At the end of the study period, whole body net fluid balance (P < 0·05) was less negative for trial CP ( − 0·26 (sd 0·27) litres) than for trial C ( − 0·52 (sd 0·30) litres), and although net negative for both the trials, it was only significantly negative after ingestion of drink C (P < 0·05). The results of the present study suggest that when matched for energy density and fat content, as well as for Na and K concentration, and when ingested after exercise-induced dehydration, a carbohydrate–milk protein solution is better retained than a carbohydrate solution. These results suggest that gram-for-gram, milk protein is more effective at augmenting fluid retention than carbohydrate.

Biochemical components in alfalfa (Medicago sativa L.), such as saponins, can act as protecting factors against bio-stresses. Saponins are also antifeedants and show oral toxicity towards higher and lower animals. Changes in saponins, such as variation in the carbon skeleton, or hydrolysis of saponin glycosides and other conjugates, may change their biological effects. The aims of this research were to study saponin variation in different growth stages of alfalfa and to investigate the biological role of saponins in the spotted alfalfa aphid, Therioaphis maculata. Saponins from alfalfa shoots in different growth stages were extracted, chemically purified and analysed by TLC. Specific saponins such as soyasaponin1 from root and shoot and two bisdesmosides of medicagenic acid, one from shoot and another from root tissues, were identified using reference compounds allowing changes in saponin composition during plant development in different shoot tissues of alfalfa to be assessed. The response of the alfalfa aphid to feeding on alfalfa in different growth stages was studied. No significant difference in the survival of aphids, from neonate to adult, was observed, but due to the antibiotic effects of saponins, two differences were found in the onset of nymph production and cumulative nymph production. The results show that the saponin composition in alfalfa changes with plant development and this, in turn, can often negatively affect the development of specific insect pests such as the spotted alfalfa aphid, suggesting a possible biological role of alfalfa saponins.

The pancreatic enzyme secretory phospholipase A2 group IB (sPLA2 IB) hydrolyses phospholipids at the sn-2 position, resulting in a NEFA and a lyso-phospholipid, which are then absorbed by the enterocytes. The sPLA2 IB is a member of a family of nineteen enzymes sharing the same catalytic ability, of which nine are cytosolic and ten are secretory. Presently, there are no pharmacological tools to separate between the different secretory enzymes when measuring the enzymatic activity. Thus, it is important to support activity data with more precise techniques when isolation of intestinal content is not possible for analysis, as in the case of small teleost larvae, where the whole animal is sometimes analysed. In the present study, we characterise the sPLA2 IB gene in Atlantic cod (Gadus morhua) and describe its ontogeny at the genetic and protein level and compare this to the total sPLA2 activity level. A positive correlation was found between the expression of sPLA2 IB mRNA and protein. Both remained stable and low during the larval stage followed by an increase from day 62 posthatch, coinciding with the development of the pyloric ceaca. Meanwhile, total sPLA2 enzyme activity in cod was stable and relatively high during the early stages when larvae were fed live prey, followed by a decrease in activity when the fish were weaned to a formulated diet. Thus, the expression of sPLA2 IB mRNA and protein did not correlate with total sPLA2 activity.

Supplementing broiler diets with conventional vegetable oils has little effect on the long-chain n-3 PUFA (LC n-3 PUFA) content of the meat. The present study investigated the effect on fatty acid composition and sensory characteristics of chicken meat when broilers were fed oil extracted from soyabeans (SDASOY) that had been genetically engineered to produce C18 : 4n-3 (stearidonic acid (SDA), 240 mg/g oil). Three diets were fed to 120 birds (eight replicate pens of five birds) from 15 d to slaughter (41–50 d). Diets were identical apart from the oil added to them (45 and 50 g/kg as fed in the grower and finisher phases, respectively), which was either SDASOY, near-isogenic soya (CON) or fish oil (FISH). The LC n-3 PUFA content of the meat increased in the order CON, SDASOY and FISH. In breast meat with skin, the SDA concentration was 522, 13 and 37 (sem 14·4) mg/100 g meat for SDASOY, CON and FISH, respectively. Equivalent values for C20 : 5n-3 (EPA) were 53, 13 and 140 (sem 8·4); for C22 : 5n-3 (docosapentaenoic acid (DPA)) 65, 15 and 101 (sem 3·5); for C22 : 6n-3 (DHA) 19, 9 and 181 (sem 4·4). Leg meat (with skin) values for SDA were 861, 23 and 68 (sem 30·1); for EPA 87, 9 and 258 (sem 7·5); for DPA 95, 20 and 165 (sem 5·0); for DHA 29, 10 and 278 (sem 8·4). Aroma, taste and aftertaste of freshly cooked breast meat were not affected. Fishy aromas, tastes and aftertastes were associated with LC n-3 PUFA content of the meat, being most noticeable in the FISH leg meat (both freshly cooked and reheated) and in the reheated SDASOY leg meat.

The objective of the present study was to investigate whether weight loss is associated with changes in serum concentrations of lutein (L) and zeaxanthin (Z), and/or macular pigment optical density (MPOD). We recruited 104 overweight subjects into this randomised controlled weight loss study. For the intervention group (I group), weight was assessed weekly and body composition, including BMI (kg/m2) and body fat (kg and percentage), was assessed at baseline, 6 and 12 months. Weight loss was encouraged using dietary and exercise programmes. MPOD was measured by heterochromatic flicker photometry and serum concentrations of L and Z by HPLC (at baseline, 1, 3, 6 and 12 months). The control (C) group was assessed at baseline and 12 months. Repeated-measures ANOVA (RMA) demonstrated significant weight loss in the I group over the study period (P = 0·000). There was no significant weight change in the C group (P = 0·993). RMA of dietary L and Z, serum L and Z, and MPOD demonstrated no significant time or time × group interaction effect in any of these parameters (P>0·05 for all), with the exception of a significant decrease in the dietary intake of Z seen in both groups, over the study period (P < 0·05). There was a positive and significant relationship between body fat loss (kg) and increase in serum concentrations of L in the I group (r 0·521; P = 0·006). Our finding that a reduction in body composition (e.g. fat mass) is related to increases in serum concentrations of L is consistent with the hypothesis that body fat acts as a reservoir for this carotenoid, and that weight loss can positively influence circulating carotenoid levels.

Historically, measurement of gastrointestinal transit time has required collection and X-raying of faecal samples for up to 7 d after swallowing radio-opaque markers; a tedious, labour-intensive technique for both subjects and investigators. Recently, a wireless motility capsule (SmartPill®), which uses gut pH, pressure and temperature to measure transit time, has been developed. This device, however, has not been validated with dietary interventions. Therefore, we conducted a controlled cross-over trial to determine whether the device could detect a significant difference in transit time after ten healthy subjects (five men and five women) consumed 9 g of wheat bran (WB) or an equal volume, low-fibre control for 3 d. A paired t test was used to determine differences in transit times. Colonic transit time decreased by 10·8 (sd 6·6) h (P = 0·006) on the WB treatment. Whole-gut transit time also decreased by 8·9 (sd 5·4) h (P = 0·02) after the consumption of WB. Gastric emptying time and small-bowel transit time did not differ between treatments. Despite encouraging results, the present study had several limitations including short duration, lack of randomisation and unusable data due to delayed gastric emptying of the capsule. With minimal participant burden, the SmartPill technology appears to be a potentially useful tool for assessing transit time after a dietary intervention. This technology could be considered for digestive studies with novel fibres and other ingredients that are promoted for gut health.

A 2 × 2 factorial experiment (ten sows per treatment) was conducted to investigate the effect of maternal dietary supplementation with a seaweed extract (SWE; 0 v. 10·0 g/d) and fish oil (FO; 0 v. 100 g/d) inclusion from day 109 of gestation until weaning (day 26) on pig performance post-weaning (PW) and intestinal morphology, selected microflora and immune status of pigs 9 d PW. The SWE contained laminarin (10 %), fucoidan (8 %) and ash (82 %) and the FO contained 40 % EPA and 25 % DHA. Pigs weaned from SWE-supplemented sows had higher daily gain (P = 0·063) between days 0 and 21 PW and pigs weaned from FO-supplemented sows had higher daily gain (P < 0·05) and gain to feed ratio (P < 0·01) between days 7 and 14 PW. There was an interaction between maternal SWE and FO supplementation on caecal Escherichia coli numbers (P < 0·05) and the villous height to crypt depth ratio in the ileum (P < 0·01) and jejunum (P < 0·05) in pigs 9 d PW. Pigs weaned from SWE-supplemented sows had lower caecal E. coli and a higher villous height to crypt depth ratio in the ileum and jejunum compared with non-SWE-supplemented sows (P < 0·05). There was no effect of SWE on E. coli numbers and villous height to crypt depth ratio with FO inclusion. Maternal FO supplementation induced an increase in colonic mRNA abundance of IL-1α and IL-6 (P < 0·05), while SWE supplementation induced an increase in ileal TNF-α (P < 0·01) and colonic TFF3 mRNA expression (P < 0·05). In conclusion, these results demonstrate that SWE and FO supplementation to the maternal diet influenced the gastrointestinal environment and performance of the weaned pig.

Small birth weight and excess of early protein intake are suspected to enhance later obesity risk. The present study was undertaken to determine the impact of neonatal diets differing in protein content on growth, body composition and hormonal status of 70-d-old pigs born with normal weight (NW) or small weight (SW). At 7 d of age, male and female suckled piglets were assigned to the NW (approximately 1·4 kg at birth) or SW (approximately 0·99 kg at birth) groups. They were fed milk replacers formulated to provide an adequate protein (AP) or a high protein (HP) supply for 3 weeks. From weaning to 70 d of age, all animals received ad libitum the same standard diet. Growth rates were higher (P < 0·05) in HP piglets than in AP piglets during formula feeding and remained higher (P < 0·05) only in HP male pigs thereafter. No difference in feed consumption was detected between groups during the periods examined. Carcass lipid content and the relative weight of perirenal adipose tissue did not differ between the AP and HP pigs. Whereas plasma leptin concentration was higher (P < 0·05) in HP pigs than in AP pigs with a marked difference in SW pigs, plasma insulin-like growth factor (IGF)-I concentration and expression of IGF system genes were not affected by the diets. In summary, a HP intake during the suckling period induced an increase in growth rate that persisted only in male pigs during the post-weaning period. This response was not associated with any difference in adiposity parameters in this period.

Aplastic anaemia (AA) is a disease characterised by bone marrow hypocellularity and peripheral blood pancytopenia. AA is also associated with mitochondrial aberrations. The present study was undertaken primarily to test the hypothesis that a nutrient mixture could affect the nutritional rehabilitation of mitochondrial aberrations in AA mice. BALB/c AA mice were induced by a combination of hypodermic injections of acetylphenylhydrazine (100 mg/kg), X-rays (2·0 Gy) and intraperitoneal injections of cyclophosphamide (80 mg/kg). We treated these mice with nutrient mixture-supplemented diets in a dose-dependent manner (1445·55, 963·7, 674·59 mg/kg per d), and the effects of the nutrient mixture for mitochondrial rehabilitation were analysed in AA mice. Transmission electron microscopy showed that mitochondrial ultrastructural abnormalities in bone marrow cells, splenocytes and hepatocytes of the nutrient mixture groups were restored markedly, compared with the AA group. Mitochondrial membrane potentials of the nutrient mixture groups were increased remarkably. Western blot analysis also revealed that the nutrient mixture significantly inhibited cytochrome c release of mitochondria in the AA group. Furthermore, the mitochondrial DNA content of the nutrient mixture groups was also increased. Our data suggest that the nutrient mixture may promote the rehabilitation of mitochondrial aberrations, and consequently protects against mitochondrial dysfunction in AA mice.

The aim of this 28 d experiment was to examine the physiological response of growing rats to a dietary combination of prebiotic chicory fructans, with polyphenols originating from different parts of the chicory plant, i.e. roots, root peels, seeds and leaves. A total of forty rats were assigned to groups fed the following diets characterised by a similar content of oligofructose and inulin: control, with 10 % of a root extract (a low level of dietary polyphenols, 0·05 %), with 6·5 % of a root peel extract (a medium level of dietary polyphenols, 0·107 %), with a combination of 8 % of a peel extract and 0·8 % of a seed extract (a high level of dietary polyphenols, 0·208 %) and with 2·5 % of a leaf extract (a medium level of dietary polyphenols, 0·106 %, with chicoric acid constituting half of them). Chicory seeds are the richest source of polyphenols, especially abundant in dicaffeoylquinic acids. When applied as a dietary supplement, the mixture of monocaffeoylquinic and dicaffeoylquinic acids, from the extracts made of roots, root peels and seeds, elicited more favourable changes in parameters of the antioxidative status of the body and in the activity of bacterial β-glucuronidase in the faeces and caecal digesta. In turn, the extract from chicory leaves, containing considerable quantities of chicoric acid and polyphenolic glycosides, apart from chlorogenic acids, also triggered desirable changes in the lipid profile of the blood serum. The high concentration of polyphenols in the extracts examined enables their application as dietary supplements to be administered in low doses.

The present study investigates whether excessive fat accumulation and hyperinsulinaemia during catch-up growth on high-fat diets are altered by n-6 and n-3 PUFA derived from oils rich in either linoleic acid (LA), α-linolenic acid (ALA), arachidonic acid (AA) or DHA. It has been shown that, compared with food-restricted rats refed a high-fat (lard) diet low in PUFA, those refed isoenergetically on diets enriched in LA or ALA, independently of the n-6:n-3 ratio, show improved insulin sensitivity, lower fat mass and higher lean mass, the magnitude of which is related to the proportion of total PUFA precursors (LA+ALA) consumed. These relationships are best fitted by quadratic regression models (r2>0·8, P < 0·001), with threshold values for an impact on body composition corresponding to PUFA precursors contributing 25–30 % of energy intake. Isoenergetic refeeding on high-fat diets enriched in AA or DHA also led to improved body composition, with increases in lean mass as predicted by the quadratic model for PUFA precursors, but decreases in fat mass, which are disproportionately greater than predicted values; insulin sensitivity, however, was not improved. These findings pertaining to the impact of dietary intake of PUFA precursors (LA and ALA) and their elongated–desaturated products (AA and DHA), on body composition and insulin sensitivity, provide important insights into the search for diets aimed at counteracting the pathophysiological consequences of catch-up growth. In particular, diets enriched in essential fatty acids (LA and/or ALA) markedly improve insulin sensitivity and composition of weight regained, independently of the n-6:n-3 fatty acid ratio.

The effect of the dietary n-3 long-chain PUFA, DHA (22 : 6n-3), on the growth of pre-term infants is controversial. We tested the effect of higher-dose DHA (approximately 1 % dietary fatty acids) on the growth of pre-term infants to 18 months corrected age compared with standard feeding practice (0·2–0·3 % DHA) in a randomised controlled trial. Infants born < 33 weeks gestation (n 657) were randomly allocated to receive breast milk and/or formula with higher DHA or standard DHA according to a concealed schedule stratified for sex and birth-weight ( < 1250 and ≥ 1250 g). The dietary arachidonic acid content of both diets was constant at approximately 0·4 % total fatty acids. The intervention was from day 2 to 5 of life until the infant's expected date of delivery (EDD). Growth was assessed at EDD, and at 4, 12 and 18 months corrected age. There was no effect of higher DHA on weight or head circumference at any age, but infants fed higher DHA were 0·7 cm (95 % CI 0·1, 1·4 cm; P = 0·02) longer at 18 months corrected age. There was an interaction effect between treatment and birth weight strata for weight (P = 0·01) and length (P = 0·04). Higher DHA resulted in increased length in infants born weighing ≥ 1250 g at 4 months corrected age and in both weight and length at 12 and 18 months corrected age. Our data show that DHA up to 1 % total dietary fatty acids does not adversely affect growth.

Gut hormones play key roles in the regulation of energy homeostasis. However, little is known about the long- and short-term effects of changing dietary fat content on gut hormones. We aim to examine the effects of changing dietary fat content on plasma gut hormone concentrations in diet-induced obese (DIO) and diet-resistant (DR) rats. After inducing obesity with a high-fat (HF) diet, male Sprague–Dawley rats were divided into three groups according to their body-weight gain: DIO; DR; control (CON). The DIO and DR rats were further divided in random into two groups. One continued on a HF diet and the other switched to a low-fat (LF) diet for an additional 4 weeks. Finally, each group was randomly divided into three subgroups (n 8): fasted; fasted-refed HF; fasted-refed LF diet groups. Replacing a HF diet with a LF diet for 4 weeks resulted in less fat mass, higher fasting and post-HF plasma ghrelin concentration and lower postprandial plasma cholecystokinin concentration in the DIO and DR rats. Acute switching dietary fat resulted in significantly higher post-HF plasma ghrelin concentrations than post-LF ghrelin concentrations in the DR rats on LF diet (DRLF) and DIO rats on LF diet (DIOLF) rats, and significantly higher post-HF obestatin concentrations than post-LF obestatin concentrations in the CON, DR rats on HF diet (DRHF) and DRLF rats. Dietary fat content appears to play a role in the gut hormone profile, which may consequently influence fat mass.

The aim of the present study was to examine the association between dietary patterns and weight change prospectively. We followed up 1231 adults aged 20 years and older (mean age 49·3 years) from 2002 to 2007. Food intake was assessed at baseline by an FFQ. Factor analysis was used to identify dietary patterns. Nutrient intake was measured by food weighing plus consecutive individual 3 d food records. Body weight and height were measured. The mean 5-year weight gain among all participants was 0·8 (sd 4·7) kg. The mean weight changes across quartiles of the ‘traditional’ pattern (rice, fresh vegetables, pork and wheat flour) were 2·0, 0·6, 0·6 and 0·0 kg. The corresponding values were 0·4, 0·5, 0·7 and 1·6 kg across quartiles of the ‘vegetable-rich’ pattern. No significant association between the ‘macho’ dietary pattern (meat and alcohol), the ‘sweet tooth’ pattern (drinks and cake) and weight gain was found. In multivariate linear regression, using the first quartile as the reference, participants in the highest quartile of the ‘traditional’ pattern had a β of − 2·18 (95 % CI − 2·91, − 1·45) for weight gain. However, the β from weight change of the highest quartile of the ‘vegetable-rich’ pattern was 1·00 (95 % CI 0·25, 1·74). In conclusion, the ‘traditional’ dietary pattern was negatively and the ‘vegetable-rich’ pattern was positively associated with weight gain in Chinese adults.

Polyphenols exert beneficial effects in atherosclerosis. The crucial step in atherosclerosis is the recruitment of monocytes to the subendothelial space, induced by endothelial adhesion molecules through the activation of factors such as NF-κB. We studied the effect of a dealcoholised lager beer (DLB) and a dealcoholised dark beer (DDB) on atherosclerotic lesions, and the underlying mechanisms. Dealcoholised beers were administered in the diet (42 ml/kg body weight per d) to 4-week-old male apoE knockout (apoE − / − ) mice for 20 weeks. The atherosclerotic lesions in the thoracic aorta were reduced by 44 % (P = 0·003) and 51 % (P < 0·001) in DLB- and DDB-treated mice, respectively. Also, the mRNA expressions of the endothelial adhesion molecules in the total aorta were decreased: P-selectin showed a 17 % (P = 0·004) reduction in DDB-treated mice; vascular cell adhesion molecule-1 (VCAM-1) was decreased by 20 % (P = 0·012) and 32 % (P = 0·001) in DLB- and DDB-treated mice, respectively; intercellular adhesion molecule-1 (ICAM-1) showed a 14 % (P = 0·014) reduction in DLB-treated mice. The protein expressions of these molecules and NF-κB were studied in the aortic root. P-selectin was decreased by 37 % (P = 0·012) in DDB-treated mice; VCAM-1 was reduced by 48 % (P = 0·001) and 54 % (P < 0·001) in DLB- and DDB-treated mice, respectively; ICAM-1 was decreased by 25 % (P = 0·028) and 30 % (P = 0·018) in DLB- and DDB-treated mice, respectively; NF-κB was reduced by 46 % (P = 0·042) in DDB-treated mice. In conclusion, dealcoholised beers protected apoE − / −  mice against atherosclerosis, through the modulation of endothelial adhesion molecules, possibly induced by NF-κB.