The developing fetus requires an adequate supply of fatty acids, in particular PUFA, for optimal growth and development. Little is known about the transfer of fatty acids by the placenta into the fetal circulation. However, the molecular form in which fatty acids are transferred into the fetal circulation may influence their metabolism and hence their availability to specific tissues. The aim of the present study was to determine which lipid pools in the fetal circulation become enriched in fatty acids from the placenta by comparing the fatty acid compositions of individual lipid pools between umbilical venous (UV) and umbilical arterial (UA) plasma. Plasma from the UV and UA was collected after delivery from ten uncomplicated pregnancies, and the fatty acid composition of each lipid class was determined by GC. Total NEFA concentration in the UV was twofold higher than in the UA (P < 0·05) due to enrichment in 16 : 0, 16 : 1n-7, 18 : 1n-9, 18 : 1n-7, 18 : 2n-6, 20 : 3n-6, 20 : 4n-6, 24 : 0 and 22 : 6n-3. Total cholesteryl ester concentration was twofold higher in the UV than in the UA (P < 0·05) due to enrichment in 16 : 0, 16 : 1n-7, 18 : 0, 18 : 1n-9, 18 : 1n-7, 18 : 2n-6 and 20 : 4n-6. There were no significant UV–UA differences in the total concentration or composition of TAG or phosphatidylcholine. The present study demonstrates differential enrichment across the placenta of fatty acids into specific lipid pools in the fetal circulation. Such partitioning may facilitate supply of individual fatty acids to specific fetal tissues.

The melanocortin-4 receptor (MC4R) is an essential regulator of food intake and energy homeostasis. Previous data suggest an influence of MC4R activity on TAG levels. Thus, the aim of the present study was to determine whether the presence of the rs12970134 polymorphism near the MC4R gene could influence postprandial lipoprotein metabolism in healthy subjects. A total of eighty-eight volunteers were selected, fifty-three homozygous for the common genotype (G/G) and thirty-five carriers for the minor A-allele (G/A and A/A). They were given a fat-rich meal containing 1 g fat and 7 mg cholesterol/kg body weight and vitamin A (60 000 IU/m2 body surface). Fat accounted for 60 % of energy, and protein and carbohydrates accounted for 15 and 25 % of energy, respectively. Blood samples were taken at time 0, every 1 h until 6 h and every 2·5 h until 11 h. Total cholesterol and TAG in plasma, and cholesterol, TAG and retinyl palmitate in TAG-rich lipoproteins (TRL, large and small TRL) were separated by ultracentrifugation. Individuals carrying the G/G genotype displayed a higher postprandial response of plasma TAG (P = 0·033), total cholesterol (P = 0·019) and large TRL–TAG (P = 0·023) than did carriers of the minor A-allele. Furthermore, G/G subjects showed a greater postprandial response of small TRL–apoB48 than did carriers of the A-allele (P = 0·032). These results suggest that the rs12970134 polymorphism near the MC4R gene region may partly explain the inter-individual differences in postprandial lipoprotein response in healthy subjects.

Following concerns about the nutritional content of school lunches and the increased prevalence of overweight and obesity in the UK, changes to the standards of school meals were made. From September 2008, all primary schools in England were required, by law, to be fully compliant with the new food-based standards (FBS) and nutrient-based standards (NBS) for school lunches. The aim of the present survey was to evaluate the introduction of the NBS for school lunches on the nutritional profile of food and drink items provided by schools and chosen by pupils at lunchtime. A nationally representative sample of 6696 pupils from 136 primary schools in England aged 3–12 years and having school lunches was recruited. Data were collected on lunchtime food and drink provision at each school and on pupil food and drink choices at lunchtime. Caterers also provided planned menus, recipes and other cooking information. Compliance with both the FBS and NBS was then assessed. Results show that even when the FBS was met, many schools did not provide a school lunch that met the NBS as well. The average school lunch eaten was significantly lower in fat, saturated fat and Na in schools that met both the FBS and NBS for school lunches compared with schools that met only the FBS. Change in school lunch policy has contributed to improvements in pupils' choices and the nutritional profile of foods selected at lunchtime.

β-(1,3)-d-Glucan with β-(1,6) branches has been reported to have various pharmacological activities, such as anti-tumour and anti-infection activities, which result from its immunomodulating effects. Gastric lesions result from an imbalance between aggressive and defensive factors. In the present study, we examined the effect of β-(1,3)-d-glucan with β-(1,6) branches isolated from Aureobasidium pullulans on the gastric ulcerogenic response in mice. Oral administration of β-glucan ameliorated gastric lesions induced by ethanol (EtOH) or HCl. This administration of β-glucan also suppressed EtOH-induced inflammatory responses, such as infiltration of neutrophils and expression of pro-inflammatory cytokines, chemokines and cell adhesion molecules (CAM) at the gastric mucosa. Of the various defensive factors, the levels of heat shock protein (HSP) 70 and mucin but not PGE2 were increased by the administration of β-glucan. β-Glucan-dependent induction of the expression of HSP70 and mucin proteins and suppression of the expression of pro-inflammatory cytokines, chemokines and CAM were also observed in cultured cells in vitro. The results of the present study suggest that β-glucan protects the gastric mucosa from the formation of irritant-induced lesions by increasing the levels of defensive factors, such as HSP70 and mucin.

The aim of the present study was to investigate the association of PLIN1 11482G>A (rs894160) and PLIN1 13041A>G (rs2304795) polymorphisms with body composition, energy and substrate metabolism, and the metabolic response to a 12-week energy-restricted diet in obese women. The study comprised a total of seventy-eight obese (BMI 34·0 (sd 2·8) kg/m2) women (age 36·7 (sd 7) years). We measured weight, height and waist circumference before and after a 12-week controlled energy-restricted diet intervention. Body fat mass and lean mass were measured by dual-energy X-ray absorptiometry. RMR and lipid oxidation rate were measured by indirect calorimetry. We also analysed fasting plasma glucose, insulin, cholesterol and leptin. Women carrying the 11482A allele had a lower reduction in waist circumference than non-A allele carriers (3·2 (sd 0·5) v. 4·6 (sd 0·6) %, respectively, P = 0·047; P for gene–diet interaction = 0·064). Moreover, women with the 11482A allele had a higher decrease in lipid oxidation rate than non-A allele carriers (58·9 (sd 6·7) v. 31·3 (sd 8·2) %, respectively, P = 0·012; P for gene–diet interaction = 0·004). There was no interaction effect between the 13041A>G polymorphism and diet-induced changes on the outcome variables (all P>0·1). These results confirm and extend previous findings suggesting that the PLIN1 11482G>A polymorphism plays a modulating role on diet-induced changes in body fat and energy metabolism in obese women.

Accumulation of muscle TAG content and modification of muscle phospholipid fatty acid pattern may have an impact on lipid metabolism, increasing the risk of developing diabetes. Some polyphenols have been reported to modulate lipid metabolism, in particular those issued from red grapes. The present study was designed to determine whether a grape polyphenol extract (PPE) modulates skeletal muscle TAG content and phospholipid fatty acid composition in high-fat–high-sucrose (HFHS) diet-fed rats. Muscle plasmalemmal and mitochondrial fatty acid transporters, GLUT4 and lipid metabolism pathways were also explored. The PPE decreased muscle TAG content in HFHS/PPE diet-fed rats compared with HFHS diet-fed rats and induced higher proportions of n-3 PUFA in phospholipids. The PPE significantly up-regulated GLUT4 mRNA expression. Gene and protein expression of muscle fatty acid transporter cluster of differentiation 36 (CD36) was increased in HFHS diet-fed rats but returned to control values in HFHS/PPE diet-fed rats. Carnitine palmitoyltransferase 1 protein expression was decreased with the PPE. Mitochondrial β-hydroxyacyl CoA dehydrogenase was increased in HFHS diet-fed rats and returned to control values with PPE supplementation. Lipogenesis, mitochondrial biogenesis and mitochondrial activity were not affected by the PPE. In conclusion, the PPE modulated membrane phospholipid fatty acid composition and decreased muscle TAG content in HFHS diet-fed rats. The PPE lowered CD36 gene and protein expression, probably decreasing fatty acid transport and lipid accumulation within skeletal muscle, and increased muscle GLUT4 expression. These effects of the PPE are in favour of a better insulin sensibility.

The objective of the present study was to determine the effects of soya and whey milk protein, α-lactalbumin (α-LA), on mammary gland morphology and the structural support of the gland, in pre-pubertal mice after 7 d of treatment. In Expt 1, weaned (day 21) CD1 mice were given one of the four treatments, three included dietary supplements: (1) control diet, casein, (2) soya, (3) α-LA and (4) subcutaneous injection of 2·5 μg oestradiol benzoate in 20 μl maize oil and fed the control diet. All diets were isoenergetic with equal protein concentrations. All groups that were not treated with oestradiol received the vehicle. Whole-mount analyses were performed to determine longitudinal ductal growth and terminal end bud development. DNA was extracted from the gland and assessed by spectrophotometry (260/280 nm). Tissue extracts for extracellular matrix (ECM) proteins, matrix metalloproteinase-2 (MMP2), tissue inhibitor of MMP2 (TIMP2), and serum oestradiol and mammary tissue epidermal growth factors (EGF) were measured by immunoassays. Expt 2 utilised the Her2/neu transgenic strain, with the same protocols. Statistical significance was determined by one-way ANOVA. From Expt 1 and 2, soya and α-LA significantly increased ductal elongation when compared with the oestrogen and control groups. These results were corroborated by data on total DNA and the ratio of MMP2:TIMP2. The ratio of MMP2:TIMP2 was affected by α-LA. Serum oestradiol was decreased only in the oestradiol-treated groups in both experiments. Soya is known to be oestrogenic and can act on epithelia directly. The mechanism by which α-LA affects glandular development is by modulating the ECM or by promoting the synthesis/activity of EGF.

The objective of the present study was to investigate the effects of the addition of fibre and the antioxidant N-acetylcysteine (NAC) to fat-rich diets on fetal intrauterine development in rats. A total of eighty virgin female Sprague–Dawley rats were fed a control diet, a high-fat diet (HF), a high-fat and high-fibre diet (HFF) or a high-fat NAC diet until day 19·5 of gestation. Maternal HFF consumption resulted in a significantly higher mean fetal number and placental weight than in the other groups (P < 0·05). The HFF diet significantly abrogated HF-induced decreases in maternal serum and placental superoxide anion and hydroxyl radical scavenging capacities (P < 0·05); partially abrogated HF-induced increases in maternal serum and placental malondialdehyde (MDA) and protein carbonyl concentrations (maternal serum MDA and placental protein carbonyl, P < 0·05); resulted in significantly higher fetal liver total superoxide dismutase (SOD), Cu- and Zn-containing SOD and Mn-containing SOD (Mn-SOD) activities than in the HF group (P < 0·05). Furthermore, mRNA expressions of hypoxia-inducible factor 1-α, thioredoxin 2 and Mn-SOD in fetal liver and Mn-SOD in fetal heart and placental GLUT3 in the HFF group were higher than those in the other groups (P < 0·05). The inclusion of dietary fibre in the HF diet was more effective than NAC supplementation in maintaining maternal serum and placental superoxide anion and hydroxyl radical scavenging capacities close to those of the control. These results suggest that maternal fibre intake during pregnancy is beneficial for fetal intrauterine development possibly through the improvement of maternal, placental and fetal antioxidant capacities and placental nutrient transfer capacity.

Both fish oil (FO) and curcumin have potential as anti-tumour and anti-inflammatory agents. To further explore their combined effects on dextran sodium sulphate (DSS)-induced colitis, C57BL/6 mice were randomised to four diets (2 × 2 design) differing in fatty acid content with or without curcumin supplementation (FO, FO+2 % curcumin, maize oil (control, MO) or MO+2 % curcumin). Mice were exposed to one or two cycles of DSS in the drinking-water to induce either acute or chronic intestinal inflammation, respectively. FO-fed mice exposed to the single-cycle DSS treatment exhibited the highest mortality (40 %, seventeen of forty-three) compared with MO with the lowest mortality (3 %, one of twenty-nine) (P = 0·0008). Addition of curcumin to MO increased (P = 0·003) mortality to 37 % compared with the control. Consistent with animal survival data, following the one- or two-cycle DSS treatment, both dietary FO and curcumin promoted mucosal injury/ulceration compared with MO. In contrast, compared with other diets, combined FO and curcumin feeding enhanced the resolution of chronic inflammation and suppressed (P < 0·05) a key inflammatory mediator, NF-κB, in the colon mucosa. Mucosal microarray analysis revealed that dietary FO, curcumin and FO plus curcumin combination differentially modulated the expression of genes induced by DSS treatment. These results suggest that dietary lipids and curcumin interact to regulate mucosal homeostasis and the resolution of chronic inflammation in the colon.

Vegetable oils containing α-linolenic acid (ALA; 18 : 3n-3) have been shown to modulate the functions of immunocompetent cells. The aim of the present study was to understand the modulatory effect of ALA-rich garden cress (Lepidium sativum L.) seed oil (GCO) on lipid composition, spleen lymphocyte (SL) proliferation and inflammatory mediator production by peritoneal macrophages (PMΦ) in rats. Female Wistar rats were fed diets containing either GCO (2·5, 5·0 and 10 %, w/w) or sunflower oil (SFO, 10 % w/w) for 8 weeks. Ex vivo proliferation of SL was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. IL-2 and TNF-α in SL and PMΦ were analysed by ELISA. Inflammatory mediators such as NO, leukotriene B4 (LTB4) and H2O2 were measured in mitogen-activated PMΦ. GCO significantly increased the levels of ALA, EPA and DHA, but reduced linoleic acid and arachidonic acid in SL and PMΦ lipids. GCO (10 %) significantly decreased the concanavalin A (Con-A)- and phytohaemagglutinin-mediated proliferation of SL by 54 and 38 %, respectively, in comparison with SFO. A marginal decrease in IL-2 and TNF-α was observed in Con-A-stimulated SL and lipopolysaccharide-stimulated PMΦ. LTB4 levels in Ca ionophore-stimulated PMΦ were reduced by 40 % in GCO-fed rats. NO release in response to various stimuli was significantly decreased in PMΦ of GCO-fed rats. The present study is the first report on the modulatory efficacy of GCO on immunomediators in rats. GCO modulated inflammatory mediators such as NO and LTB4, and thus may play a role in alleviating inflammatory conditions favourably.

Besides being cholesterol-lowering agents, phytosterols (PS) can inhibit the growth and development of tumours. The anti-neoplastic activity is accounted for by PS incorporation into cell membranes, resulting in the interference of membrane functionality. The similarity between the PS cholesterol-lowering and anti-neoplastic effective doses deserves attention on the possible adverse effects even in non-neoplastic cells. To date, few studies have addressed the clarification of this important issue. In the present study, we supplemented primary, non-neoplastic neonatal rat cardiomyocytes with two different PS concentrations (3 or 6 μg/ml), both within the range of human plasma concentration. Cardiac cells were chosen as an experimental model since the heart has been reported as the target organ for subchronic toxicity of PS. Following supplementation, a dose-dependent incorporation of PS and a decrease in cholesterol content were clearly evidenced. PS did not induce apoptosis but caused a reduction in metabolic activity (measured as 3-(4,5-dimethyldiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) conversion) and a slowing down of cell growth. The lower MTT conversion and the similar lactate dehydrogenase release could suggest that PS more efficiently target mitochondria than plasma membrane integrity. The replacement of cholesterol by PS could also have caused the observed slowing down of cell growth and the reduction in metabolic activity, which could rely on the PS increase, cholesterol decrease, or both. The present study is the first report on the effect of PS in cardiac cells, and although it is difficult to translate the obtained results to the health of heart tissue, it raises concerns about the safety of long-term exposure to physiologically relevant PS concentrations.

For conducting effective risk management in long-stay elderly people at a health service facility, we performed an open case-controlled study to evaluate the effect of the intake of probiotic-fermented milk containing Lactobacillus casei strain Shirota (LcS-fermented milk) on norovirus gastroenteritis occurring in the winter season during the intake period. A total of seventy-seven elderly people (mean age 84 years) were enrolled in the study. During a 1-month period, there was no significant difference in the incidence of norovirus gastroenteritis between the LcS-fermented milk-administered (n 39) and the non-administered (n 38) groups; however, the mean duration of fever of >37°C after the onset of gastroenteritis was 1·5 (sd 1·7) d in the former and 2·9 (sd 2·3) d in the latter group, showing a significant shortening in the former group (P < 0·05). RT-quantitative PCR analysis targeting ribosomal RNA showed both Bifidobacterium and Lactobacillus to be significantly dominant, whereas Enterobacteriaceae decreased in faecal samples from the administered group (n 10, mean age 83 years), with a significant increase in faecal acetic acid concentration. Continuous intake of LcS-fermented milk could positively contribute to the alleviation of fever caused by norovirus gastroenteritis by correcting the imbalance of the intestinal microflora peculiar to the elderly, although such consumption could not protect them from the disease.

It has been suggested that antioxidants attenuate oxidative stress and prevent oxidative stress-related diseases. Paradoxically, randomised controlled trials (RCT) using pharmacological doses of antioxidant supplements have demonstrated harmful effects in smokers. The aim of the present study was to test the compliance, tolerability and safety of two food-based antioxidant-rich diets in smokers. One of the diets provided antioxidants at levels similar to that used in RCT using supplements which previously have generated harmful effects. The present study followed a randomised, parallel-arm dietary intervention for 8 weeks (n 102) in male smokers (age ≥ 45 years). Participants were randomised to either antioxidant-rich diet, kiwi fruit or control groups. The antioxidant-rich foods provided about 300 mmol antioxidants/week from a wide range of plant-based food items. The kiwi fruit group consumed three kiwi fruits/d. Compliance to both diets was good. Only mild, undesirable events were reported by a minority of the participants. The safety of both diets was demonstrated as no potentially harmful or pro-oxidative effects were observed. In the antioxidant-rich diet group, the mean intake of antioxidants increased from 30 mmol/d at baseline to 62 mmol/d during the intervention. In conclusion, we have demonstrated that male smokers can comply with two food-based antioxidant-rich diets. Furthermore, the present study is the first to demonstrate the tolerability and safety of dietary antioxidants at levels similar to dosages provided in RCT using supplements. Such diets may be useful in future studies investigating whether dietary antioxidants may reduce oxidative stress and related diseases.

Certain forms of dietary Se may have advantages for improving human Se status and regulating the risk for disease, such as cancers, including colorectal cancer (CRC). The present study compared the effects of a Se-enriched milk protein (dairy-Se) with a Se-rich yeast (yeast-Se) on plasma Se levels and rectal selenoprotein gene expression since we reasoned that if these genes were not regulated, there was little potential for regulating the risk for CRC in this organ. A total of twenty-three healthy volunteers with plasma Se in the lower half of the population range were supplemented with dairy-Se (150 μg/d) or yeast-Se (150 μg/d) for 6 weeks, followed by 6 weeks of washout period. Blood was sampled every 2 weeks, and rectal biopsies were obtained before and after Se supplementation and after the washout period. Plasma Se levels and glutathione peroxidase (GPx) activity, and rectal mRNA of selenoprotein P (SeP), cytosolic GPx-1 (GPx-1), gastrointestinal GPx-2 (GPx-2) and thioredoxin reductase-1 (TrxR-1) were measured. Plasma Se levels increased rapidly in both Se groups (P < 0·001); plasma GPx activity was not significantly changed. Rectal SeP mRNA increased at 6 weeks compared with baseline in both Se groups (P < 0·05); only dairy-Se resulted in a sustained elevation of SeP after the washout period (P < 0·05). Rectal GPx-1 and GPx-2 mRNA were higher with dairy-Se (P < 0·05) than with yeast-Se at 6 weeks. In conclusion, three rectal selenoprotein mRNA were differentially regulated by dairy-Se and yeast-Se. Changes in rectal selenoproteins are not predicted by changes in plasma Se; dairy-Se effectively regulates the expression of several rectal selenoproteins of relevance to the risk for CRC.

In healthy older subjects, the glycaemic response to carbohydrate-containing meals is dependent on gastric emptying and intestinal absorption; when the latter is slowed, the magnitude of the rise in glucose is attenuated. The oligosaccharide α-cyclodextrin has been reported to diminish the glycaemic response to starch in young adults; this effect has been attributed to the inhibition of pancreatic amylase. We examined the effects of α-cyclodextrin on gastric emptying of, and the glycaemic and insulinaemic responses to, oral sucrose in healthy older subjects; as sucrose is hydrolysed by intestinal disaccharides, any effect(s) of α-cyclodextrin would not be attributable to amylase inhibition. A total of ten subjects (seven males and three females, age 68–76 years) were studied on 2 d. Gastric emptying, blood glucose and serum insulin were measured after ingestion of a 300 ml drink containing 100 g sucrose, labelled with 99mTc-sulphur colloid, with or without 10 g α-cyclodextrin. Gastric emptying was slowed slightly by α-cyclodextrin; this effect was evident between 135 and 195 min and was associated with a slight increase (P < 0·05) in distal stomach retention. After α-cyclodextrin, blood glucose was slightly less (P < 0·05) at 60 min, and serum insulin was less (P < 0·0005) at 90 and 120 min. There was no difference in the incremental areas under the curve (iAUC) for blood glucose, but there was a trend for the iAUC for serum insulin to be lower (P = 0·09) after α-cyclodextrin. We conclude that in a dose of 10 g, α-cyclodextrin has modest effects to slow gastric emptying of, and modify the glycaemic and insulinaemic responses to, oral sucrose, probably due to delayed intestinal carbohydrate absorption.

There is a belief that caffeinated drinks, such as tea, may adversely affect hydration. This was investigated in a randomised controlled trial. Healthy resting males (n 21) were recruited from the general population. Following 24 h of abstention from caffeine, alcohol and vigorous physical activity, including a 10 h overnight fast, all men underwent four separate test days in a counter-balanced order with a 5 d washout in between. The test beverages, provided at regular intervals, were 4 × 240 ml black (i.e. regular) tea and 6 × 240 ml black tea, providing 168 or 252 mg of caffeine. The controls were identical amounts of boiled water. The tea was prepared in a standardised way from tea bags and included 20 ml of semi-skimmed milk. All food taken during the 12 h intervention period was controlled, and subjects remained at rest. No other beverages were offered. Blood was sampled at 0, 1, 2, 4, 8 and 12 h, and a 24 h urine sample was collected. Outcome variables were whole blood cell count, Na, K, bicarbonate, total protein, urea, creatinine and osmolality for blood; and total volume, colour, Na, K, creatinine and osmolality for urine. Although data for all twenty-one participants were included in the analysis (mean age 36 years and mean BMI 25·8 kg/m2), nineteen men completed all conditions. Statistical analysis, using a factorial ANOVA approach within PROC MIXED, revealed no significant differences between tea and water for any of the mean blood or urine measurements. It was concluded that black tea, in the amounts studied, offered similar hydrating properties to water.

Hyperemesis gravidarum (hyperemesis), characterised by severe nausea and vomiting in early pregnancy, has an unknown aetiology. The aim of the present study was to investigate food and nutrient intake before pregnancy and the risk of developing hyperemesis in women participating in the Norwegian Mother and Child Cohort Study. From 1999 to 2002, a total of 7710 pregnant women answered a FFQ about their diet during the 12 months before becoming pregnant and a questionnaire about illnesses during pregnancy, including hyperemesis. Only women who were hospitalised for hyperemesis were included as cases. Nutrient intakes during the year before pregnancy did not differ between the ninety-nine women who developed hyperemesis and the 7611 who did not. However, the intake of seafood, allium vegetables and water was significantly lower among women who developed hyperemesis than among women in the non-hyperemesis group. Relative risks of hyperemesis were approximated as OR, and confounder control was performed with multiple logistic regression. Women in the upper tertile of seafood consumption had a lower risk of developing hyperemesis than those in the lower tertile (OR 0·56, 95 % CI 0·32, 0·98), and women in the second tertile of water intake had a lower risk of developing hyperemesis than those in the first tertile (OR 0·43, 95 % CI 0·25, 0·73). The findings suggest that a moderate intake of water and adherence to a healthy diet that includes vegetables and fish are associated with a lower risk of developing hyperemesis.

Diet-induced overweight rats exhibit delayed cutaneous healing; however, when receiving an obesogenic diet, some rats are susceptible to developing the overweight phenotype, whereas others are resistant. We investigated cutaneous healing in diet-induced obesity (DIO)-prone and diet-resistant (DR) rats. Male rats were fed with a standard (control) or a high-saturated fat (30 % fat, w/w) diet for 20 weeks. Then, the experimental group was subdivided into DIO (n 17) and DR (n 16) groups. An excision lesion was made, and the animals were killed 7 or 14 d later. The average body weight was 29 and 25 % higher in the DIO group compared with the C and DR groups. Retroperitoneal fat was higher in the DIO group than in the control and DR groups (518 and 92 %) and was higher in the DR group than in the control group (223 %). The DIO group presented glucose intolerance, and both the DIO and DR groups presented delayed wound contraction (50 %) and re-epithelialisation (20 %). Compared with the DR group, the DIO group displayed higher amounts of inflammatory cells as well as higher levels of lipid peroxidation (P < 0·05). Myofibroblastic differentiation and vessel remodelling were delayed in both the DIO and DR groups. Nitrite levels were lower in the DIO group (340 % less) than in the DR group. TNF-α expression was increased in the DIO group (130 %) compared with the DR group. Our results showed that DIO as well as DR rats present delays in cutaneous wound healing, even though the DR group does not have an overweight phenotype.

Rodents respond to a chronic high-fat diet (HFD) in two ways: some readily become obese (obesity prone, OP) and others do not (obesity resistant, OR). Although several hypotheses have been proposed, the mechanisms underlying the inter-individual susceptibility to diet-induced obesity remain to be fully defined. In the present study, two-dimensional gel electrophoresis (2-DE) combined with matrix-assisted laser desorption ionisation time-of-flight MS was carried out for identification of differentially expressed liver proteins in OP and OR rats fed a HFD, in an attempt to discover marker proteins involved in susceptibility and/or resistance to obesity in rat liver. The 2-DE analysis demonstrated that forty spots from 380 visualised spots were differentially regulated between the groups. Among these forty spots, twelve were differentially expressed proteins between OP and OR rats, reaching statistical significance. Of these, five proteins have already been linked to obesity; however, seven proteins involved in obesity susceptibility or resistance were identified for the first time in the present study. In order to validate the proteomic results and gain insight into the metabolic changes between the OP and OR groups, we further confirmed the expression pattern of some proteins of interest by Western blot analysis. Combined results of proteomic analysis with Western blot analysis revealed that reduced lipogenesis and increased fat oxidation were achieved in the livers of OR rats. In conclusion, the present proteomic study is an important advance over the previous steps required for identification of OP and OR rats, and should prove valuable in the search for the pathogenesis of obesity in humans.