Intra-uterine growth retardation has been linked to the development of type 2 diabetes in later life. Mitochondrial changes have been suggested as a link between fetal malnutrition and adult insulin resistance. Taurine has been implicated in this process. We investigated whether protein malnutrition in early life alters mitochondria of the pancreatic islets in adulthood, and whether taurine supplementation restores these changes. Male offspring of rats fed a control diet, a low-protein diet or a low-protein diet supplemented with taurine during pregnancy and lactation were weaned onto the control diet. In each group, at 20 weeks of age, intravenous glucose tolerance tests, euglycaemic–hyperinsulinaemic clamp studies, morphometric analysis of the pancreatic islets and ultra-structural analysis of the mitochondria of the β-cells were performed. The expressions of cytochrome c oxidase (COX) I and mitochondrial respiratory chain complex II were also measured. Fetal protein-malnourished rats showed decreased pancreatic islet mass and reduced insulin-secretory responses to a glucose load. These rats also showed reduced mitochondrial DNA-encoded COX I gene expression in the islets. Electron microscopic examination showed abnormal mitochondrial shapes in the β-cells of fetal protein-malnourished rats. Taurine supplementation to the low-protein diet restored all these changes. Our findings indicate that a maternal protein-restriction diet causes long-lasting mitochondrial changes that may contribute to the development of type 2 diabetes later in life. The lack of taurine may be a key causative factor for these dysfunctional mitochondrial changes.

Medium-chain fatty acids (MCFA) are widely used in diets for patients with obesity. To develop a delivery system for suppressing dietary fat accumulation into adipose tissue, MCFA were encapsulated in nanoliposomes (NL), which can overcome the drawbacks of MCFA and keep their properties unchanged. In the present study, crude liposomes were first produced by the thin-layer dispersion method, and then dynamic high-pressure microfluidisation (DHPM) and DHPM combined with freeze–thawing methods were used to prepare MCFA NL (NL-1 and NL-2, respectively). NL-1 exhibited smaller average size (77·6 (sd 4·3) nm), higher zeta potential ( − 40·8 (sd 1·7) mV) and entrapment efficiency (73·3 (sd 16·1) %) and better stability, while NL-2 showed narrower distribution (polydispersion index 0·193 (sd 0·016)). The body fat reduction property of NL-1 and NL-2 were evaluated by short-term (2 weeks) and long-term (6 weeks) experiments of mice. In contrast to the MCFA group, the NL groups had overcome the poor palatability of MCFA because the normal diet of mice was maintained. The body fat and total cholesterol (TCH) of NL-1 (1·54 (sd 0·30) g, P = 0·039 and 2·33 (sd 0·44) mmol/l, P = 0·021, respectively) and NL-2 (1·58 (sd 0·69) g, P = 0·041 and 2·29 (sd 0·38) mmol/l, P = 0·015, respectively) significantly decreased when compared with the control group (2·11 (sd 0·82) g and 2·99 (sd 0·48) mmol/l, respectively). The TAG concentration of the NL-1 group (0·55 (sd 0·14) mmol/l) was remarkably lower (P = 0·045) than the control group (0·94 (sd 0·37) mmol/l). No significant difference in weight and fat gain, TCH and TAG was detected between the MCFA NL and MCFA groups. Therefore, MCFA NL could be potential nutritional candidates for obesity to suppress body fat accumulation.

It is well established that plant phenolics elicit various biological activities, with positive effects on health. Palm oil production results in large volumes of aqueous by-products containing phenolics. In the present study, we describe the effects of oil palm phenolics (OPP) on several degenerative conditions using various animal models. OPP reduced blood pressure in a NO-deficient rat model, protected against ischaemia-induced cardiac arrhythmia in rats and reduced plaque formation in rabbits fed an atherogenic diet. In Nile rats, a spontaneous model of the metabolic syndrome and type 2 diabetes, OPP protected against multiple aspects of the syndrome and diabetes progression. In tumour-inoculated mice, OPP protected against cancer progression. Microarray studies on the tumours showed differential transcriptome profiles that suggest anti-tumour molecular mechanisms involved in OPP action. Thus, initial studies suggest that OPP may have potential against several chronic disease outcomes in mammals.

A model was used to investigate two mechanisms describing reductions in food intake (anorexia) observed during gastrointestinal parasitism in lambs, and to explore relationships between anorexia and food composition. The mechanisms were either a reduction in intrinsic growth rate, leading to a consequent reduction in food intake (mechanism 1; M1), or a direct reduction in food intake (mechanism 2; M2). For both mechanisms, lambs growing from 2 to 6 months of age were modelled, with one of three levels of trickle challenge with Teladorsagia circumcincta. Scenarios were simulated for feeds varying in either protein or energy content, or both. Major differences were found between the predictions resulting from M1 and M2 on low-energy foods that constrained the intake of uninfected lambs through bulk. With M1, food intake was governed by the first operating constraint, whereas with M2 an additivity of constraints was observed. On the other foods, the duration of anorexia increased with increasing energy content of feed for M1, whilst the duration of anorexia decreased with increasing protein content of feed for M2.For foods that did not have an impact upon lambs' gastrointestinal tract capacity, published data were consistent with predictions of M2. Due to an absence of experimental data, no conclusions could be drawn for relationships between anorexia and food composition in the presence of other limiting constraints, such as bulk for low-energy foods. In conclusion, available experimental data and model predictions were consistent with anorexia having an impact directly on food intake, and with impacts of anorexia increasing with decreasing protein content.

The incidence of obesity and type 2 diabetes mellitus (T2DM) is increasing, and new experimental models are required to investigate the diverse aspects of these polygenic diseases, which are intimately linked in terms of aetiology. Feline T2DM has been shown to closely resemble human T2DM in terms of its clinical, pathological and physiological features. Our aim was to develop a feline model of diet-induced weight gain, adiposity and metabolic deregulation, and to examine correlates of weight and body fat change, insulin homeostasis, lipid profile, adipokines and clinical chemistry, in order to study associations which may shed light on the mechanism of diet-induced metabolic dysregulation. We used a combination of partially hydrogenated vegetable shortening and high-fructose corn syrup to generate a high-fat–high-fructose diet. The effects of this diet were compared with an isoenergetic standard chow, either in the presence or absence of 1·125 % dietary monosodium glutamate (MSG). Dual-energy X-ray absorptiometry body imaging and a glucose tolerance test were performed. The present results indicate that dietary MSG increased weight gain and adiposity, and reduced insulin sensitivity (P < 0·05), whereas high-fat–high-fructose feeding resulted in elevated cortisol and markers of liver dysfunction (P < 0·01). The combination of all three dietary constituents resulted in lower insulin levels and elevated serum β-hydroxybutyrate and cortisol (P < 0·05). This combination also resulted in a lower first-phase insulin release during glucose tolerance testing (P < 0·001). In conclusion, markers of insulin deregulation and metabolic dysfunction associated with adiposity and T2DM can be induced by dietary factors in a feline model.

Low-molecular-weight fucoidan (LMWF) has been broadly studied in recent years due to its numerous biological properties. Nevertheless, there have been no reports about the effects of LMWF on myogenic differentiation (MyoD). The objective of the present study was to demonstrate the impact of LMWF on myogenesis in C2C12 cells. The ultimate aim was to establish whether LMWF regulates myogenesis similar to heparin as a partial regulator of myogenesis. LMWF was prepared at a minimal size by ultra-filtration compared with crude fucoidan. We treated C2C12 cells with LMWF and/or heparin during MyoD. The data from the present study are the first to suggest that LMWF suppresses the expression of the myogenic regulatory factors and the myocyte enhancer factors as well as the morphological changes that occur during differentiation. Additionally, the expression of the mitogen-activated protein kinase (MAPK) family was significantly inhibited by LMWF when compared with controls. The LMWF-treated group showed significantly decreased expression of reactive oxygen species (ROS) enzymes compared with control cells. Heparin was used as a positive control because it has been reported to activate MyoD. Taken together, these results suggest that LMWF might regulate MyoD through the MAPK pathway and by regulating ROS activity in C2C12 cells.

The objective of the present study was to investigate whether early undernutrition changes the chronic inflammatory response, so as to study its influence on pharmacological response to indomethacin. Rat offspring of dams fed from the first day of gestation to term or throughout the lactation period received a balanced diet (NN) or a basic regional diet (BRD) from northeast Brazil. According to their dams, the offspring were divided into three groups: NN; basic regional diet during gestation (BRD-g, undernourished during gestation); basic regional diet during gestation and lactation (BRD-gl, undernourished during gestation and lactation). At 2 months of age, Freund's adjuvant (0·2 ml) was inoculated into the plantar surface of the hind paw (day 0) of animals. All animals orally received saline (0·9 %) for 28 d. Another group of adult offspring was subjected to the same procedure as described above, but orally received indomethacin (2 mg/kg) instead of saline, and divided into three subgroups: NN treated with indomethacin (NNI); BRD-g treated with indomethacin (BRDI-g); BRD-gl treated with indomethacin (BRDI-gl). The hind paw volume was calculated on days 0 (initial paw volume), 7, 14 and 28. Hind paw swelling, blood albumin and C-reactive protein (CRP) levels and leucocyte counts were evaluated as markers of inflammation. Reduced hind paw swelling and the blood levels of serum albumin and CRP were found in the BRD-g and BRD-gl offspring. However, no difference was found in the leucocyte count. Compared with their respective saline-treated groups (NN, BRD-g and BRD-gl), the anti-inflammatory effect of indomethacin was lower in the BRDI-g and BRDI-gl groups than in the NNI group. We conclude that early undernutrition attenuated the chronic inflammatory response and the anti-inflammatory effect of indomethacin.

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 present study investigated whether the hypocholesterolaemic effect of water-insoluble fish protein (IFP) from Alaska pollock in ovariectomised (OVX) rats was affected by methionine (Met) addition. OVX rats (6 months old) were fed a cholesterol-free diet containing casein, IFP or IFP+Met as a protein source for 28 d. The ratio of Met:glycine was lower in the IFP and IFP+Met diets compared with the casein diet. Body-weight gain, food intake and liver lipids were not affected by the diet. Plasma total cholesterol concentration was lower in OVX rats fed the IFP diet compared with those fed the casein diet. The hypocholesterolaemic effect of the IFP diet was not abolished by Met addition. Amount of bile acids in the small-intestinal content and faecal excretion of bile acids were higher in OVX rats fed the IFP and IFP+Met diets compared with those fed the casein diet. Ileal bile acid transporter (IBAT) mRNA level and faecal excretion of bile acids were significantly lower and higher, respectively, in OVX rats fed the IFP diet compared with those fed the casein diet, but not in those fed the IFP+Met diet. Thus, the hypocholesterolaemic effect of the IFP diet seems to be mediated by increased faecal excretion of bile acids coupled with decreased reabsorption of bile acids from the ileum through a decrease in IBAT and the change in cholesterol metabolism linked to the amino acid profile.

The present study investigated the effects of dietary supplementation of a seaweed extract (SWE) to sows and weaned pigs on post-weaning growth performance, intestinal morphology, intestinal microflora, volatile fatty acid concentrations and immune status of pigs at days 11 and 117 post-weaning. Gestating sows (n 20) were supplemented with a SWE (0 v. 10·0 g/d) from day 107 of gestation until weaning (day 26). At weaning, pigs (four pigs per sow) were divided into two groups based on sow diet during lactation and supplemented with a SWE (0 v. 2·8 g/kg diet), resulting in four treatment groups: (1) BB (basal sows–basal pigs); (2) BS (basal sows–treated pigs); (3) SB (treated sows–basal pigs); (4) SS (treated sows–treated pigs). Pigs weaned from SWE-supplemented sows had a higher average daily gain (ADG) between days 0 and 21 (P < 0·05) post-weaning compared with pigs weaned from non-SWE-supplemented sows. Pigs offered post-weaning diets (PW) containing SWE had decreased colonic Escherichia coli populations on day 11 (P < 0·01) and decreased colonic Enterobacteriaceae numbers on day 117 (P < 0·05). Pigs offered PW containing SWE had a greater mRNA abundance of MUC2 in the colon at day 11 post-weaning (P < 0·05) compared with pigs offered unsupplemented diets. In conclusion, these results demonstrate that SWE supplementation post-weaning provides a dietary means to improve gut health and to enhance growth performance in starter pigs. Dietary SWE supplementation increased ADG during the grower–finisher (GF) phases. However, there was no growth response to SWE inclusion in GF diets when pigs were weaned from SWE-supplemented sows.

The effects of wet (canned) or dry (kibbled) diets on faecal bacterial populations in the cat were investigated in eight domestic short-haired cats (four males and four females; averaging 6 years of age and 3·4 kg) in a nested design. The cats were fed ad libitum a commercially available wet diet (moisture 82·0 %, crude protein 51·7 %, fat 28·9 %, carbohydrate (CHO) 8·9 % and ash 10·6 % DM) for 5 weeks. On the fifth week, individual feed intakes and faecal outputs were determined. Fresh faecal samples were collected twice daily, mixed for homogeneity, subsampled and stored at − 85°C until analysis. The cats were then switched to a commercially available dry diet (moisture 8·5 %, crude protein 33·0 %, fat 11·0 %, CHO 49·4 % and ash 6·6 % DM) for 5 weeks, and fresh faeces were sampled as described previously. Energy intake tended to be higher in cats fed dry diets (P < 0·10), but body weight was similar between the two feeding periods (P>0·05). Denaturing gradient gel electrophoresis (DGGE) of bacterial 16S rRNA genes amplified from DNA extracted from faeces was performed. The unweighted pair group method with arithmetic mean cluster analysis of bacterial community profiles using Pearson's correlation revealed diet-specific clustering when the same cats were fed on either a dry or a wet diet (dissimilarity between the groups, 88·6 %; P < 0·001). Subsequent cloning and sequencing of five selected distinct DGGE bands indicated that members of the Pelomonas and Fusobacteriaceae were influenced by a short-term change in diet format. This suggests that 5-week dietary exposure is sufficient to alter gastrointestinal microflora.

Diabetic nephropathy is a serious complication for diabetic patients, yet the precise mechanism that underlies the development of diabetic complications remains unknown. We hypothesised that dietary antioxidant supplementation with single N-acetylcysteine (NAC) or vitamin C combined with either vitamin E or vitamin E and NAC improves diabetic renal inflammation through the modulation of blood glucose levels, oxidative stress and inflammatory response. Experimental animals were treated with alloxan monohydrate to induce diabetes. Mice were divided into five groups and supplemented with single or a combination of antioxidants. Body weights and blood glucose levels were measured once a week. After 8 weeks of dietary antioxidant supplementation, mice were killed and blood urea N (BUN) and plasma creatinine levels were measured to evaluate renal function. NF-κB protein was indirectly demonstrated by the phosphorylated IκBα (pIκBα) level, and the expressions of oxidative stress- and inflammatory response-related proteins were also determined. We demonstrated that dietary antioxidant supplementation decreased lipid peroxidation levels demonstrated by thiobarbituric acid-reacting substances, BUN and plasma creatinine levels in diabetic kidneys. Moreover, dietary antioxidant cocktail supplementation improved blood glucose levels and selectively regulated the expressions of Cu-Zn superoxide dismutase, haeme oxygenase-1, pIκBα, inducible NO synthase, cyclo-oxygenase-2 and C-reactive protein in diabetic kidneys effectively. These findings demonstrated that diabetic renal failure was associated with inflammatory responses induced by hyperglycaemia. In addition, results in the study suggest that antioxidant cocktail supplementation may have beneficial effects on diabetic nephropathy through selective reduction of blood glucose levels and inflammatory response.

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.

Wholegrain cereals are reported to promote beneficial health effects. Wholegrain wheat and rye are almost exclusive sources of alkylresorcinols, and intact alkylresorcinols together with their plasma and urinary metabolites, 3-(3,5-dihydroxyphenyl)-1-propanoic acid (DHPPA) and 3,5-dihydroxybenzoic acid (DHBA), have been proposed as biomarkers of the intake of these foods in humans. The pharmacokinetics of alkylresorcinols and their metabolites in plasma have been determined but not that of the urinary metabolites. We aimed to characterise the urinary pharmacokinetics of alkylresorcinol metabolites in humans to evaluate their potential as biomarkers of wholegrain wheat and rye. A group of fifteen volunteers followed a low-alkylresorcinol diet for 2 d before ingesting a single dose of rye bread, containing 100 mg alkylresorcinols. Urine was collected between baseline (0 h) and 25 h after administration. Thereafter alkylresorcinol metabolites were quantified by HPLC with coulometric electrode array detection. Maximum excretion rates were observed at 5–6 h for both metabolites, DHPPA being predominant over DHBA and also possessing a greater area under the curve0–25 h. Total urinary recovery between 0 and 25 h yielded 43 % of ingested alkylresorcinols, and at 25 h significant amounts of metabolites were still retained in the body, suggesting that even a spot urine sample may be sufficient to indicate whether or not wholegrain wheat or rye is a daily dietary component. These results support the use of urinary DHPPA and DHBA as biomarkers of wholegrain wheat and rye and enable new potential for studying the association between wholegrain intake and diseases, even in the absence of dietary data.

The present study determined whether α-ketoglutarate (AKG) might affect the expression of AMP-activated protein kinase (AMPK) and energy status in the intestinal mucosa of piglets challenged with Escherichia coli lipopolysaccharide (LPS). A total of eighteen piglets (weaned at 21 d of age) were allocated to one of three treatments: (1) non-challenged (control); (2) LPS-challenged (LPS); (3) LPS+1 % AKG (LPS+AKG). Piglets in the control and LPS groups were fed a maize- and soyabean meal-based diet, and the LPS+AKG group was fed the basal diet supplemented with 1 % AKG. On days 10, 12, 14 and 16 of the trial, piglets in the LPS and LPS+AKG groups were challenged with LPS (80 μg/kg body weight), whereas piglets in the control group received the same volume of sterile saline. Pigs were euthanised 24 h after the last administration of LPS or saline to obtain intestinal mucosae for biochemical analysis. Compared with the control group, LPS administration decreased (P < 0·05) the oxidation of AKG, oleic acid, glutamine and glucose in enterocytes, decreased concentrations of ATP in the duodenal and jejunal mucosae and decreased adenylate energy charge (AMP:ATP ratio) in the jejunal and ileal mucosae. Additionally, LPS treatment reduced (P < 0·05) mucosal concentrations of phosphorylated AMPK in the jejunum and ileum as well as acetyl-CoA carboxylase in all segments of the small intestine. The adverse effects of LPS were reversed by AKG. Collectively, these results indicate that dietary supplementation with 1 % AKG beneficially modulates the AMPK signalling pathway to improve energy status in the small intestine of LPS-challenged piglets.

The aim of the present study was to evaluate the vitamin and mineral content of bone and raw food rations fed to adult dogs in Germany. Pet owners completed a standardised feeding questionnaire. The composition of 95 rations was calculated from mean data for foodstuffs using nutrition balancing software. Typical ration ingredients were meats, fish, offal, dairy products, eggs, oil, nuts, cod liver oil and natural and commercial supplements. The supply of nutrients was compared with the recommended allowance (RA). Of the rations that were used, 10 % supplied < 25 % of the RA of Ca. In these rations, Ca:P was below 0·6:1, and vitamin D was below RA. About half of the rations supplied less iodine than the minimum requirement. Many of the rations had low Zn and Cu supply, and 25 % of the rations supplied only 70 % of RA for vitamin A or less. A total of 60 % of the rations had one or more of the above-mentioned imbalance. The remaining 40 % of rations either had minor problems like Ca excess from bones or they were balanced.

The present study analysed the effects of the flavanol ( − )-epicatechin in rats after chronic inhibition of NO synthesis with NG-nitro-l-arginine methyl ester (l-NAME), at doses equivalent to those achieved in the studies involving human subjects. Wistar rats were randomly divided into four groups: (1) control-vehicle, (2) l-NAME, (3) l-NAME-epicatechin 2 (l-NAME-Epi 2) and (4) l-NAME-epicatechin 10 (l-NAME-Epi 10). Rats were daily given by oral administration for 4 weeks: vehicle, ( − )-epicatechin 2 or 10 mg/kg. Animals in the l-NAME groups daily received l-NAME 75 mg/100 ml in drinking-water. The evolution in systolic blood pressure and heart rate, and morphological and plasma variables, proteinuria, vascular superoxide, reactivity and protein expression at the end of the experiment were analysed. Chronic ( − )-epicatechin treatment did not modify the development of hypertension and only weakly affected the endothelial dysfunction induced by l-NAME but prevented the cardiac hypertrophy, the renal parenchyma and vascular lesions and proteinuria, and blunted the prostanoid-mediated enhanced endothelium-dependent vasoconstrictor responses and the cyclo-oxygenase-2 and endothelial NO synthase (eNOS) up-regulation. Furthermore, ( − )-epicatechin also increased Akt and eNOS phosphorylation and prevented the l-NAME-induced increase in systemic (plasma malonyldialdehyde and urinary 8-iso-PGF2α) and vascular (dihydroethidium staining, NADPH oxidase activity and p22phox up-regulation) oxidative stress, proinflammatory status (intercellular adhesion molecule-1, IL-1β and TNFα up-regulation) and extracellular-signal-regulated kinase 1/2 phosphorylation. The present study shows for the first time that chronic oral administration of ( − )-epicatechin does not improve hypertension but reduced pro-atherogenic pathways such as oxidative stress and proinflammatory status of the vascular wall induced by blockade of NO production.

Multiple pathways including oxidative stress and mitochondrial damage are implicated in neurodegeneration during Parkinson's disease (PD). The current PD drugs provide only symptomatic relief and have limitations in terms of adverse effects and inability to prevent neurodegeneration. Therefore, there is a demand for novel compound(s)/products that could target multiple pathways and protect the dying midbrain dopaminergic neurons, with potential utility as adjunctive therapy along with conventional drugs. Turmeric is a spice used in traditional Indian cuisine and medicine with antioxidant, anti-inflammatory and potential neuroprotective properties. To explore the neuroprotective property of turmeric in PD, mice were subjected to dietary supplementation with aqueous suspensions of turmeric for 3 months, mimicking its chronic consumption and challenged in vivo with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Brain samples from untreated and treated groups were characterised based on mitochondrial complex I (CI) activity, protein nitration and tyrosine hydroxylase immunoreactivity. Chronic turmeric supplementation induced the enzyme activity of γ-glutamyl cysteine ligase, which in turn increased glutathione levels and protected against peroxynitrite-mediated inhibition of brain CI. These mice were also protected against MPTP-mediated protein nitration, CI inhibition and degeneration of substantia nigra neurons in the brain. We conclude that chronic dietary consumption of turmeric protects the brain against neurotoxic insults, with potential application in neurodegeneration. Further characterisation of the active constituents of turmeric that potentially promote neuroprotection could improve the utility of dietary turmeric in brain function and disease.

Uterine infections during pregnancy predispose to pre-term birth and postnatal morbidity, but it is unknown how prenatal bacterial exposure affects maturation of the immature gut. We hypothesised that a prenatal exposure to gram-negative lipopolysaccharide (LPS) has immunomodulatory effects that improve resistance towards necrotising enterocolitis (NEC) in pre-term neonates. At approximately 85 % gestation, pig fetuses were injected intramuscularly with saline or LPS (0·014 mg/kg), or intra-amniotically with LPS (0·4 mg/kg). Pigs were delivered by caesarean section 3–5 d later and fed colostrum (C) or formula (F) for 48 h. Gut indices did not differ between pigs injected intramuscularly with saline or LPS, and these groups were therefore pooled into two control groups according to diet (control-F, n 32 and control-C, n 11). Control-F pigs showed reduced villus heights, mucosal structure, gut integrity, digestive enzymes, elevated NEC incidence (38 v. 0 %, P < 0·05) and several differentially expressed immune-related genes, relative to control-C pigs. Compared with the control-F and control-C groups, values in formula-fed pigs given intra-amniotic LPS formula (n 17) were intermediate for villus height, enzyme activities, intestinal permeability and NEC incidence (18 %, P = 0·2 relative to control-F), and numbers of differentially expressed immune genes. In conclusion, prenatal exposure of the fetal gut to Gram-negative bacteria may modulate the immediate postnatal response to an enteral diet and colonising bacteria.

The objective of the present study was to investigate age-related differences in erythrocyte membrane fluidity (EMF) and changes in antioxidant capacity following supplementation. A total of seventy-four children were randomly divided into two groups: group A1 was the placebo-controlled group and group A2 was supplemented daily with 600 μg retinol, 1·0 mg β-carotene, 100 mg tocopherol, 300 mg ascorbic acid and 200 μg Se. A total of ninety young people were randomly divided into B1 and B2 groups, and ninety-one elderly subjects were divided into C1 and C2 groups. Groups B1 and C1 were placebo-controlled groups, and groups B2 and C2 were daily supplemented with 900 μg retinol, 1·5 mg β-carotene, 200 mg tocopherol, 500 mg ascorbic acid and 400 μg Se. Results showed that plasma malondialdehyde (MDA) was 5·35 μmol/l in children, which was lower than in young and elderly people. The MDA levels of the young and elderly individuals in the treated groups were significantly lower compared with the control groups, but the supplementation did not alter MDA levels in children. At baseline, there was a lower value of polarisation (ρ) and microviscosity (η) in children, indicating a higher EMF, than in both the young and elderly subjects. After the 2-month trial, the ρ and η values of young and elderly subjects in the treated groups decreased significantly in comparison with the placebo groups, indicating an increase in EMF. In conclusion, there was a background of higher MDA levels and lower EMF in young and elderly people than in children, which could be improved by antioxidant supplementation.