Since its introduction in 1981, the glycaemic index (GI) has been a useful tool for classifying the glycaemic effects of carbohydrate foods. Consumption of a low-GI diet has been associated with a reduced risk of developing CVD, diabetes mellitus and certain cancers. WISP (Tinuviel Software, Llanfechell, Anglesey, UK) is a nutrition software package used for the analysis of food intake records and 24 h recalls. Within its database, WISP contains the GI values of foods based on the International Tables 2002. The aim of the present study is to describe in detail a methodology for adding and amending GI values to the WISP database in a clinical or research setting, using data from the updated International Tables 2008.

The present experiment was conducted to determine proteome changes in Longissimus muscle of finishing pigs fed conjugated linoleic acid (CLA), in association with alteration of intramuscular fat content. Previously, seventy-two Duroc × Landrace × Large White gilts (approximately 60 kg) had been fed maize–soyabean meal-based diets with 0, 12·5 and 25 g CLA/kg diet. The CLA contained 369·1 mg/g cis-9, trans-11 CLA, 374·6 mg/g trans-10, cis-12 CLA and 53·7 mg/g other isomers. Six pigs per treatment were slaughtered when they reached a body weight of approximately 100 kg. Data published from a previous experiment demonstrated that supplementation with 12·5 or 25 g CLA/kg diet increased intramuscular fat content (P < 0·05). The present study investigated the proteome changes in Longissimus muscle of control and pigs supplemented with 25 g CLA/kg diet. CLA significantly influenced the abundance of proteins related to energy metabolism, fatty acid oxidation and synthesis, amino acid metabolism, defence, transport and other miscellaneous processes (P < 0·05). The increase in intramuscular fat content was positively correlated with the increased abundance of carbonic anhydrase 3 and aspartate aminotransferase (P < 0·05). We suggest that the proteome changes in Longissimus muscle contributed to greater intramuscular lipid content in CLA-supplemented pigs.

Previous animal and human studies have shown protective effects of Ca on the resistance to enteropathogenic infections. Most interventions were performed with calcium phosphate and little is known about the protective effect of other dietary sources of Ca. Therefore, we investigated the efficacy of several Ca salts to enhance intestinal resistance to Salmonella enteritidis infection. Rats (n 7–8 per group) were fed a high-fat, Western human-style, purified diet with a low Ca content (20 mmol calcium phosphate/kg; negative control group) or the same diet supplemented with either (extra) calcium phosphate, milk Ca, calcium chloride or calcium carbonate (total of 100 mmol Ca supplement/kg). Diets contained Cr-EDTA for assessment of incremental changes in intestinal permeability. After an adaptation period of 2 weeks, animals were orally infected with S. enteritidis to mimic a human-relevant foodborne infection. Ca supplement-induced changes on faecal lactobacilli and enterobacteria were studied before infection. Changes in intestinal permeability were determined by measuring urinary Cr with time. Persistence of Salmonella was determined by studying faecal excretion of this pathogen in time. Overall, all Ca salts increased resistance towards Salmonella. After infection, body weight gain and food intake were higher in the calcium phosphate group. Calcium phosphate and milk Ca decreased faecal enterobacteria before infection. All Ca salts decreased infection-induced intestinal permeability and persistence of Salmonella. Calcium phosphate, milk Ca, calcium carbonate and calcium chloride are able to enhance the intestinal resistance to Salmonella in rats.

Under commercial conditions, weaning of piglets is associated with social, environmental and dietary stress. Consequently, small-intestinal barrier and absorptive functions deteriorate within a short time after weaning. Most studies that have assessed small-intestinal permeability in pigs after weaning used either Ussing chambers or orally administered marker probes. Paracellular barrier function and active absorption decrease when pigs are weaned at 3 weeks of age or earlier. However, when weaned at 4 weeks of age or later, the barrier function is less affected, and active absorption is not affected or is increased. Weaning stress is a critical factor in relation to the compromised paracellular barrier function after weaning. Adequate feed intake levels after weaning prevent the loss of the intestinal barrier function. Transcellular transport of macromolecules and passive transcellular absorption decrease after weaning. This may reflect a natural intestinal maturation process that is enhanced by the weaning process and prevents the pig from an antigen overload. It seems that passive and active absorption after weaning adapt accurately to the new environment when pigs are weaned after 3 weeks of age. However, when weaned at 3 weeks of age or earlier, the decrease in active absorption indicates that pigs are unable to sufficiently adapt to the new environment. To improve weaning strategies, future studies should distinguish whether the effect of feed intake on barrier function can be directed to a lack of a specific nutrient, i.e. energy or protein.

Risk of developing the metabolic syndrome may be influenced by nutritional environment early in life. We examined the effects of high-fibre (HF) and high-protein (HP) diets consumed during pregnancy and lactation on satiety hormones and expression of genes involved in glucose and lipid metabolism in offspring. Wistar dams were fed a control (C), HF or HP diets during pregnancy and lactation. At parturition, litters were culled to ten pups. At 21 d, all pups were weaned onto C diet. At 7, 14, 21, 28 and 35 d after birth, blood was analysed for satiety hormones and tissues for mRNA expression in offspring. No differences were observed in litter size or birth weight. At 21 d, offspring of HF dams had greater adjusted intestinal mass and lower liver weight than those of C but not of HP dams. Plasma glucose at 28 d and amylin at 7, 14 and 28 d were lower in HF v. C and HP offspring. Glucagon-like peptide-1 was higher in HP offspring than in HF offspring at 7 d but was higher in HF v. C offspring at 21 d. Offspring of HF dams had higher glucose transporter (GLUT2 and Na+-dependent glucose/galactose transporter) mRNA expression at 21 d v. C and HP offspring. In brown adipose tissue, HF and HP up-regulated uncoupling protein-1 and PPAR-γ coactivator. HP was associated with increased resistin and IL-6 mRNA expression. The present study demonstrates that maternal diet composition differentially regulates circulating satiety hormones and genes involved in glucose transport and energy metabolism in offspring. These early changes could have long-term consequences for obesity risk.

Chronic subcutaneous (s.c.) administration of d-galactose (DG) to BL/6J mice has been shown to induce oxidative stress and is considered a model to mimic accelerated ageing. Fructo-oligosaccharide (FO) is a well-defined prebiotic and its fermentation by lactic acid bacteria has been shown to exert antioxidative capacity. The present study was aimed to determine whether FO attenuated DG-induced oxidative stress and hepatopathy in Balb/cJ mice. Mice (12 weeks of age, n 40) were divided into control (s.c. saline), DG (s.c. 1·2 g/kg body weight), DG+FO (5 %, w/w) and DG+vitamin E (0·2 %, w/w) groups and were killed after 52 d of treatment. Results indicated that DG significantly decreased the hepatic superoxide dismutase and glutathione peroxidase activities. These alterations were ameliorated both by FO and vitamin E. DG increased the hepatic TAG content approximately by 7·2 % compared with the vehicle control, which was in agreement with the histological alteration. FO, similar to vitamin E, almost normalised the hepatic TAG content and ameliorated the histological characteristics of fatty liver. Similarly, the increased plasma alanine aminotransferase activity induced by DG was normalised by FO and vitamin E, respectively. Faecal bifidobacteria counts were greater in the DG+FO and DG+vitamin E groups compared with the DG group, respectively. In conclusion, the present study indicated that FO diminished the altered hepatic antioxidative enzyme activities and morphology caused by chronic DG administration in Balb/cJ mice, partially associated with its prebiotic role in the colon.

Phospholipid hydroperoxides (PLOOH) accumulate abnormally in the erythrocytes of dementia patients, and dietary xanthophylls (polar carotenoids such as astaxanthin) are hypothesised to prevent the accumulation. In the present study, we conducted a randomised, double-blind, placebo-controlled human trial to assess the efficacy of 12-week astaxanthin supplementation (6 or 12 mg/d) on both astaxanthin and PLOOH levels in the erythrocytes of thirty middle-aged and senior subjects. After 12 weeks of treatment, erythrocyte astaxanthin concentrations were higher in both the 6 and 12 mg astaxanthin groups than in the placebo group. In contrast, erythrocyte PLOOH concentrations were lower in the astaxanthin groups than in the placebo group. In the plasma, somewhat lower PLOOH levels were found after astaxanthin treatment. These results suggest that astaxanthin supplementation results in improved erythrocyte antioxidant status and decreased PLOOH levels, which may contribute to the prevention of dementia.

Paraoxonase 1 (PON1) is an enzyme that is mainly synthesised in the liver and protects LDL from oxidation, thereby exhibiting antiatherogenic properties. Using a luciferase reporter gene assay, we tested curcumin for its ability to induce PON1 in Huh7 hepatocytes in culture. Curcumin ( ≥ 10 μmol/l) dose-dependently induced PON1 transactivation in Huh7 cells. However, dietary supplementation of female B6C3F1 mice with curcumin (500 mg/kg diet) for 2 weeks did not increase the hepatic PON1 mRNA and protein levels. No curcumin was detectable in the plasma of the 12 h fasted mice. In conclusion, curcumin may be a potent PON1 inducer in cultured cells in vitro, but not in the liver of curcumin-fed mice because of its low concentrations in vivo.

Sideritis caesarea (SC) Duman, Aytac&Baser is a member of the Lamiaceae family. The present study was designed to investigate the antioxidant properties of the aerial parts of island green tea SC against TCA effects in rats. Biomarkers selected for monitoring antioxidant capacity were the activities of glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase, catalase (CAT), GSH level and malondialdehyde (MDA) content in various organs of rats. Three experimental groups, A (untreated = control), B (only TCA-treated) and C (TCA+SC-treated), were studied. At the end of the 50 d experiment, the MDA content in tissues increased significantly in group B, whereas no significant changes were observed in group C as compared with that of the control group. Antioxidant enzyme activities such as SOD and CAT increased significantly in the brain, liver and kidneys of group B but decreased significantly in group C as compared with group B. The GSH level and GR activity increased significantly in the brain and liver of group C as compared with the control and TCA-exposed rats. Hence, the study reveals that the constituents present in SC impart protection against chemical-induced oxidative injury that may result in the development of cancer.

Dietary flaxseed (FS) inhibited the growth of human breast tumours and enhanced the effectiveness of tamoxifen (TAM) in athymic mice with low oestradiol (E2) levels. The present study determined whether the n-3 fatty acid-rich cotyledon fraction of FS (FC), alone or in combination with TAM, has a similar effect and thus can substitute for FS. In a 2 × 2 factorial design, ovariectomised mice with established oestrogen receptor (ER)-positive breast tumours (MCF-7) were treated as follows: groups 1 and 2 were fed the basal diet (BD, control) and FC diet (82 g FC/kg), respectively. Groups 3 and 4 with TAM implants (5 mg) were fed the BD and FC diet, respectively. At 8 weeks post-treatment, mice were euthanised, and tumours were analysed by immunohistochemistry and real-time PCR. BD, FC and FC/TAM groups significantly decreased tumour area, but the TAM group did not. Tumour regression in the FC/TAM group was greater compared to the TAM group. FC lowered cell proliferation but had no effect on apoptosis; the opposite was observed with TAM. FC suppressed mRNA expressions of pS2 and insulin-like growth factor 1 receptor (IGF-1R) and protein expressions of ERα, phosphospecific ERα, human epidermal growth factor receptor 2 (HER2), phosphospecific HER2 (pHER2) and amplified in breast 1 (AIB1), while TAM up-regulated mRNA expressions of Bcl2, progesterone receptor and IGF-1R and protein expression of pHER2, and down-regulated ERβ mRNA. FC modulated the effect of TAM on tumour growth biomarkers. In conclusion, FC reduced the growth of ER+human breast tumours at low circulating E2, alone and combined with TAM, in part through modulation of ER −  and growth factor-mediated signalling pathways; it may substitute for FS in increasing the effectiveness of TAM.

Experimental studies suggest that B vitamins such as niacin, folate, riboflavin, vitamin B6 and vitamin B12 may protect against DNA damage induced by ionising radiation (IR). However, to date, data from IR-exposed human populations are not available. We examined the intakes of these B vitamins and their food sources in relation to the frequency of chromosome translocations as a biomarker of cumulative DNA damage, in eighty-two male airline pilots. Dietary intakes were estimated by using a self-administered semi-quantitative FFQ. Translocations in peripheral blood lymphocytes were scored by using fluorescence in situ hybridisation whole-chromosome painting. Negative binomial regression was used to estimate rate ratios and 95 % CI, adjusted for age and occupational and lifestyle factors. We observed a significant inverse association between translocation frequency and dietary intake of niacin (P = 0·02): adjusted rate ratio for subjects in the highest tertile compared with the lowest tertile was 0·58 (95 % CI 0·40, 0·83). Translocation frequency was not associated with total niacin intake from food and supplements as well as dietary or total intake of folate, riboflavin or vitamin B6 or B12. However, the adjusted rate ratios were significant for subjects with ≥ median compared with < median intake of whole grains (P = 0·03) and red and processed meat (P = 0·01): 0·69 (95 % CI 0·50, 0·96) and 1·56 (95 % CI 1·13, 2·16), respectively. Our data suggest that a high intake of niacin from food or a diet high in whole grains but low in red and processed meat may protect against cumulative DNA damage in IR-exposed persons.

There is increasing interest in the potential chronic beneficial effects of dietary n-3 PUFA on the metabolic syndrome (MetS) and associated cardiovascular complications. We have recently established that increased dietary n-3 PUFA has a profound acute benefit on fasting lipids and the postprandial pro-inflammatory response in the JCR:LA-cp rat, a model of the MetS. However, it is unclear to what extent chronic dietary n-3 PUFA intervention can modulate the progression of end-stage metabolic and vascular complications. The present study aimed to determine the chronic effects of dietary n-3 PUFA supplementation on fasting and non-fasting dyslipidaemia, insulin resistance and vascular complications in the JCR:LA-cp rodent model. JCR:LA-cp rats were fed an isoenergetic lipid-balanced diet supplemented with 5 % n-3 PUFA (w/w) of the total fat (fish oil-derived EPA/DHA) for 16 weeks. Fasting and non-fasting (postprandial) plasma lipid profile was assessed. Hepatic and adipose tissue was probed for the expression of lipogenic proteins (acyl-CoA carboxylase (ACC), fatty acid synthase (FAS) and sterol regulatory element-binding protein-1 (SREBP-1)), while the activity of Jun N-terminal kinase (JNK) was assessed via Western blot to target phosphorylated JNK protein in primary enterocytes. The frequency of myocardial lesions was assessed by haematoxylin and eosin staining. Increased dietary n-3 PUFA improved both the fasting and postprandial lipid profiles (TAG, cholesterol and apoB48) in the JCR:LA-cp rat, potentially via the down-regulation of the hepatic or adipose tissue expression of lipogenic enzymes (ACC, FAS and SREBP-1). Rats fed the 5 % n-3 PUFA diet had lower (58·2 %; P < 0·01) enterocytic phosphorylated JNK protein and secreted less cholesterol (30 %; P < 0·05) into mesenteric lymph compared with the control. The chronic metabolic benefits of dietary n-3 PUFA may underlie the potential to reduce vascular complications during the MetS, including the observed reduction in the frequency (approximately 80 %) of late-stage 3 myocardial lesions.

Green tea is rich in polyphenolic antioxidants and has widely reported but largely unsubstantiated health benefits. In the present study, genoprotective effects of two types of green tea were studied both in an in vitro and in a human supplementation trial. For the in vitro study, human lymphocytes were pre-incubated in tea (0·005–0·1 %, w/v), washed and subjected to oxidant challenge induced by H2O2. In a placebo-controlled, cross-over supplementation study, eighteen healthy volunteers took 2 × 150 ml/d of 1 % (w/v) green tea (‘Longjing’ green tea or ‘screw-shaped’ green tea) or water (control) for 4 weeks (n 6). Subjects took all the three treatments in a random order, with 6 weeks' washout between each treatment. Fasting blood and urine were collected before and after each treatment. The comet assay was used to measure the resistance of lymphocytic DNA to H2O2-induced challenge. Basal oxidation-induced DNA damage was measured using the formamidopyrimidine glycosylase (Fpg) enzyme-assisted comet assay. Urine 7,8-dihydro-2-deoxyguanosine (8-oxodG, mol/mmol creatinine), a biomarker of whole-body oxidative stress, was measured by liquid chromatography with tandem MS. In vitro testing results of tea-treated cells showed increased (P < 0·05) resistance of DNA to the challenge. In the supplementation trial, a significant (P < 0·05) increase in resistance was also observed. Furthermore, the FPg comet data showed >20 % decrease in DNA damage with tea supplementation: mean and standard deviation changes in %DNA in comet tail in the Fpg-assisted comet assay were: − 5·96 (sd 3·83) % after Longjing tea; − 6·22 (sd 3·34) % after screw-shaped tea; +0·91 (sd 5·79) % after water (P < 0·05). No significant changes in urine 8-oxodG were seen. The results indicate that green tea has significant genoprotective effects and provide evidence for green tea as a ‘functional food’.

Hepatitis B virus (HBV)- and hepatitis C virus (HCV)-related chronic infections represent a major health problem worldwide. Although the efficacy of HBV and HCV treatment has improved, several important problems remain. Current recommended antiviral treatments are associated with considerable expense, adverse effects and poor efficacy in some patients. Thus, several alternative approaches have been attempted. To review the clinical experiences investigating the use of lipid- and water-soluble vitamins in the treatment of HBV- and HCV-related chronic infections, PubMed, the Cochrane Library, MEDLINE and EMBASE were searched for clinical studies on the use of vitamins in the treatment of HBV- and HCV-related hepatitis, alone or in combination with other antiviral options. Different randomised clinical trials and small case series have evaluated the potential virological and/or biochemical effects of several vitamins. The heterogeneous study designs and populations, the small number of patients enrolled, the weakness of endpoints and the different treatment schedules and follow-up periods make the results largely inconclusive. Only well-designed randomised controlled trials with well-selected endpoints will ascertain whether vitamins have any role in chronic viral hepatitis. Until such time, the use of vitamins cannot be recommended as a therapy for patients with chronic hepatitis B or C.

The present study reviews the possible role of Se status during pregnancy regarding adverse pregnancy outcomes, with emphasis on those related to diminished antioxidant activity and increased oxidative stress. Studies have reported that Se could play an important role in adverse outcomes such as miscarriages, neural tube defects, diaphragmatic hernia, premature birth, low birth weight, pre-eclampsia, glucose intolerance and gestational diabetes. Also, low Se status has been associated with adverse outcomes among HIV-infected pregnant women and their offspring. Nevertheless, the function of Se in the aetiology of pregnancy complications is yet to be elucidated. Available evidence presents the following limitations: most study designs do not allow conclusions about causal relationships; study populations, selection of subjects, research setting, procedures for defining sample size and analytical methods are often poorly described; many studies fail to adjust for important confounding variables. In addition, population studies assessing the relationship between Se intake during pregnancy and health outcomes are scarce. Further research is still needed to clarify the role of Se status in adverse pregnancy outcomes, especially those related to augmented oxidative stress.