The slow digestible disaccharide isomaltulose (iso; Palatinose™) is available as novel functional carbohydrate ingredient for manufacturing of low glycaemic foods and beverages. Although basically characterised, various information on physiological effects of iso are still lacking. Thus, the objective of the present study was to expand scientific knowledge of physiological characteristics of iso by a set of three human intervention trials. Using an ileostomy model, iso was found to be essentially absorbed, irrespective of the nature of food (beverage and solid food). Apparent digestibility of 50 g iso from two different meals was 95·5 and 98·8 %; apparent absorption was 93·6 and 96·1 %, respectively. In healthy volunteers, a single dose intake of iso resulted in lower postprandial blood glucose and insulin responses than did sucrose (suc), while showing prolonged blood glucose delivery over 3 h test. In a 4-week trial with hyperlipidaemic individuals, regular consumption of 50 g/d iso within a Western-type diet was well tolerated and did not affect blood lipids. Fasting blood glucose and insulin resistance were lower after the 4-week iso intervention compared with baseline. This would be consistent with possible beneficial metabolic effects as a consequence of the lower and prolonged glycaemic response and lower insulinaemic burden. However, there was no significant difference at 4 weeks after iso compared with suc. In conclusion, the study shows that iso is completely available from the small intestine, irrespective of food matrix, leading to a prolonged delivery of blood glucose. Regular iso consumption is well tolerated also in subjects with increased risk for vascular diseases.

Dietary beans and peas provide fibre, resistant starch and other nutrients that are often lacking in the human diet. The influence of native starches of beans and peas (and microwaved preparations) on N utilisation, biochemical indices in blood serum and caecal ecosystem state (SCFA, bacterial enzymes, micro-organisms) was studied in vivo. The native pea starch contained more resistant starch compared with its bean counterpart (31 v. 17 %); however, processing decreased these amounts to 25 v. 10 %. N digestibility was found to decrease considerably in all experimental groups. A considerable reduction was observed in glucose and total cholesterol concentration in rat blood serum as a result of feeding both dietary legume starch preparations under microwave treatment. This indicates that starch of bean origin activated glycolytic bacterial enzymes; however, all the analysed starches were found to reduce the activity of β-glucuronidase. In addition, both dietary bean starches significantly induced the formation of SCFA in the caecal digesta. As compared with the control group, a significant decrease in the pH of caecal and colonic digesta was demonstrated for both bean starch preparations. In comparison with the diet with native pea starch, its microwaved preparation reduced the concentrations of acetic, butyric and propionic acids among caecal SCFA and increased the pH of caecal and colonic digesta. The atherogenic index was significantly lower in rats fed microwaved pea starch. All investigated starch preparations increased the population of Bifidobacterium spp. in caecal digesta, but were also good substrates for opportunistic Enterococcus or Escherichia coli.

The health-promoting effects of various constituents of the olive tree (Olea europaea) are mainly associated with hypoglycaemic and insulin-sensitising activities and have been widely demonstrated in the metabolic syndrome and type 2 diabetes. However, their biological activity in autoimmune type 1 diabetes (T1D) is poorly characterised. Therefore, the influence of O. europaea-derived components present in dry olive leaf extract (DOLE) was examined in two established preclinical models of human T1D, which differ in some aspects of diabetogenesis: multiple low-dose streptozotocin-induced diabetes in susceptible C57BL/6 and CBA/H mouse strains; cyclophosphamide-accelerated diabetes in non-obese diabetic mice. In both T1D models, in vivo administration of DOLE significantly reduced clinical signs of diabetes (hyperglycaemia and body weight loss) and led to complete suppression of histopathological changes in pancreatic islets. In line with these, insulin expression and release were restored in DOLE-treated mice. Interestingly, inducible NO synthase expression and NO production were significantly elevated in peripheral tissues but were down-regulated within the local environment of the endocrine pancreas. This interference was reflected in NO-mediated suppression of T lymphocyte proliferation and lower production of the proinflammatory cytokines interferon-γ, IL-17 and TNF-α in the spleen, with subsequent blockade of β-cell destruction. The results suggest that DOLE interferes with development of autoimmune diabetes by down-regulating production of proinflammatory and cytotoxic mediators. Therefore, the potential use of a DOLE-enriched diet for prophylaxis/treatment of human T1D, and possibly other autoimmune diseases, is worthy of further investigation.

The present cross-sectional study set out to determine the nutritional status of infants aged 0–3 months with the WHO Multicentre Growth Reference (WHO-MGR) and examine the relationship between undernutrition and congenital or early-onset sensorineural hearing loss (CESHL) rarely reported for developing countries. The nutritional status of all infants attending community-based clinics for routine Bacille de Calmette-Guérin (BCG) immunisation from July 2005 to December 2006 was determined by weight-for-age, weight-for-length and BMI-for-age based on the WHO-MGR. Hearing loss status was determined by tympanometry, auditory brainstem response (ABR) and visual response audiometry after a two-stage screening with transient evoked otoacoustic emissions and automated ABR. The relationship between nutritional status and CESHL were explored after adjusting for potentially confounding maternal and infant characteristics using multivariable logistic regression analyses. Of the 3386 infants who completed the hearing evaluation protocol, seventy-one were confirmed with hearing loss (>30 dB hearing level). More than one-third (37·9 %) of all infants and over half (54·9 %) of those with CESHL were undernourished by at least one measure of growth. Stunting (35·3 %) was the most prevalent nutritional deficit in infants with CESHL. In the final logistic model, infants with any undernourished physical state were significantly likely to have CESHL (OR 1·67; 95 % CI 1·03, 2·77) and of a severe-to-profound degree (OR 3·92; 95 % CI 1·38, 11·17) compared with infants without any undernourishment. Prospective studies to establish the full spectrum of the relationship between undernutrition and CESHL, particularly in resource-poor countries, are therefore warranted.

High dietary intake of fats has been thought to be one of the major risk factors for the development of CVD. Less is known about the possible influence of fats from various sources on haemorheological abnormalities, which are considered an important factor in the pathogenesis of these diseases. The goal of the present study was to investigate effects of high-fat diets enriched in unsaturated fatty acids (USFA), SFA or trans-fatty acids (TFA), respectively, on haemorheological parameters in rats. Wistar female rats were divided into four groups and fed diets based on the AIN-93M formulation containing approximately 10 % energy from soyabean oil (control group) or 40 % energy from soyabean oil (USFA), palm oil (SFA) and vegetable shortening (TFA) for 8 weeks. The results showed that rats fed high-fat diets exhibited significant increases in serum TAG levels (P < 0·01), plasma viscosity (P < 0·01), whole blood viscosity (P < 0·01) and internal viscosity (P < 0·01) compared to the controls. The TFA group showed a significant decrease in erythrocyte deformability (P < 0·01) and increase in internal viscosity (P < 0·01) compared with the other groups. In addition, a significant increase in blood levels of free radicals (P < 0·01) was found in the TFA group, suggesting that the attack of oxygen-free radicals could be responsible for the impaired erythrocyte deformability. These impairments could be partly responsible for the development of various circulatory disorders. The present haemorheological study provides additional insights into the potential adverse effects of trans-fat and high-fat diets on haemorheological parameters.

The effects of long-term dietary supplementation of fish oil (n-3 PUFA-rich) in adult male pigs on body condition as well as insulin sensitivity and secretion were examined. Fifteen Duroc boars aged 204·5 (sd 9·4) d (body weight 145·8 (sd 16·8) kg) received daily 2·5 kg basal diet with a supplement of: (1) 62 g hydrogenated animal fat (n 5); (2) 60 g menhaden oil containing 10·8 g DHA and 9·0 g EPA (n 6); (3) 60 g tuna oil containing 19·8 g DHA and 3·9 g EPA (n 4). Rations were balanced to be isoenergetic. After 7 months of treatments, oral glucose and meal tolerance tests were conducted after insertion of a catheter into the jugular vein. Dietary supplementation with n-3 PUFA altered the blood plasma profile: DHA and EPA increased whereas arachidonic acid decreased (P < 0·01). Plasma glucose, insulin and C-peptide responses to oral glucose and the test meal were not affected by treatments (P>0·34). For all animals, total body fat estimated from body weight and back fat thickness was correlated with both β-cell function (by homeostasis model assessment (HOMA); r+0·63) and insulin sensitivity (index of whole-body insulin sensitivity and by HOMA; r − 0·63 and r+0·66, respectively). In conclusion, long-term supplementation with dietary n-3 PUFA did not affect insulin metabolism in healthy adult male pigs. The relationship between body fat and insulin sensitivity, well documented in human subjects, suggests that the adult male pig could be a promising animal model for studies on insulin metabolism.

We investigated the effects of amla (Emblica officinalis Gaertn.) on fructose-induced metabolic syndrome using a rat model. Male Wistar rats were fed a high-fructose (65 %) diet or standard chow for 1 week, and treated with an ethyl acetate (EtOAc) extract of amla, a polyphenol-rich fraction, at 10 or 20 mg/kg body weight per d, or vehicle, for 2 weeks. Serum glucose, TAG, total cholesterol and blood pressure levels of the high-fructose diet-fed rats were increased compared with those of the normal rats (P < 0·001). However, the EtOAc extract of amla ameliorated the high fructose-induced metabolic syndrome, including hypertriacylglycerolaemia and hypercholesterolaemia. Also, the elevated levels of hepatic TAG and total cholesterol in rats given the high-fructose diet were significantly reduced by 33·8 and 24·6 %, respectively (P < 0·001), on the administration of the EtOAc extract of amla at the dose of 20 mg/kg with the regulation of sterol regulatory element-binding protein (SREBP)-1 expression. The protein levels of PPARα and SREBP-2 were not affected by the feeding of the high-fructose diet or EtOAc extract of amla. In addition, oral administration of the amla extract at the dose of 20 mg/kg significantly inhibited the increased serum and hepatic mitochondrial thiobarbituric acid-reactive substance levels (21·1 and 43·1 %, respectively; P < 0·001). Furthermore, the amla extract inhibited the increase of cyclo-oxygenase-2 with the regulation of NF-κB and bcl-2 proteins in the liver, while the elevated expression level of bax was significantly decreased by 8·5 and 10·2 % at the doses of 10 and 20 mg/kg body weight per d, respectively. These findings suggest that fructose-induced metabolic syndrome is attenuated by the polyphenol-rich fraction of amla.

Capsinoids are non-pungent compounds with molecular structures similar to capsaicin, which has accepted thermogenic properties. To assess the acute effect of a plant-derived preparation of capsinoids on energy metabolism, we determined RMR and non-protein respiratory quotient (NPRQ) after ingestion of different doses of the capsinoids. Thirteen healthy subjects received four doses of the capsinoids (1, 3, 6 and 12 mg) and placebo using a crossover, randomised, double-blind trial. After a 10 h overnight fast as inpatients, RMR was measured by indirect calorimetry for 45 min before and 120 min after ingesting capsinoids or placebo. Blood pressure and axillary temperature were measured before ( − 55 and − 5 min) and after (60 and 120 min) dosing. Before dosing, mean RMR was 6247 (se 92) kJ/d and NPRQ was 0·86 (se 0·01). At 120 min after dosing, metabolic rate and NPRQ remained similar across the four capsinoids and placebo doses. Capsinoids also had no influence on blood pressure or axillary temperature. Capsinoids provided in four doses did not affect metabolic rate and fuel partitioning in human subjects when measured 2 h after exposure. Longer exposure and higher capsinoids doses may be required to cause meaningful acute effects on energy metabolism.

Inflammatory bowel disease (IBD) is a major source of morbidity in children and adults. Its incidence is rising, particularly in young people. IBD carries a lifelong risk of cancer, which is proportional to disease duration. Drug and surgical treatments rarely offer cure and often carry a high side effect burden. Dietary therapy is highly effective in Crohn's disease. For these reasons, there is much interest in developing novel dietary treatments in IBD. Curcumin, a component of the spice turmeric, and an anti-inflammatory and anti-cancer agent, shows preclinical and clinical potential in IBD. Its mechanisms of action are unknown. Our aim was to assess the effect of curcumin on key disease mediators p38 mitogen-activated protein kinase (MAPK), IL-1β, IL-10 and matrix metalloproteinase-3 (MMP-3) in the gut of children and adults with IBD. Colonic mucosal biopsies and colonic myofibroblasts (CMF) from children and adults with active IBD were cultured ex vivo with curcumin. p38 MAPK, NF-κB and MMP-3 were measured by immunoblotting. IL-1β and IL-10 were measured by ELISA. We show reduced p38 MAPK activation in curcumin-treated mucosal biopsies, enhanced IL-10 and reduced IL-1β. We demonstrate dose-dependent suppression of MMP-3 in CMF with curcumin. We conclude that curcumin, a naturally occurring food substance with no known human toxicity, holds promise as a novel therapy in IBD.

Prebiotic fibres have been proposed to promote weight loss and lower serum cholesterol; however, the mechanisms are not fully understood. The aim of the present research was to identify possible mechanisms through which prebiotic fibres improve serum lipids. Lean and obese JCR:La-cp rats aged 8 weeks consumed one of three diets supplemented with 0, 10 or 20 % prebiotic fibre for 10 weeks. Rats were anaesthetised and a fasting blood sample was taken for lipid analysis. Real-time PCR was used to determine gene expression for cholesterol and fatty acid regulatory genes in liver tissue. Liver and caecal digesta cholesterol and TAG content were quantified. Both doses of prebiotic fibre lowered serum cholesterol levels by 24 % in the obese hyperlipidaemic rats (P < 0·05). This change was associated with an increase in caecal digesta as well as an up-regulation of genes involved in cholesterol synthesis and bile production. Additionally, there was a 42 % reduction in TAG accumulation in the liver of the obese rats with 10 % prebiotic diet (P < 0·05); however, no change in liver fatty acid synthase (FAS). Prebiotic fibres appear to lower cholesterol levels through increased cholesterol excretion in the form of bile and inhibit the accumulation of TAG in the liver through a mechanism unrelated to FAS. These effects appear to be limited to the obese model and particularly the 10 % dose. The present work is significant as it provides insight into the mechanisms of action for prebiotic fibres on lipid metabolism and furthers the development of dietary treatments for hypercholesterolaemia.

Intake of lignans has been assessed in different study populations, but so far none of the studies has compared the daily intake of lignans and the urinary excretion of plant and enterolignans. We assessed the intake of lariciresinol, pinoresinol, secoisolariciresinol and matairesinol in 100 Finnish men consuming their habitual omnivorous diet, and measured the 24 h urinary excretion of plant and enterolignans to compare the intake and metabolism. Dietary determinants of lignan intake and their urinary excretion were also determined. The mean intake of lignans was 1224 (sd 539) μg/d, of which lariciresinol and pinoresinol covered 78 %. Almost half (47 %) of the intake of lignans was explained by the intake of rye products, berries, coffee, tea and roots. The urinary excretion of plant lignans corresponded to 17 % and enterolignans to 92 % of the intake of lignans. The urinary excretion of plant lignans was explained 14 % by the intake of rye products and intake of coffee, and consequently 3–7 % by the intake of water-insoluble fibre. The urinary excretion of enterolactone was explained 11 % by the intake of vegetables and rye products, 14 % by the intake of water-soluble fibre and only 4 % by the intake of lariciresinol. Although the assessed intake of lignans corresponded well with the urinary excretion of lignans, the enterolactone production in the human body depended more on the dietary sources of lignans than the absolute intake of lignans.

It has been demonstrated that intact plasma alkylresorcinols (AR) and urinary AR metabolites could be used as biomarkers of whole-grain intake. Thereafter, we developed the method for the plasma AR metabolites, which is more convenient and requires less sample pretreatment than the analysis of intact plasma AR. The aim of the present study is to evaluate whether AR metabolites measured in plasma, in the same population, could also be considered as useful biomarkers of cereal fibre. Fifty-six women were recruited in a cross-sectional and observational study. Dietary intake (5-d record) and plasma AR metabolites (3,5-dihydroxybenzoic acid, DHBA; 3-(3,5-dihydroxyphenyl)-1-propanoic acid, DHPPA) were measured. The relationship between plasma AR metabolites and cereal fibre intake was examined using partial correlation and stepwise regression. Cereal fibre intake correlated significantly with plasma DHBA (r 0·411; P = 0·002) and DHPPA (r 0·463; P = 0·000) even after adjustment for BMI and age. Thus, plasma AR metabolites correlate with cereal fibre intake as noted with plasma intact AR and urinary AR metabolites. We observed that plasma DHPPA was the independent predictor of cereal fibre intake, explaining 18 % of the variance (adjusted r2 0·176; P = 0·002). In epidemiological screening, it might be easier to obtain and to collect plasma than urine samples. In addition, the plasma AR metabolites half-life seems longer than those of intact plasma AR, and their measurements are more convenient, and faster. Thus, sum of plasma AR metabolites and more specifically plasma DHPPA seems to be good and specific biomarkers of cereal fibre intake.

Cholesterol-lowering effects of oats have been demonstrated in both animals and human subjects. However, the crucial properties of oat-containing diets that determine their health effects need to be further investigated to optimise their use. A mouse model would be a valuable tool, but few such studies have been published to date. We investigated the effects of oat bran on plasma cholesterol and lipoproteins in two substrains of C57BL/6 mice. Western diet was made atherogenic by the addition of 0·8 % cholesterol and 0·1 % cholic acid. After 4 weeks on atherogenic diet, total plasma cholesterol had increased from 1·86–2·53 to 3·77–4·40 mmol/l. In C57BL/6NCrl mice, inclusion of 27 and 40 % oat bran reduced total plasma cholesterol by 19 and 24 %, respectively, reduced the shift from HDL to LDL+VLDL and caused increased faecal cholesterol excretion. There was no effect of oat bran on plasma levels of the inflammatory markers fibrinogen, serum amyloid A or TNF-α. Contrary to findings in C57BL/6NCrl mice, there was no sustained effect of oat bran (27 or 40 %) on plasma cholesterol in C57BL/6JBomTac mice after 4 weeks of feeding. Thus, C57BL/6NCrl mice fed an atherogenic diet are a good model for studies of physiological effects of oats, whereas a substrain derived from C57BL/6J, raised in a different breeding environment and likely possessing functional genetic differences from C57BL/6N, is considerably less responsive to oats. The present finding that two substrains of mice respond differently to oats is of practical value, but can also help to elucidate mechanisms of the cholesterol-lowering effect of oats.

We used a factorial approach to distinguish maintenance from growth requirements for protein, lysine and methionine in the black tiger shrimp, Penaeus monodon. Juvenile P. monodon (initial weight 2·4 g) were fed during 6 weeks one of ten semi-purified diets based on casein and purified amino acids (AA) as N source. The diets contained four levels of crude protein (CP, from 5 to 54 % DM diet) with two levels (% CP) of lysine or methionine (normal or 30 % deficient). Requirements were determined using linear and non-linear regression models. We could thus obtain the first ever data on maintenance (N equilibrium) requirements for CP and AA in P. monodon. CP requirements for maintenance (4·5 g/kg body weight (BW) per d) represented approximately 19 % of the CP requirement for maximal N gain (23·9 g/kg BW per d). The marginal efficiency of utilisation reached a maximum of 38 % for N, 0·77 for lysine and 1·62 for methionine using N gain as response. Lysine requirements were 0·20 g/kg BW per d for N maintenance and 1·40 g/kg BW per d for maximal N gain. Methionine requirements were 0·11 g/kg BW per d for N maintenance and 0·70 g/kg BW per d for maximal N gain. The lysine (5·8 %) and methionine (2·9 %) requirements for maximal N gain, expressed as percentage of protein requirement, agree with literature data using a dose–response technique with smaller P. monodon. The observed interaction between dietary CP and methionine for N gain demonstrates that requirements for indispensable AA (expressed as % CP) cannot be evaluated separately from CP requirements.

Zn and DHA have putative neuroprotective effects and these two essential nutrients are known to interact biochemically. We aimed to identify novel protein candidates that are differentially expressed in human neuronal cell line M17 in response to Zn and DHA that would explain the molecular basis of this interaction. Two-dimensional gel electrophoresis and MS were applied to identify major protein expression changes in the protein lysates of human Ml7 neuronal cells that had been grown in the presence and absence of Zn and DHA. Proteomic findings were further investigated using Western immunoblot and real-time PCR analyses. Four protein spots, which had significant differential expression, were identified and selected for in-gel trypsin digestion followed by matrix-assisted laser desorption ionisation MS analysis. The resultant peptide mass fingerprint for each spot allowed their respective identities to be deduced. Two human histone variants H3 and H4 were identified. Both H3 and H4 were downregulated by Zn in the absence of DHA (Zn effect) and upregulated by DHA (DHA effect) in the presence of Zn (physiological condition). These proteomic findings were further supported by Western immunoblot and real-time PCR analyses using H3- and H4-specific monoclonal antibodies and oligonucleotide primers, respectively. We propose that dietary Zn and DHA cause a global effect on gene expression, which is mediated by histones. Such novel information provides possible clues to the molecular basis of neuroprotection by Zn and DHA that may contribute to the future treatment, prevention and management of neurodegenerative diseases such as Alzheimer's disease.

Oral supplementation with bovine colostrum (COL) has been shown to enhance immunity in human subjects. However, there is limited research on the use of bovine COL supplementation to counter exercise-induced immunodepression, as a model of stress-induced immunodepression, and previous research has focused primarily on salivary IgA. The aim of the present study was to determine the effects of bovine COL supplementation on exercise-induced changes in innate immunity (neutrophil function and salivary lysozyme) in addition to salivary IgA. Twenty healthy, active men cycled for 2 h at approximately 64 % maximal oxygen uptake after 4 weeks of daily bovine COL (n 10) or placebo (PLA, n 10) supplementation. Blood and saliva samples were obtained before and after supplementation, before and after exercise. Exercise induced significant increases in markers of physiological stress and stress to the immune system (circulating neutrophils, neutrophil:lymphocyte ratio, immature granulocytes, atypical lymphocytes and plasma cortisol), but there were no differences between the COL and PLA groups. Significant group × time interactions (two-way mixed model ANOVA) were observed for neutrophil function (stimulated degranulation) and salivary lysozyme concentration and release (P < 0·05). Significant exercise-induced decreases were observed in these parameters, and bovine COL supplementation either speeded the recovery (neutrophil function) or prevented the decrease (salivary lysozyme) in these measures of innate immunity. These results suggest that 4 weeks of bovine COL supplementation limits the immunodepressive effects induced by an acute prolonged physical stressor, such as exercise, which may confer some benefits to host defence.

Exposure to diets high in fat and sucrose can induce hyperinsulinaemia, affect Ca and Mg metabolism, and alter bone mineralisation and mechanical properties. The present study assessed morphological and mechanical changes in a murine model exposed to a high-fat/sucrose (HFS) diet, as well as corresponding molecular and endocrine markers of bone turnover. Female C57BL/6 mice (aged 9 weeks) consumed either a low-fat, complex carbohydrate diet or an HFS diet for 10 weeks. At the end of the 10 weeks, serum was collected for biochemical analysis. Tibiae from half the mice (n 15) were randomly selected to be micro-computed tomography scanned and tested to failure in cantilever bending, while the remaining half were prepared for real-time PCR analysis. Serum tartrate-resistant acid phosphatase was significantly elevated in HFS mice, while osteocalcin remained unchanged. Both body mass and percentage body fat were greater in mice fed HFS diet. After adjusting for body mass, tibial structural and morphological properties were adversely affected in the HFS cohort. Cortical thickness, cross-sectional area, and load at maximum were all significantly lower in mice fed HFS diet. Receptor activator of nuclear factor κβ ligand (RANKL) mRNA was significantly upregulated in HFS mice, but osteoprotegerin/RANKL mRNA ratio remained unchanged between cohorts. Moreover, cyclo-oxygenase-2 mRNA tended to be increased in HFS. Thus, ingestion of an HFS diet had a significant adverse effect on mouse bone morphology and mechanics, and these effects were likely due to elevated osteoclast activity associated with the inflammatory state of obesity, and not necessarily osteoclast recruitment/proliferation.

Diets rich in fruits and vegetables are associated with lower risk of cancer which may be conferred in part by the antioxidant properties of these foods. However, antioxidant supplementation or increased consumption of antioxidant-rich foods has been reported to have inconsistent effects on DNA damage. The present work (the DART study) investigated the extent of inter-individual variation in DNA damage, the capacity for base excision repair (BER) and the responses of both variables to supplementation with an antioxidant supplement for 6 weeks. There was a wide inter-individual variation in endogenous lymphocyte DNA strand breaks (8-fold variation), in damage after a challenge with H2O2 (16-fold variation) and in DNA repair (41-fold variation) measured using the comet assay. When stratified into tertiles according to the pre-supplementation level of endogenous DNA damage, there was a statistically significant decrease in DNA damage after supplementation in the tertile with the highest pre-supplementation level of damage. There was no effect of supplementation on BER. Endogenous DNA damage level before supplementation was significantly different (P = 0·037) between the three genotypes for the Val16Ala single nucleotide polymorphism in manganese superoxide dismutase (rs4880) with individuals homozygous/wild type showing less damage than those carrying the alanine variant.

Consumption of different types of oil may have different effects on cardiovascular risk. The exact role of maize oil, cod liver oil, soya oil and extra virgin olive oil on endothelial function, oxidative stress and inflammation is unknown. We evaluated the effect of acute consumption of these types of oil on endothelial function, oxidative stress and inflammation in healthy adults. Thirty-seven healthy volunteers were randomised to receive an oral amount of each type of oil or water. Endothelial function was evaluated by gauge-strain plethysmography at baseline and 1, 2 and 3 h after consumption. Oxidative stress status was determined by total lipid peroxides (PEROX), while inflammatory process was estimated by measuring the soluble form of vascular adhesion molecule 1. Serum levels of the two previous markers were measured at baseline and 3 h after oil consumption. Reactive hyperaemia (RH) was significantly decreased after maize oil consumption compared with controls (P < 0·05). However, the consumption of cod liver oil and soya oil induced a significant improvement of RH after 1 h, compared with controls (P < 0·05). There was no significant effect of any type of oil consumption on endothelium-independent dilatation, total lipid PEROX and vascular adhesion molecule 1 serum levels. Consumption of maize oil leads to impaired endothelial function, while soya oil and cod liver oil slightly improve endothelial function. However, all types of oils did not affect inflammatory process and systemic oxidative stress, suggesting that their effect on endothelial function may not be mediated by free radicals bioavailability.

Genistein and daidzein are known to have both beneficial and adverse effects on human health due to their many biological actions at the cellular level. Both isoflavones have been shown to inhibit GLUT-mediated glucose transport across the plasma membrane of mammalian cells. Since lysosomal membrane transport is essential for maintaining cellular homeostasis, the present study examined the effects of genistein and daidzein on glucose and sulphate transport in isolated rat liver lysosomes. Both genistein and daidzein significantly inhibited lysosomal glucose uptake. Genistein was a more potent glucose transport inhibitor than daidzein, with a half-maximum inhibitory concentration (IC50) of 45 μmol/l compared with 71 μmol/l for daidzein. Uptake kinetics of d-glucose showed a significant decrease in Vmax (control:genistein treat = 1489 (sem 91):507 (sem 76) pmol/unit of β-hexosaminidase per 15 s) without a change in Km. The presence of 50 μm-genistein in the medium also reduced glucose efflux from lysosomes preloaded with 100 mm-d-glucose. Genistein also inhibited lysosomal sulphate transport. Similar to its effects on glucose uptake kinetics, genistein treatment caused a significant decrease in sulphate uptake Vmax (control:genistein treat = 87 (sem 4):59 (sem 5) pmol/unit of β-hexosaminidase per 30 s), while the Km was not affected. The evidence provided by the present study suggests that the most likely mechanism of lysosomal glucose transport inhibition by genistein is via direct interaction between genistein and the transporter, rather than mediation by tyrosine kinase inactivation. Genistein likely has a similar mechanism of directly inhibiting sulphate transporter.