A positive energy balance (energy intake>energy expenditure), in which total fat intake plays an important role, is commonly regarded as a major factor contributing to obesity. Adipose tissue development, i.e. both size (hypertrophy) and number (hyperplasia), is stimulated by high dietary fat intake during early postnatal development, a susceptibility that now appears to continue well into adulthood. Recent human and animal studies suggest that by altering rates of adipocyte differentiation and proliferation, differences in the composition of dietary fat may also contribute to adipose tissue development. At least in rodent models, the relative intake of n-6 to n-3 PUFA is clearly emerging as a new factor in this development. In these models, higher linoleate intake raises tissue arachidonic acid, which increases prostacyclin production and, in turn, stimulates signalling pathways implicated in adipogenesis. Signalling pathways stimulated by arachidonic acid probably include phospholipase and/or cyclo-oxygenase activation and may be linked as much to relatively low intake of n-3 PUFA as to excessive dietary linoleate. One factor potentially contributing to oversight about the apparent role of dietary n-6 PUFA (especially excess dietary linoleate) in adipose tissue development is the historical overestimation of linoleate requirements and the enthusiasm for higher intake of ‘essential fatty acids’. More research is needed to address whether disequilibration of dietary PUFA intake contributes to the risk of obesity in humans.

Recent evidence shows that specific fatty acids affect cell metabolism, modifying the balance between fatty acid oxidation and lipogenesis. These effects may have important implications in addressing the present epidemic of nutrition-related chronic disease. Intake of dietary saturated and n-6 PUFA have increased while n-3 fatty acid intake has decreased. Obesity, type 2 diabetes and insulin resistance are highly prevalent, and both are strongly related to disorders of lipid metabolism characterized by an increased plasma and intracellular fatty acid availability. Thus, it has been hypothesized that change in the quality of dietary fat supply is able to modify the degree of insulin sensitivity. Animal studies provide support for this notion. However, there is limited human data either from normal or diabetic subjects. This review aims to analyse human studies that address this question. To this purpose, the experimental design, dietary compliance, insulin-sensitivity method used and confounding variables are discussed in order to identify the role of dietary fat quality as a risk factor for insulin resistance. Most studies (twelve of fifteen) found no effect relating to fat quality on insulin sensitivity. However, multiple study design flaws limit the validity of this conclusion. In contrast, one of the better designed studies found that consumption of a high-saturated-fat diet decreased insulin sensitivity in comparison to a high-monounsaturated-fat diet. We conclude that the role of dietary fat quality on insulin sensitivity in human subjects should be further studied, using experimental designs that address the limitations of existing data sets.

Invasion in and translocation across enterocytes are major events during Campylobacter jejuni-induced enteritis in humans. C. jejuniin vitro infection of cell monolayers typically results in loss of tight junction integrity, which could contribute to translocation. In the present study, we wanted to investigate whether butyrate is able to confer protection to Caco-2 cells against C. jejuni invasion, thus reducing paracellular permeability and limiting C. jejuni translocation. Protection of Caco-2 cells against C. jejuni invasion was assessed using a gentamicin protection assay. Transwell systems were used to investigate the impact of butyrate on translocation of C. jejuni across a Caco-2 monolayer and its effect on transepithelial resistance during infection. Butyrate protected Caco-2 cells against C. jejuni invasion in a concentration-dependent manner. Differentiated Caco-2 cells were less susceptible to C. jejuni invasion than 3-d-old undifferentiated cells and higher concentrations of butyrate and longer incubation times were needed to become refractive for invasion. C. jejuni translocation over Caco-2 monolayers was reduced when monolayers were treated with butyrate and this was accompanied by an enhanced drop in transepithelial resistance. The present study showed that butyrate is able to protect Caco-2 cells from two major virulence mechanisms of C. jejuni, namely invasion and translocation, but not from a decline in transepithelial resistance.

The dietary fibre and fermentability characteristics of local root crops and legumes were determined. Total, soluble and insoluble fibre were determined in six root crops (kamote, gabi, potato, tugi, ube, cassava) and ten legumes (mungbean, soyabean, peanut, pole sitao, cowpea, chickpea, green pea, lima bean, kidney bean and pigeon pea) using Association of Official Analytical Chemists methods. The dietary fibre from test foods was isolated and fermented in vitro using human faecal inoculum simulating conditions in the human colon. The SCFA, e.g. acetate, propionate, butyrate, produced after fibre fermentation was measured using HPLC. The dietary fibre content of root crops ranged from 4·6 to 13·5 g/100 g while legumes ranged from 20·9 to 46·9 g/100 g, suggesting that root crops and legumes are good sources of dietary fibre. Significant amounts of SCFA were produced after in vitro fermentation of the fibre isolate of both root crops and legumes. The best sources (as mmol/g fibre isolate) of acetate among the legumes were pole sitao (5·6 (sem 0·5)) and mungbean (5·3 (sem 0·1)) and among the root crops, tugi (2·5 (sem 0·4)) and cassava (2·4 (sem 0·1)); of propionate, kidney bean (7·2 (sem 1·5)) and pigeon pea (3·3 (sem 0·2)) for legumes, and tugi (1·8 (sem 0·2)) for root crops; and of butyrate, peanut (6·0 (sem 0·2)) and cowpea (5·4 (sem 0·2)) for legumes, and tugi (0·8 (sem 0·0)) and cassava (0·8 (sem 0·0)) for root crops. In conclusion, root crops and legumes are good sources of dietary fibre and produced SCFA after fibre fermentation, such as acetate, propionate and butyrate. SCFA production after in vitro fermentation can be estimated using human faecal inoculum and can be used to model the human colon.

In contrast to some extensively examined food mutagens, for example, aflatoxins, N-nitrosamines and heterocyclic amines, some other food contaminants, in particular polycyclic aromatic hydrocarbons (PAH) and other aromatic compounds, have received less attention. Therefore, exploring the relationships between dietary habits and the levels of biomarkers related to exposure to aromatic compounds is highly relevant. We have investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort the association between dietary items (food groups and nutrients) and aromatic DNA adducts and 4-aminobiphenyl-Hb adducts. Both types of adducts are biomarkers of carcinogen exposure and possibly of cancer risk, and were measured, respectively, in leucocytes and erythrocytes of 1086 (DNA adducts) and 190 (Hb adducts) non-smokers. An inverse, statistically significant, association has been found between DNA adduct levels and dietary fibre intake (P = 0·02), vitamin E (P = 0·04) and alcohol (P = 0·03) but not with other nutrients or food groups. Also, an inverse association between fibre and fruit intake, and BMI and 4-aminobiphenyl-Hb adducts (P = 0·03, 0·04, and 0·03 respectively) was observed. After multivariate regression analysis these inverse correlations remained statistically significant, except for the correlation adducts v. fruit intake. The present study suggests that fibre intake in the usual range can modify the level of DNA or Hb aromatic adducts, but such role seems to be quantitatively modest. Fibres could reduce the formation of DNA adducts in different manners, by diluting potential food mutagens and carcinogens in the gastrointestinal tract, by speeding their transit through the colon and by binding carcinogenic substances.

The present study evaluates for the first time in dogs, the kinetics of green tea catechins and their metabolic forms in plasma and urine. Ten beagles were administered 173 mg (12·35 mg/kg body weight) of catechins as a green tea extract, in capsules. Blood samples were collected during 24 h after intake and urine samples were collected during the following periods of time: 0–2, 2–6, 6–8 and 8–24 h. Two catechins with a galloyl moiety and three conjugated metabolites were detected in plasma. Most of the detected forms in plasma reached their maximum plasma concentration (Cmax) at around 1 h. Median Cmax for ( − )-epigallocatechin-3-gallate (EGCG), ( − )-epicatechin-3-gallate (ECG), ( − )-epigallocatechin glucuronide (EGC-glucuronide), ( − )-epicatechin glucuronide (EC-glucuronide), ( − )-epicatechin sulphate (EC-sulphate) were 0·3 (range 0·1–1·9), 0·1 (range 0–0·4), 0·8 (range 0·2–3·9), 0·2 (range 0·1–1·7) and 1 (range 0·3–3·4) μmol/l, respectively. The areas under the plasma concentration v. time curves (AUC0 → 24) were 427 (range 102–1185) μmol/l × min for EGC-glucuronide, 112 (range 53–919) μmol/l × min for EC-sulphate, 71 (range 26–306) μmol/l × min for EGCG, 40 (range 12–258) μmol/l × min for EC-glucuronide and 14 (range 0·1–124) μmol/l × min for ECG. The values of mean residence time (MRT0 → 24) were 5 (range 2–16), 2 (range 1–11), 10 (range 2–13), 3 (range 2–16) and 2·4 (range 1–18) h for EGCG, ECG, EGC-glucuronide, EC-glucuronide and EC-sulphate, respectively. In urine, catechins were present as conjugated forms, suggesting bile excretion of EGCG and ECG. Green tea catechins are absorbed following an oral administration and EGC-glucuronide is the metabolic form that remains in the organism for a longer period of time, suggesting that this compound could suffer an enterohepatic cycle.

This study tested the hypothesis that protein source is a factor determining the impact of the diet on lipid metabolism in hamsters. Twenty-eight hamsters of similar body weight were assigned for a period of 8 weeks to one of the following four diets (seven per group) containing either 20 % (w/w) casein (CAS), beef protein (BF), wheat gluten (WG) or soya protein (SOY). The fat composition of the diet was the same (15·5 % w/w) in all groups and provided SFA, MUFA and PUFA representative of the average Canadian diet. After an overnight fast, blood and liver were collected for the measurement of serum lipids, fatty acid composition of liver phospholipids and mRNA levels of selected genes involved in lipid metabolism. WG resulted in lower total cholesterol, HDL-cholesterol and non-HDL-cholesterol but, along with SOY, in higher mRNA levels of cholesterol 7 α-hydroxylase and LDL receptor. Furthermore, both WG and SOY resulted in lower 18 : 3n-3, 20 : 4n-6, total n-6 PUFA, 18 : 1n-9 and total MUFA, but higher 22 : 6n-3, total n-3 PUFA, 22 : 6n-3/18 : 3n-3 and 22 : 5n-3/18 : 3n-3 ratios in liver phospholipids, and higher hepatic Δ6-desaturase mRNA levels. These results show that the impact of dietary protein on lipid metabolism is source-dependent and associated with changes in mRNA abundances of key hepatic enzymes and receptors.

This study examined the effect of purified soyabean phosphatidylcholine (SPC) on circulating plasma lipids and nutrient digestibility in juvenile common carp. The fish (100 (SD 15) g, 25°C) were fed, for 4 weeks, a casein-based diet containing either 12 % soyabean oil (diet SBO) or 8 % SBO plus 4 % SPC (diet SPC). The lipid, protein and energy contents of the faeces were analysed for the determination of apparent digestibility. At the end of the trial, the fish were fasted for 48 h and fed a single meal. Plasma lipids were then analysed over the next 48 h. The growth (1·63 v. 1·26 % per d) and apparent lipid digestibility (96·3 v. 92·1 %) were higher in SPC- than in SBO-fed fish. The amplitude of the postprandial (8 h after the meal) TAG peak was identical in fish from both treatments, despite the 33 % lower amount of TAG in diet SPC. Both observations support the idea that SPC stimulates intestinal TAG uptakes. The lower TAG:phospholipid ratio of the secreted plasma lipids at the time of absorption suggests a larger number of smaller intestinal lipoproteins in SPC- than SBO-fed fish, possibly due to the recycling of absorbed lysophosphatidylcholine for chylomicron formation. In the 48 h unfed state, phospholipid levels remained approximately 20 % higher in SPC-fed than in SBO-fed fish, but we observed no hypocholesterolaemic effect of SPC. In summary, the present data support earlier histological indications of a positive role of dietary phosphatidylcholine in intestinal TAG uptakes in carp.

The purpose of the present study was to determine the effects of an exercise training programme in high-fat-fed rats on in vitro lipolysis in a visceral (mesenteric) and a non-visceral fat depot (retroperitoneal) and its relationship to perilipin content. Two groups of female rats were fed a high-fat diet (42 % as energy) for 8 weeks, one remaining sedentary (Sed) and the other being exercise trained (Tr) for this entire period. Rats were killed after 2 and 8 weeks of their respective treatment. The significantly (P < 0·01) higher levels in mesenteric and retroperitoneal fat pad weights, plasma leptin, NEFA and glucose observed with time in Sed high-fat-fed rats were significantly (P < 0·05) attenuated in Tr animals. Isoproterenol-stimulated (10− 5–10− 4 m) lipolysis in the mesenteric, but not in the retroperitoneal tissue, was significantly (P < 0·05) lower (about 57 %) in Tr than in Sed rats after 8 weeks of high-fat feeding. The isoproterenol-stimulated lipolysis in the mesenteric tissue of 8-week Tr high-fat-fed rats was lowered to the level measured in 2-week fat-fed rats although mesenteric fat accumulation was still significantly (P < 0·01) higher in 8- than in 2-week Tr rats. Perilipin content (Western blot) was not affected by the exercise training programme. These results indicate that exercise training resulted in a reduction in the high-fat diet-induced elevated levels of lipolysis in the mesenteric tissue. This response appears to be independent of the perilipin content.

Hypovitaminosis D is common in Asian Indians. Physicians often prescribe 1500 μg (60 000 IU) cholecalciferol per week for 8 weeks for vitamin D deficiency in India. Its efficacy to increase serum 25-hydroxy vitamin D (25(OH)D) over short (2 months) and long (1 year) term is not known. We supplemented a group of twenty-eight apparently healthy Asian Indians detected to have low serum 25(OH)D (mean 13·5 (sd 3·0) nmol/l) on screening during January–March 2005. Serum parathyroid hormone (PTH) level was supranormal in 30 % of them. Oral supplementation included 1500 μg cholecalciferol per week and 1g elemental Ca daily for 8 weeks. Serum 25(OH)D, total Ca, inorganic P and intact (i) PTH were reassessed in twenty-three subjects (twelve females and eleven males) who had follow up at both 8 weeks and 1 year. At 8 weeks the mean 25(OH)D levels increased to 82·4 (sd 20·7) nmol/l and serum PTH normalized in all. Twenty-two of the twenty-three subjects had 25(OH)D levels>49·9 nmol/l. At 1 year, though the mean 25(OH)D level of 24·7 (sd 10·9) nmol/l was significantly higher than the baseline, all subjects were 25(OH)D deficient. Five subjects with supranormal iPTH at baseline showed recurrence of biochemical hyperparathyroidism. Thus, with 8 weeks of cholecalciferol supplementation in Asian Indians with chronic hypovitaminosis D, mean serum 25(OH)D levels would be normalized and serum PTH value would be reduced to half. However, such quick supplementation would not maintain their 25(OH)D levels in the sufficient range for 1 year. For sustained improvement in 25(OH)D levels vitamin D supplementation has to be ongoing after the initial cholecalciferol loading.

We examined the in vitro and in vivo effects of a probiotic, Escherichia coli strain M-17 (EC-M17), on NF-κB signalling, cytokine secretion and efficacy in dextran sulfate sodium (DSS)-induced murine colitis. NF-κB signalling was assessed using an NF-κB luciferase reporter cell line that was stimulated with TNF-α (100 ng/ml). p65 Nuclear binding and cytokine secretion (TNF-α, IL-1β and IL-6) were evaluated using a RAW 264·7 macrophage cell line that was exposed to lipopolysaccharide (LPS; 5 μg/ml). Mice were administered vehicle, EC-M17, metronidazole, or EC-M17 plus metronidazole for 13 d. During the final 6 d, mice also received 2 % DSS. Parameters evaluated included disease activity index (DAI), histology, myeloperoxidase and NF-κB p65. EC-M17 dose dependently inhibited TNF-α-induced NF-κB signalling. At 5 × 109 colony-forming units/ml, EC-M17 inhibited NF-κB by >95 %. LPS-induced nuclear p65 binding was significantly inhibited (78 %; P < 0·05) in RAW 264·7 macrophages at 1 × 108 colony-forming units/ml. EC-M17 also inhibited (by >90 %) the LPS-induced secretion of TNF-α, IL-1β and IL-6. In mice with DSS-induced colitis, EC-M17, metronidazole, and EC-M17 plus metronidazole significantly reduced DAI and colonic histology scores. Both EC-M17 and metronidazole reduced colonic IL-12, IL-6, IL-1β and interferon-γ. The combination of EC-M17 plus metronidazole resulted in more substantial cytokine reductions than were found with either treatment alone, and combination therapy significantly (P < 0·05 in both cases) reduced IL-1β compared with EC-M17 and colonic histology scores compared with metronidazole. Alone, and in combination with metronidazole, EC-M17 improved murine colitis, probably due to an inhibitory effect on NF-κB signalling.

Recent studies support beneficial effects of polyphenols in various chronic inflammatory diseases, for example, the inflammatory bowel diseases. Inhibition of NF-κB activation by polyphenols could explain part of their anti-inflammatory properties, but few data are available on the intestine. The purpose of the present study was thus to investigate the effects of some polyphenols on NF-κB activation using human intestinal Caco-2 cells. Effects of standard polyphenols (50 μmol/l) were studied on different cellular events associated with NF-κB activation: (i) NF-κB activity using cells transiently transfected with a NF-κB–luciferase construct and stimulated by inflammatory agents (IL-1β, TNF-α or lipopolysaccharides (LPS)); (ii) phosphorylation of the inhibitor of κB (IκB-α) analysed by Western blot; (iii) secretion of IL-8 quantified by ELISA assay. Results showed that chrysin and ellagic acid inhibited NF-κB activity, whereas genistein and resveratrol increased it. These effects were independent of the nature of the inducer, indicating that polyphenols may modulate NF-κB activation by acting on a common event to the cytokine- and LPS-mediated cascades. Chrysin strongly reduced (2·5-fold) IL-1β-induced IκB-α phosphorylation, whereas ellagic acid increased it (1·7-fold). Ellagic acid, genistein and epigallocatechin gallate reduced (4- to 8-fold) IL-1β-induced IL-8 secretion, while resveratrol promoted (1·7-fold) the secretion. Chrysin also diminished IL-8 secretion by 1·6-fold (but P>0·05). The data indicate that polyphenols can modulate the NF-κB activation pathway in the intestine. Chrysin could block NF-κB activation via the inhibition of IκB-α phosphorylation. The other molecular targets of the active polyphenols are still to be identified.

This study evaluated whether arginine (Arg) supplementation could attenuate gut injury induced by Escherichia coli lipopolysaccharide (LPS) challenge through an anti-inflammatory role in weaned pigs. Pigs were allotted to four treatments including: (1) non-challenged control; (2) LPS-challenged control; (3) LPS+0·5 % Arg; (4) LPS+1·0 % Arg. On day 16, pigs were injected with LPS or sterile saline. At 6 h post-injection, pigs were killed for evaluation of small intestinal morphology and intestinal gene expression. Within 48 h of challenge, 0·5 % Arg alleviated the weight loss induced by LPS challenge (P = 0·025). In all three intestinal segments, 0·5 or 1·0 % Arg mitigated intestinal morphology impairment (e.g. lower villus height and higher crypt depth) induced by LPS challenge (P < 0·05), and alleviated the decrease of crypt cell proliferation and the increase of villus cell apoptosis after LPS challenge (P < 0·01). The 0·5 % Arg prevented the elevation of jejunal IL-6 mRNA abundance (P = 0·082), and jejunal (P = 0·030) and ileal (P = 0·039) TNF-α mRNA abundance induced by LPS challenge. The 1·0 % Arg alleviated the elevation of jejunal IL-6 mRNA abundance (P = 0·053) and jejunal TNF-α mRNA abundance (P = 0·003) induced by LPS challenge. The 0·5 % Arg increased PPARγ mRNA abundance in all three intestinal segments (P < 0·10), and 1·0 % Arg increased duodenal PPARγ mRNA abundance (P = 0·094). These results indicate that Arg supplementation has beneficial effects in alleviating gut mucosal injury induced by LPS challenge. Additionally, it is possible that the protective effects of Arg on the intestine are associated with decreasing the expression of intestinal pro-inflammatory cytokines through activating PPARγ expression.

There is a need to further our understanding of the role that the equine hindgut ecosystem plays in digestive processes and diseases. The aim of the present study was to utilise the real-time PCR technique to determine the abundance of candidate cellulolytic (Ruminococcus flavefaciens; Fibrobacter succinogenes) and non-cellulolytic (Streptococcus bovis) bacteria in lumen contents from the caecum, ventral and dorsal colon, and rectum of healthy horses (n 14). Total DNA was extracted from frozen and lyophilised lumen contents, and PCR primers and Taqman® probes were designed based on 16S rDNA sequences for specific detection of candidate bacterial species. Overall, in frozen and lyophilised digesta, there were significantly (P < 0·01) fewer candidate bacteria in the caecum than the dorsal colon and rectum. In frozen digesta, candidate bacteria levels were similar between the ventral colon, dorsal colon and rectum, but in lyophilised digesta there were significantly (P < 0·05) higher levels of bacteria in the dorsal colon and rectum. Frozen digesta contained disparate levels of candidate bacteria such that R. flavefaciens > F. succinogenes > S. bovis (P < 0·05), while in lyophilised digesta R. flavefaciens was present in significantly (P < 0·05) greater amounts than F. succinogenes and S. bovis. R. flavefaciens and F. succinogenes were abundant at significantly (P < 0·05) greater levels in lyophilised digesta v. frozen digesta, with no difference in S. bovis levels. These data indicate that for these bacteria at least, faeces are a suitable model for studying the bacterial ecosystem within the equine colon. The present study also indicates that the preservation method of digesta affects levels of bacteria detected.

During atherogenesis, a pathological accumulation of lipids occurs within aortic intimal macrophages through uptake of plasma oxidised LDL (oxLDL). The aim of the present study was to determine whether macrophage uptake of plasma oxLDL and LDL susceptibility to oxidation may be determined by quantity and quality of dietary fat. Twenty healthy young men were subjected to three dietary periods, each lasting 4 weeks. The first was an SFA-enriched diet (38 % fat, 20 % SFA), which was followed by a carbohydrate (CHO)-rich diet (30 % fat, < 10 % SFA, 55 % CHO) or a MUFA olive oil-rich diet (38 % fat, 22 % MUFA) following a randomised cross-over design. After each diet period, LDL particles were oxidised with Cu ions to determine LDL susceptibility to oxidation and subsequently incubated with the U937-macrophage cell line to determine the percentage of uptake of plasma oxLDL. The shift from the MUFA diet to the SFA- or CHO-rich diets reduced the resistance of LDL particles to oxidation, decreasing lag time (P = 0·038) and increasing the propagation rate (P = 0·001). Furthermore, the MUFA-rich diet demonstrated reduced macrophage uptake of plasma oxLDL (P = 0·031) as compared with the SFA-rich diet. Finally, macrophage uptake of plasma oxLDL was correlated (r 0·45; P = 0·040) with total amount of conjugated dienes after LDL oxidation. Our data suggest that a MUFA-rich diet may have favourable effects on cardiovascular risk since it prevents the oxidative modifications of LDL and reduces macrophage uptake of plasma oxLDL.

Little is known about the effect of dietary carbohydrate, glycaemic index (GI) and glycaemic load (GL) on the risk of the metabolic syndrome, especially in populations with white rice as the staple food. The study examined the cross-sectional relationship between carbohydrate, GI, GL and risk of the metabolic syndrome. There were a total of 910 middle-aged Korean adults. Dietary carbohydrate, GI and GL were determined by an interview-administered FFQ. The metabolic syndrome was defined using the modified criteria published in the Third Report of the National Cholesterol Education Program Adult Treatment Panel III. The risk of developing the metabolic syndrome was positively related to dietary carbohydrate (P for trend = 0·03), GI (P for trend = 0·03) and GL intakes (P for trend = 0·02) in women after adjusting for potential confounding variables. Among the components of developing the metabolic syndrome, the risk of high TAG and low HDL-cholesterol were positively related to high GI and GL intakes in women. The risk of developing the metabolic syndrome was considerably higher in the highest quintiles of carbohydrate (OR 6·44; 95 % CI 2·16, 19·2), GI (OR 10·4; 95 % CI 3·24, 33·3) and GL intakes (OR 6·68; 95 % CI 2·30, 19·4) than in the lowest quintiles among women with a BMI ≥ 25 kg/m2. However, there was no difference in risk across quintiles of carbohydrate, GI and GL among women with a BMI < 25 kg/m2. In conclusion, both the quantity and quality of carbohydrate intake has a positive relationship with the risk of the metabolic syndrome in women but this relationship was dependent on the BMI level.

Oxidative modification of LDL is thought to play an important role in the development of atherosclerosis. Susceptibility of LDL to peroxidation may partly depend on the compositional characteristics of the antioxidant and fatty acid content. The aim of this study was to examine the association between levels of antibodies to oxidized LDL and the various serum fatty acids in women. A total of 465 women aged 18–65 years were selected randomly from the adult population census of Pizarra, a town in southern Spain. Measurement of anti-oxidized-LDL was done by ELISA and the fatty acid composition of serum phospholipids was determined by GC. The levels of anti-oxidized-LDL antibodies were significantly related with age (r − 0·341, P < 0·001), BMI (r − 0·239, P < 0·001), waist:hip ratio (r − 0·285, P < 0·001), glucose (r − 0·208, P < 0·001), cholesterol (r − 0·243, P < 0·001), LDL-cholesterol (r − 0·185, P = 0·002), EPA (r − 0·159, P = 0·003), DHA (r − 0·121, P = 0·026), and the sum of the serum phospholipid n-3 PUFA (r − 0·141, P = 0·009). Multiple regression analysis showed that the variables that explained the behaviour of the levels of anti-oxidized-LDL antibodies were age (P < 0·001) and the serum phospholipid EPA (P < 0·001). This study showed that the fatty acid composition of serum phospholipids, and especially the percentage of EPA, was inversely related with the levels of anti-oxidized-LDL antibodies.

The calculation of body composition using bioelectrical impedance analysis in sick and hospitalized patients is hampered due to altered hydration state. We wanted to investigate how disease-related malnutrition assessed by the Subjective Global Assessment (SGA) is reflected in the bioelectrical impedance vector analysis. Patients with benign gastrointestinal disease (n 242) were entered in the study. Nutritional status was assessed by SGA. Arm muscle and fat area were estimated by anthropometry, muscle function was determined by hand grip strength. Whole body impedance measurements were made at 50 kHz. Ninety-eight patients were considered well nourished (SGA A), ninety-four were classified moderately malnourished (SGA B) and fifty patients were classified severely malnourished (SGA C) according to the SGA. The mean vector was significantly displaced between SGA C and SGA A and B, showing comparable resistance with a significantly reduced reactance, indicating comparable hydration but loss of dielectrical mass of soft tissues. This distinctive vector migration was not seen when studying the patients grouped according to BMI. In conclusion, disease-related malnutrition as assessed by the SGA is associated with a distinctive bioelectrical vector migration, implying that abnormal tissue structure and not reduced body mass only occurs in disease-related malnutrition. These disturbances are not seen in underweight according to BMI. Bioelectrical impedance vector analysis appears to be an attractive tool to identify disease-related malnutrition and to monitor nutritional intervention.

Previous studies with folate/methyl-deficient rat models proposed the role of folate deficiency in hepatocarcinogenesis and tumour progression. We investigated the relationship between folate status and tumour progression in patients with hepatocellular carcinoma (HCC). Ninety HCC patients (age 62 (sd 10) years) recruited through the Department of Internal Medicine, Chi-Mei Hospital, participated in this cross-sectional study. According to the clinical criteria, 44 % showed marginal folate deficiency (serum folate 7–14 nmol/l; folate intake 278 (sd 212) μg/d), and 16 % were folate deficient ( < 7 nmol/l; 207 (sd 113) μg/d). Serum folate showed inverse correlations with three elements of tumour progression: tumour size (r − 0·29; P = 0·005), tumour multiplicity (r − 0·24; P = 0·018) and metastasis (r − 0·39; P = 0·0001). When HCC progression was categorised into stages I to IV, serum folate decreased as HCC stage progressed (stage I, 24·5 (sd 11·5); stage IV, 10·3 (sd 3·3) nmol/l; P = 0·032). After adjustment for age, sex, lifestyle and dietary factors, patients with low blood folate status (serum folate < 14 nmol/l) had increased risks for advanced tumour progression in large tumours (OR 7·1 (95 % CI 2·27, 21·9); P = 0·0007), tumour multiplicity (OR 3·2 (95 % CI 1·07, 3·51); P = 0·004) and metastasis (OR 4·5 (95 % CI 1·11, 18·4); P = 0·03) relative to those with normal folate status. Further controlling for liver injury, tumour proliferation and tumour stage, however, negated the effect of folate on advanced tumour progression. The data thus suggest that low blood folate status could be a risk factor for tumour progression, which is modulated by clinical lesions present in HCC patients. Future studies with larger sample sizes are warranted to explore the joint effects of low folate and hepatic lesions in human HCC malignancy.

We evaluated whether plant stanol esters mixed with different vegetable oil spreads improved arterial health. A total of 200 adults with serum cholesterol >5 mmol/l were randomised to consume camelina, rapeseed or sunflower oil spread with stanol (2 g/d) ester or sunflower oil spread without stanol ester (controls) for 3 months. Non-invasive ultrasound was used to measure carotid artery compliance (CAC) and brachial artery flow-mediated endothelial dependent vasodilatation (FMD) at baseline and after the intervention as markers of arterial health. Plant stanol esters reduced LDL-cholesterol by 9 % compared with controls (P < 0·001) similarly in the different treatment groups. In the combined treatment groups (n 147), CAC or FMD were not changed from controls (n 47). In a subgroup analysis, division of subjects at baseline into below and over sex-specific 50th percentiles of CAC and FMD revealed that low CAC was improved from 1·23 to 1·59 % per 10 mmHg in the treatment group (n 69), and from 1·42 to 1·47 % per 10 mmHg in controls (n 25), (P = 0·0035 between groups). Low FMD was improved from 6·9 % to 8·6 % in the treatment group (n 73) and from 6·6 % to 6·8 % in controls (n 24) (P = 0·05 between groups). In the respective high-median groups, CAC and FMD were not changed in spite of significantly lowered LDL-cholesterol. In conclusion, consumption of plant stanol ester for 3 months had no overall significant effect on arterial elasticity and endothelial function. A controlled study is needed to test whether beneficial changes are obtained in subjects with initially reduced arterial elasticity and endothelial function.