The present review assesses the potential of the Phaseolus vulgaris α-amylase inhibitor isoform 1 (α-AI1) starch blockers as a widely used remedy against obesity and diabetes. Consumption of the α-amylase inhibitor causes marginal intraluminal α-amylase activity facilitated by the inhibitor's appropriate structural, physico-chemical and functional properties. As a result there is decreased postprandial plasma hyperglycaemia and insulin levels, increased resistance of starch to digestion and increased activity of colorectal bacteria. The efficacy and safety of the amylase inhibitor extracts, however, depend on the processing and extraction techniques used. The extracts are potential ingredients in foods for increased carbohydrate tolerance in diabetics, decreased energy intake for reducing obesity and for increased resistant starch. Research developments in the distribution and biosynthesis of the α-amylase inhibitor, relevant physico-chemical properties, the molecular starch-blocking mechanism, anti-obesity and anti-diabetes effects, safety of extracts and the need for research into their potential anti-colorectal cancer effect are discussed.

Trans-vaccenic acid (TVA) is a natural trans fatty acid found in ruminant food produce. It is converted to the cis-9, trans-11 isomer of conjugated linoleic acid (c9, t11-CLA) by the action of stearoyl-CoA desaturase (SCD) in tissue. c9, t11-CLA has been associated with anti-inflammatory effects and also affects lipid metabolism. The aim of the present study was to determine if TVA is bioconverted to c9, t11-CLA in intestinal epithelial cells and to ascertain whether TVA has effects similar to c9, t11-CLA on markers of inflammation relevant to inflammatory bowel disease. The present study demonstrated that TVA treatment led to significant bioconversion into c9, t11-CLA in Caco-2 cells. Treatment with both TVA and c9, t11-CLA resulted in alteration of cellular fatty acid profile and SCD activity in the Caco-2 cell line. However, CLA, but not TVA, significantly modulated transcription of TNF-α, IL-12, IL-6 and production of IL-12 by these cells. Thus the present study established that TVA treatment can alter SCD desaturation indices and induce compositional changes in the fatty acid profile of the Caco-2 cell model of the human intestinal epithelium but this is not associated with functional effects on markers of the inflammatory response.

Angiopoietin-like protein 4 (Angptl4)/FIAF (fasting-induced adipose factor) was first identified as a target for PPAR and to be strongly induced in white adipose tissue (WAT) by fasting. Here we have examined the regulation of the expression and release of this adipokine in mouse WAT and in 3T3-L1 adipocytes. Angptl4/FIAF expression was measured by RT-PCR and real-time PCR; plasma Angptl4/FIAF and release of the protein in cell culture was determined by western blotting. The Angptl4/FIAF gene was expressed in each of the major WAT depots of mice, the mRNA level in WAT being similar to the liver and much higher (>50-fold) than skeletal muscle. Fasting mice (18 h) resulted in a substantial increase in Angptl4/FIAF mRNA in liver and muscle (9·5- and 21-fold, respectively); however, there was no effect of fasting on Angptl4/FIAF mRNA in WAT and the plasma level of Angptl4/FIAF was unchanged. The Angptl4/FIAF gene was expressed in 3T3-L1 adipocytes before and after differentiation, the level increasing post-differentiation; Angptl4/FIAF was released into the culture medium. Insulin, leptin, dexamethasone, noradrenaline, TNFα and several IL (IL-1β, IL-6, IL-10, IL-18) had little effect on Angptl4/FIAF mRNA levels in 3T3-L1 adipocytes. However, a major stimulation of Angptl4/FIAF expression was observed with rosiglitazone and the inflammatory prostaglandins PGD2 and PGJ2. Angptl4/FIAF does not act as an adipose tissue signal of nutritional status, but is markedly induced by fasting in liver and skeletal muscle.

Anthocyanins are a class of flavonoids, widely spread throughout the plant kingdom, exhibiting important antioxidant and anti-inflammatory actions as well as chemotherapeutic effects; nonetheless, little is known about the molecular mechanisms by which these activities are exerted. The present study is aimed at investigating molecular mechanisms involved in the chemotherapeutic effects induced by both cyanidin-3-O-β glucopyranoside (CY3G) and its aglycon form, cyanidin chloride (CY), in human colon cancer cells (CaCo2). The effect on cell growth, reactive oxygen species (ROS) formation and cell cycle/stress proteins modification, including ataxia teleangectasia mutated protein (ATM), p53, p21, 8-oxoguanine DNA glycosylase (OGG1), 70 kDa heat shock protein (HSP70) and topoisomerase IIβ, as well as on DNA fragmentation, was determined. CY and CY3G treatment affect cell growth and cell proliferation, this latter in a moderately dose-dependent way. Interestingly, ROS level is decreased by any concentration of CY and, only at the lowest concentration, by CY3G. Moreover, the two molecules exert their activities increasing ATM, topoisomerase II, HSP70 and p53 expression. The analysis of DNA fragmentation by Comet assay evidences: (1) a dose-dependent increase in DNA damage only after treatment with CY3G; (2) a more evident trend in the DNA fragmentation when the treatment is performed on agarose embedded cells (cellular atypical Comet); (3) a highly dose-dependent DNA fragmentation induced by CY when the treatment is carried out on agarose embedded naked DNA (acellular atypical Comet). The present findings substantiate a possible chemotherapeutic role of anthocyanins and suggest that CY and CY3G act on CaCo2 by different mechanisms, respectively, ROS-dependent and ROS-independent.

We have previously reported the anticarcinogenic effects of an olive fruit extract composed of pentacyclic triterpenes, the main components of which are maslinic acid (73·25 %) and oleanolic acid (25·75 %). Here we examined the effects of the individual components on proliferation, necrosis and apoptosis rates by fluorescence-based techniques in human HT-29 colon cancer cells. Oleanolic acid showed moderate antiproliferative activity, with an ec50 of 160·6 (se 10·6) μmol/l, and moderate cytotoxicity at high concentrations ( ≥ 250 μmol/l). On the other hand, maslinic acid inhibited cell growth with an ec50 of 101·2 (se 7·8) μmol/l, without necrotic effects. Oleanolic acid, which lacks a hydroxyl group at the carbon 2 position, failed to activate caspase-3 as a prime apoptosis protease. In contrast, maslinic acid increased caspase-3-like activity at 10, 25 and 50 μmol/l by 3-, 3·5- and 5-fold over control cells, respectively. The detection of ROS in the mitochondria, which serve as pro-apoptotic signal, evidenced the different bioactivity of the two triterpenes. Confocal microscopy analysis revealed that maslinic acid generated superoxide anions while oleanolic acid-treated cells did not differ from the control. Completion of apoptosis by maslinic acid was confirmed microscopically by the increase in plasma membrane permeability, and detection of DNA fragmentation. In conclusion, the anticancer activity observed for olive fruit extracts seems to originate from maslinic acid but not from oleanolic acid. Maslinic acid therefore is a promising new compound for the chemoprevention of colon cancers.

The molecular basis of the positive association between apoE4 genotype and CVD remains unclear. There is direct in vitro evidence indicating that apoE4 is a poorer antioxidant relative to the apoE3 isoform, with some indirect in vivo evidence also available. Therefore it was hypothesised that apoE4 carriers may benefit from α-tocopherol (α-Toc) supplementation. Targeted replacement mice expressing the human apoE3 and apoE4 were fed with a diet poor (0 mg/kg diet) or rich (200 mg/kg diet) in α-Toc for 12 weeks. Neither apoE genotype nor dietary α-Toc exerted any effects on the antioxidant defence system, including glutathione, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase activities. In addition, no differences were observed in mitogen-induced lymphocyte proliferation. α-Toc concentrations were modestly higher in plasma and lower in tissues of apoE4 compared with apoE3 mice, with the greatest differences evident in the lung, suggesting that an apoE4 genotype may reduce α-Toc delivery to tissues. A tendency towards increased plasma F2-isoprostanes in apoE4 mice was observed, while liver thiobarbituric acid-reactive substances did not differ between apoE3 and apoE4 mice. In addition, C-reactive protein (CRP) concentrations were reduced in apoE4 mice indicating that this positive effect on CRP may in part negate the increased CVD risk associated with an apoE4 genotype.

Multiparous sows (n 17) were included in a controlled cross-over-study in order to investigate the influence of a natural source of conjugated linoleic acid (CLA) (alpine butter) on the milk fatty acid composition of lactating sows (as an animal model for lactating women) and on the growth performance of their progeny. The usual fat source of a standard lactation diet was replaced by either CLA-rich alpine butter or margarine (control diet). Compared with the margarine diet, feeding the alpine butter-supplemented diet increased (P < 0·001) the CLA concentration in the milk fat (742·3 (sd 272·0) v. 107·7 (sd 34·7) mg/100 g fat). Eleven of fourteen CLA isomers were higher (P ≤ 0·004) in milk fat after feeding the alpine butter-supplemented diet but the transfer was not proportional. The milk fat concentration of the sow milk and the level of SFA, MUFA and PUFA were not (P>0·05) affected. Growth performance of the progeny was similar for both dietary treatments. In summary, the findings show that adding alpine butter to the diet does not provoke a milk fat depression and does not alter the composition of total SFA, MUFA and PUFA in sow milk but increases its CLA concentration.

Ingestion of dietary protein is known to induce both insulin and glucagon secretion. These responses may be affected by the dose and the form (intact or hydrolysed) in which protein is ingested. The aim of the study was to investigate the effect of different amounts of intact protein and protein hydrolysate of a vegetable (soya) and animal (whey) protein on insulin and glucagon responses and to study the effect of increasing protein loads for both intact protein and protein hydrolysate in man. The study employed a repeated-measures design with Latin-square randomisation and single-blind trials. Twelve healthy non-obese males ingested three doses (0·3, 0·4 and 0·6 g/kg body weight) of intact soya protein (SPI) and soya protein hydrolysate (SPH). Another group of twelve healthy male subjects ingested three doses (0·3, 0·4 and 0·6 g/kg body weight) of intact whey protein (WPI) and whey protein hydrolysate (WPH). Blood was sampled before (t = 0) and 15, 30, 60, 90 and 120 min after protein ingestion for insulin, glucagon and glucose determination. SPI induced a higher total area under the curve for insulin and glucagon than SPH while no difference between WPI and WPH was found. Insulin and glucagon responses increased with increasing protein load for SPI, SPH, WPI and WPH, but the effect was more pronounced for glucagon. A higher dose of protein or its hydrolysate will result in a lower insulin:glucagon ratio, an important parameter for the control of postprandial substrate metabolism. In conclusion, insulin and glucagon responses were protein and hydrolysate specific.

Two feeding trials were conducted with pigs to determine the effects of blueberry supplementation on plasma lipid levels and other indices of cardiovascular benefit. In the first trial, where basal diets contained a high level of plant-based components (70 % soya, oats and barley), supplementation with 1, 2 and 4 % blueberries resulted in a decrease in total, LDL- and HDL-cholesterol. The greatest reduction was observed in the 2 % blueberry-fed pigs, where total, LDL- and HDL-cholesterol were reduced 11·7, 15·1 and 8·3 %, respectively. In the second trial where basal diets contained only 20 % (w/w) of soya, oats and barley, the lipid-modulating effect of blueberries was attenuated, so that supplementation with 1·5 % blueberries reduced total cholesterol by 8 %, which occurred only in pigs whose diets had been supplemented with cholesterol (0·08 %), NaCl (0·11 %) and fructose (9 %). In the first feeding trial, blueberry supplementation had no effect on blood platelet activity. Blueberry supplementation also had no effect on the susceptibility of leucocyte DNA to oxidation in the first trial and no effect on the susceptibility of LDL to oxidation in the second trial. Results of these two feeding trials are discussed in relation to the effects of basal diet composition on lipid-modulating effects of blueberries.

Effects of dietary α-lipoic acid on hepatic and serum lipid concentrations and the activity and mRNA levels of lipogenic enzymes were examined in rats. Rats were fed experimental diets containing varying amounts of lipoic acid (0, 1, 2·5, 5 g/kg) for 21 d. Lipoic acid profoundly decreased serum and liver concentrations of TAG, and also lowered serum concentrations of phospholipid and NEFA, and the concentration of cholesterol in the liver. A hypoglycaemic effect of this compound was also observed. Lipoic acid dose-dependently decreased the activity and mRNA levels of fatty acid synthase, ATP-citrate lyase, glucose 6-phosphate dehydrogenase, malic enzyme and pyruvate kinase in the liver despite that reductions were considerably attenuated in the NADPH-producing enzymes. This compound also dose-dependently lowered the mRNA levels of spot 14, adiponutrin, stearoyl-CoA desaturase 1, and Δ5- and Δ6-desaturases. In addition, lipoic acid dose-dependently lowered serum concentrations of insulin and leptin, but increased those of adiponectin. Lipoic acid appeared to reduce hepatic lipogenesis and hence decreases serum and liver lipid levels. Alterations in serum concentrations of insulin and (or) adiponectin may trigger this consequence.

The effect of feed protein type on body composition and growth has been examined. Evidence exists that whey protein concentrate is effective at limiting body fat expansion. The presence of caseinomacropeptide, a mixture of glycosylated and non-glycosylated carbohydrate residues, in particular glycomacropeptide (GMP) in whey protein concentrate may be important for this effect. The influence of whey protein isolate (WPI) and GMP on weight gain and body composition was examined by feeding Wistar rats ad libitum for 7 weeks with five semi-purified American Institute of Nutrition-based diets differing in protein type: (1) casein; (2) barbequed beef; (3) control WPI (no GMP); (4) WPI+GMP at 100 g/kg; (5) WPI+GMP at 200 g/kg. Body composition was assessed, and plasma samples were assayed for TAG, insulin and glucose. Body-weight gain was lower ( − 21 %) on the control WPI diet relative to casein, with a non-significant influence associated with GMP inclusion ( − 30 %), the effect being equivalent at both levels of GMP addition. Renal and carcass fat mass were reduced in the highest GMP diet when compared with WPI (P < 0·05). Plasma insulin was lowered by GMP at the highest addition compared with WPI alone ( − 53 %; P < 0·01). Plasma TAG in the WPI+GMP (200 g/kg) group were lower ( − 27 %; P < 0·05) than the casein and beef groups. In conclusion, GMP appears to have a significant additional influence when combined with WPI on fat accumulation. WPI alone appears to have the predominant influence accounting for 70 % of the overall effect on body-weight gain. Mechanisms for this effect have not been identified but food intake was not responsible.

Numerous studies have indicated that increased vulnerability to oxidative stress may be the main factor involved in functional declines during normal and pathological ageing, and that antioxidant agents, such as polyphenols, may improve or prevent these deficits. We examined whether 1-year administration of a cocoa polyphenolic extract (Acticoa powder), orally delivered at the dose of 24 mg/kg per d between 15 and 27 months of age, affects the onset of age-related cognitive deficits, urinary free dopamine levels and lifespan in old Wistar-Unilever rats. Acticoa powder improved cognitive performances in light extinction and water maze paradigms, increased lifespan and preserved high urinary free dopamine levels. These results suggest that Acticoa powder may be beneficial in retarding age-related brain impairments, including cognitive deficits in normal ageing and perhaps neurodegenerative diseases. Further studies are required to elucidate the mechanisms of cocoa polyphenols in neuroprotection and to explore their effects in man.

The objective of the present study was to characterise some important antioxidant enzymes and their relationships with retinoids and lipid peroxidation during rainbow trout (Oncorhynchus mykiss) early development. Eggs were incubated at 7°C until the swim-up stage whereupon fry were fed two semi-purified diets with 0 % (CO) and 8 % (OX) oxidised lipid respectively for 2 months at 17°C. The activities and gene expression of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) were determined as well as the levels of retinoids, F2-isoprostanes and lipid-soluble fluorescent products (LSFP) at various developmental stages. Only SOD had a detectable activity in embryos which increased during development and was linked with an increase of mitochondrial (SOD2) and cytosolic (SOD1) gene expression. SOD1 and SOD2 mRNA were more abundant in fry fed OX than in fry fed CO. CAT activity and gene expression also increased during development and were higher in fry fed OX compared with fry fed CO. Activity of Se-dependent GPX (Se-GPX) increased during development. The gene expression of cytosolic Se-GPX (GPX1) increased from hatching to 2-month-fed fry. Both phospholipid-hydroperoxide GPX and GPX1 genes were more expressed in fry fed OX than in fry fed CO. Retinoids decreased during development and, by 2 months, were lowered in fry fed OX compared with those fed CO. The levels of LSFP were higher in fry fed OX compared with fry fed CO. The present study demonstrates that antioxidant defence systems are active all through the development of rainbow trout and modulated by feeding oxidised lipid.

Animal studies suggest that conjugated linoleic acid (CLA) may modulate the immune response, while studies in healthy human subjects have shown little effect and results are controversial. However, the effects of CLA may be more prominent in situations of immune imbalance, such as allergy. We studied the effects of the natural CLA isomer, cis-9, trans-11-CLA, on allergy symptoms and immunological parameters in subjects with birch pollen allergy. In a randomised, placebo-controlled study, forty subjects (20–46 years) with diagnosed birch pollen allergy received 2 g CLA/d in capsules, which contained 65·3 % cis-9, trans-11-CLA and 8·5 % trans-10, cis-12-CLA (n 20), or placebo (high-oleic acid sunflower-seed oil) (n 20) for 12 weeks. The supplementation began 8 weeks before the birch pollen season and continued throughout the season. Allergy symptoms and use of medication were recorded daily. Lymphocyte subsets, cytokine production, immunoglobulins, C-reactive protein, lipid and glucose metabolism and lipid peroxidation were assessed before and after supplementation. The CLA group reported a better overall feeling of wellbeing (P < 0·05) and less sneezing (P < 0·05) during the pollen season. CLA supplementation decreased the in vitro production of TNF-α (P < 0·01), interferon-γ (P < 0·05) and IL-5 (P < 0·05). Total plasma IgE and birch-specific IgE concentrations did not differ between groups, whereas plasma IgA (P < 0·05), granulocyte macrophage colony-stimulating factor (P < 0·05) and eosinophil-derived neurotoxin (P < 0·05) concentrations were lower after CLA supplementation. Urinary excretion of 8-iso-PGF2α, a major F2-isoprostane (P < 0·01), and 15-keto-dihydro-PGF2α, a primary PGF2α metabolite (P < 0·05), increased in the CLA group. The results suggest that cis-9, trans-11-CLA has modest anti-inflammatory effects in allergic subjects.

Saponins are naturally occurring amphiphilic molecules and have been associated with many biological activities. The aim of the present study was to investigate whether soya saponins trigger the onset of soyabean-induced enteritis in Atlantic salmon (Salmo salar L.), and to examine if dietary soya saponins increase the epithelial permeability of the distal intestine in Atlantic salmon. Seven experimental diets containing different levels of soya saponins were fed to seawater-adapted Atlantic salmon for 53 d. The diets included a fishmeal-based control diet, two fishmeal-based diets with different levels of added soya saponins, one diet containing 25 % lupin kernel meal, two diets based on 25 % lupin kernel meal with different levels of added soya saponins, and one diet containing 25 % defatted soyabean meal. The effect on intestinal morphology, intestinal epithelial permeability and faecal DM content was examined. Fish fed 25 % defatted soyabean meal displayed severe enteritis, whereas fish fed 25 % lupin kernel meal had normal intestinal morphology. The combination of soya saponins and fishmeal did not induce morphological changes but fish fed soya saponins in combination with lupin kernel meal displayed significant enteritis. Increased epithelial permeability was observed in fish fed 25 % defatted soyabean meal and in fish fed soya saponin concentrate independent of the protein source in the feed. The study demonstrates that soya saponins, in combination with one or several unidentified components present in legumes, induce an inflammatory reaction in the distal intestine of Atlantic salmon. Soya saponins increase the intestinal epithelial permeability but do not, per se, induce enteritis.

Elderly individuals are more susceptible to gastrointestinal problems such as constipation than young adults. Furthermore, the common use of non-steroidal anti-inflammatory drugs (NSAID) among the elderly is known to further increase such gastrointestinal ailments. To describe the specific changes in elderly, intestinal microbes, their metabolites and immune markers were measured from faecal samples obtained from fifty-five elderly individuals (aged 68–88 years), using either NSAID or not, and fourteen young adults (aged 21–39 years). The faecal DM content increased with age but was significantly lower among the elderly NSAID users. The microbial metabolism was especially influenced by NSAID use and/or ageing, although fewer changes were observed in the composition of the microbial community, whilst the level of aerobes was increased in the elderly and the level of Clostridium coccoides–Eubacterium rectale reduced in the elderly NSAID users as compared with young adults. An increase in the concentrations of some branched SCFA and l-lactate but a decrease in some major SCFA concentrations were observed. Evidently, the decreased defecation frequency in the elderly directed colonic fermentation toward an unfavourable microbial metabolism but this was partially offset by the use of NSAID. Irrespective of the use of NSAID, the elderly subjects had significantly lower concentrations of faecal PGE2 than the young adults, reflecting possibly a reduced immune response. According to the present study more attention should be paid to the development of dietary products that seek to enhance bowel function, saccharolytic fermentation and immune stimulation in the elderly population.

Fermentation products, SCFA, particularly butyrate, are considered a sign of ‘good’ bowel health but the influence of bacterial population composition and diet on inter-individual difference in metabolites and colonic health is poorly understood. Faecal specimens were collected weekly from eight healthy human volunteers over 12 weeks. Dietary intake was self-reported and ten macronutrient factors were analysed at selected weekly periods. Faecal weight, pH and moisture were recorded, and SCFA concentrations were measured in all samples. From each specimen, DNA was prepared and eubacterial 16S rRNA gene PCR performed. Bacterial population profiles were captured by denaturing gradient gel electrophoresis (DGGE) of PCR products, and multivariate statistical analysis was performed. Faecal weight, pH and moisture varied widely within and between individuals. Average total SCFA concentrations over 12 weeks ranged from 36·9 to 144·4 mmol/kg in 48 h specimens and faecal butyrate concentrations ranged from 1·8 to 48·5 mmol/kg. Two individuals with butyrate concentrations below 10 mmol/kg were considered to be ‘low butyrate types’ and may represent an at-risk population for bowel health. Dietary fat, sugar and carbohydrate showed weak correlation with SCFA (R − 0·612, P = 0·015; R 0·607, P = 0·016; R 0·610, P = 0·016, respectively) and butyrate concentrations (R − 0·593, P = 0·02; R 0·504, P = 0·054; R 0·528, P = 0·043, respectively). Multivariate analysis of DGGE bacterial profiles demonstrated concise and repeated grouping of intra-individual samples, but these were combined with distinct inter-individual differences (analysis of similarities P < 0·001, R ≥ 0·99) The exact relationship of these SCFA values to the overall bacterial profiles and SCFA-producer bacterial groups was not direct nor linear.

The purpose of the present study was to evaluate the effect of Ramadan fasting on insulin sensitivity in subjects with the metabolic syndrome. Males (n 55; age 34·1 (sd 8·9) years) with the metabolic syndrome were studied. Blood pressure, waist circumference, body weight, HDL-cholesterol (HDL-C), TAG, fasting plasma glucose (FPG), fasting blood insulin and insulin resistance indices (quantitative insulin sensitivity check index (QUICKI), homeostasis model assessment of insulin resistance (HOMA-IR) and reciprocal index of HOMA-IR (1/HOMA-IR)) were evaluated before and after 30 d of Ramadan fasting (two meals at 12 h intervals). The dietary intake was estimated by 24 h recall before and after fasting. The total daily energy intake was decreased by 234·6 (sd 88·2) kJ/d in the fasting period (P = 0·005). 1/HOMA-IR, QUICKI and HDL-C were significantly increased (P = 0·005, P = 0·001 and P = 0·004) and FPG significantly decreased (P < 0·005) after fasting. Simple linear regression analysis demonstrated that HOMA-IR, 1/HOMA-IR and QUICKI were related to waist circumference after intervention (r 0·458, P < 0·001; r − 0·396, P < 0·05; r − 0·342, P < 0·05). In conclusion, the present study showed that the combined change in the number and timing of meals and portioning of the entire intake into only two meals per d may increase insulin sensitivity in subjects with the metabolic syndrome even when the decrease in energy consumption is minimal.

The study was conducted to determine the effectiveness of a modified Mini Nutritional Assessment (MNA) for assessing the nutritional status and predicting follow-up mortality of institutionalized elderly Taiwanese. The study was conducted in a large long-term care centre in central Taiwan. Trained interviewers assisted by the caregivers elicited sociodemographic data, healthcare and disease history, and answers to the MNA screen from each subject. One researcher performed all subjects' anthropometric measurements. Plasma albumin and cholesterol concentrations were determined. Results showed that the MNA without BMI, modified according to population-specific mid-arm circumference and calf circumference cut-points, effectively predicted the nutritional risk status of the elderly regardless of cognitive status. Substituting caregiver's assessments for self-viewed nutrition and health status (questions O and P of MNA) improved the predicting power of the tool in cognition-normal subjects. Results showed that 21·9 % of the elderly were malnourished, 59·2 % were at risk of malnutrition and 18·9 % were normal according to self-assessment whereas 14·2 % were malnourished, 59·2 % were at risk of malnutrition, and 26·6 % were normal according to caregiver's evaluation. The tool was also effective in predicting 12- and 6-month follow-up mortality in cognition-normal and cognition-impaired elderly, respectively. Results indicate that a population-specific MNA can effectively predict the nutritional status and 6-month follow-up mortality of elderly Taiwanese regardless of cognitive condition. Easier and wider application of the tool will enable early detection of emerging nutritional problems and timely intervention to prevent the development of severe malnutrition in the elderly.

Traditional cardiovascular risk factors are associated with endothelial dysfunction. The vascular endothelium plays a key role in local vascular tone regulation and can be modulated by dietary fat. We propose to determine the chronic effect of three diets with different fat compositions on postprandial endothelial function and inflammatory biomarkers. Twenty healthy men followed three 4-week diets in a randomised cross-over design: a Western diet, rich in saturated fat (22 % SFA, 12 % MUFA and 0·4 % α-linolenic acid (ALA), all fractions are % of energy); a Mediterranean diet, rich in MUFA ( < 10 % SFA, 24 % MUFA and 0·4 % ALA); a low-fat diet enriched in ALA ( < 10 % SFA, 12 % MUFA and 2 % ALA). At the end of each dietary period all subjects underwent a postprandial study. Plasma concentrations of lipid parameters, soluble intercellular cell-adhesion molecule-1, soluble vascular cell-adhesion molecule-1 (sVCAM-1), nitrates and nitrites (NOx) and endothelial function studied by laser Doppler were examined at 0, 2, 4, 6 and 8 h. The endothelium-dependent vasodilatory response was greater 4 h after the ingestion of the MUFA-rich diet than after the SFA or ALA low-fat diets (P = 0·031). The 4 h postprandial plasma sVCAM-1 levels were lower after the MUFA meals than after the ALA low-fat diet (P = 0·043). The bioavailability of NOx was higher following the MUFA diet than after the SFA and ALA low-fat diets (P = 0·027). We found no differences in the other parameters measured. Chronic ingestion of a Mediterranean diet avoids the postprandial deterioration of endothelial function associated with Westernised diets in healthy individuals.