Being the metabolic syndrome a multifactorial condition, it is difficult to find adequate experimental models to study this pathology. The obese Zucker rats, which are homozygous for the fa allele, present abnormalities similar to those seen in human metabolic syndrome and are a widely extended model of insulin resistance. The usefulness of these rats as a model of non-insulin-dependent diabetes mellitus is nevertheless questionable, and they neither can be considered a clear experimental model of hypertension. Some experimental models different from the obese Zucker rats have also been used to study the metabolic syndrome. Some derive from the spontaneously hypertensive rats (SHR). In this context, the most important are the obese SHR, usually named Koletsky rats. Hyperinsulinism, associated with either normal or slightly elevated levels of blood glucose, is present in these animals, but SHR/N-corpulent rats are a more appropriated model of non-insulin-dependent diabetes mellitus. The SHR/NDmc corpulent rats, a subline of SHR/N-corpulent rats, also exhibit metabolic and histopathologic characteristics associated with human metabolic disorders. A new animal model of the metabolic syndrome, stroke-prone–SHR (SHRSP) fatty rats, was obtained by introducing a segment of the mutant leptin receptor gene from the Zucker line heterozygous for the fa gene mutation into the genetic background of the SHRSP. Very recently, it has been developed as a non-obese rat model with hypertension, fatty liver and characteristics of the metabolic syndrome by transgenic overexpression of a sterol-regulatory element-binding protein in the SHR rats. The Wistar Ottawa Karlsburg W rats are also a new strain that develops a nearly complete metabolic syndrome. Moreover, a new experimental model of low-capacity runner rats has also been developed with elevated blood pressure levels together with the other hallmarks of the metabolic syndrome.

The association between trans-fatty acids (TFA) and cancer risk is poorly understood and remains controversial. It is recognised that unique biological effects are associated with specific isoforms within families of fatty acids such as those belonging to the n-3 fatty acids. Furthermore, the interactions between diet and genetic polymorphisms are increasingly recognised for their potential risk-modifying effects on human health and disease. Therefore, the aim of the present review is to evaluate whether specific TFA isomers and genetic polymorphisms differentially modify cancer risk in prostate, colon and breast cancers in animal and human models. Potential mechanisms of action by which TFA may affect cancer development are also reviewed. Overall, across a number of experimental models and human studies, there is insufficient and inconsistent evidence linking specific TFA isomers to cancers of the prostate, colon and breast. A number of methodological limitations and experimental considerations were identified which may explain the inconsistencies observed across these studies. Therefore, further research is warranted to accurately assess the relationship between TFA and cancer risk.

There is interest in the degree to which fats in dairy foods contribute to CHD. We undertook a systematic review to investigate the effect of dairy consumption on CHD using prospective cohort studies. A systematic search of electronic databases identified studies relating dairy food intake in adulthood to episodes or death from CHD, IHD and myocardial infarction. Included studies were assessed for quality based on study methodology, validity of dietary assessment, success of follow-up, standardised assessment of CHD, IHD or myocardial infarction end points and appropriateness of statistical adjustment. Data from twelve cohorts involving >280 000 subjects were included. Most studies had follow-up of >80 %, adjusted statistically for three or more confounders and used standard criteria to determine end points. About half the studies used a validated FFQ, administered the FFQ more than once or had follow-up of >20 years. Fewer than half the studies involved subjects representative of the general population. Four of the twelve cohorts found no association between dairy intake and CHD. Eight studies reported varying relationships between different dairy foods and CHD or differential associations based on race, sex or over time. Although dairy foods contribute to the SFA composition of the diet, this systematic review could find no consistent evidence that dairy food consumption is associated with a higher risk of CHD. This could be due to the limited sensitivity of the dietary assessment methods to detect an effect of a single food in a mixed diet on complex clinical outcomes.

Deoxynivalenol (DON) is a toxic fungal metabolite found on wheat, maize and barley. We previously reported a significant association between the amount of DON in a single 24 h urine sample and the average cereal intake over 7 d for 300 UK adults. In this more detailed analysis of the data, food diary information (n 255) for the day of urine collection (model I), the previous 24 h period (model II) and the day of urine collection plus the previous 24 h combined (model III) were further examined to assess whether the recent intake of cereal correlated more strongly with urinary DON, compared with the longer-term assessment of usual cereal intake from 7 d food diaries (model IV). DON was detected in 254/255 (99·6 %) urine samples (mean 12·0 μg/d; range not detected–66 μg/d). For all the models, total cereal intake was positively associated with urinary DON (P < 0·001) in each model. The goodness of fit (adjusted R2 value) was used to assess how well each model explained the variation in urinary DON. Model I provided a better goodness of fit (adjusted R2 0·22) than model IV (adjusted R2 0·19), whereas model III provided the best fit (adjusted R2 0·27). These data suggest that the inter-individual variation in urinary DON was somewhat better explained by recent cereal intake compared with usual cereal intake assessed over 7 d.

Peroxidised phospholipid-mediated cytotoxity is involved in the pathophysiology of many diseases; for example, phospholipid hydroperoxides (PLOOH) are abnormally increased in erythrocytes of dementia patients. Dietary carotenoids (especially xanthophylls, polar carotenoids such as lutein) have gained attention as potent inhibitors against erythrocyte phospholipid hydroperoxidation, thereby making them plausible candidates for preventing diseases (i.e. dementia). To evaluate these points, we investigated whether orally administered lutein is distributed to human erythrocytes, and inhibits erythrocyte PLOOH formation. Six healthy subjects took one capsule of food-grade lutein (9·67 mg lutein per capsule) once per d for 4 weeks. Before and during the supplementation period, carotenoids and PLOOH in erythrocytes and plasma were determined by our developed HPLC technique. The administered lutein was incorporated into human erythrocytes, and erythrocyte PLOOH level decreased after the ingestion for 2 and 4 weeks. The antioxidative effect of lutein was confirmed on erythrocyte membranes, but not in plasma. These results suggest that lutein has the potential to act as an important antioxidant molecule in erythrocytes, and it thereby may contribute to the prevention of dementia. Therefore future biological and clinical studies will be required to evaluate the efficacy as well as safety of lutein in models of dementia with a realistic prospect of its use in human therapy.

Sodium butyrate (SB) provided orally favours body growth and maturation of the gastrointestinal tract (GIT) in milk-fed pigs. In weaned pigs, conflicting results have been obtained. Therefore, we hypothesised that the effects of SB (3 g/kg DM intake) depend on the period (before v. after weaning) of its oral administration. From the age of 5 d, thirty-two pigs, blocked in quadruplicates within litters, were assigned to one of four treatments: no SB (control), SB before (for 24 d), or after (for 11–12 d) weaning and SB before and after weaning (for 35–36 d). Growth performance, feed intake and various end-point indices of GIT anatomy and physiology were investigated at slaughter. The pigs supplemented with SB before weaning grew faster after weaning than the controls (P < 0·05). The feed intake was higher in pigs supplemented with SB before or after weaning (P < 0·05). SB provided before weaning improved post-weaning faecal digestibility (P < 0·05) while SB after weaning decreased ileal and faecal digestibilities (P < 0·05). Gastric digesta retention was higher when SB was provided before weaning (P < 0·05). Post-weaning administration of SB decreased the activity of three pancreatic enzymes and five intestinal enzymes (P < 0·05). IL-18 gene expression tended to be lower in the mid-jejunum in SB-supplemented pigs. The small-intestinal mucosa was thinner and jejunal villous height lower in all SB groups (P < 0·05). In conclusion, the pre-weaning SB supplementation was the most efficient to stimulate body growth and feed intake after weaning, by reducing gastric emptying and intestinal mucosa weight and by increasing feed digestibility.

The effects of dietary supplementation with fat of different fatty acid profile and chronic intermittent hypoxia (CIH) on the fatty acid composition of serum and heart lipids were analysed. Adult male Wistar rats were fed a standard non-fat diet enriched with 10 % of lard, fish oil (n-3 PUFA) or maize oil (n-6 PUFA) for 10 weeks. After 4 weeks on the diets, each group was divided in two subgroups, either exposed to CIH in a barochamber (7000 m, twenty-five exposures) or kept at normoxia. In normoxic rats, the fish oil diet increased the level of conjugated dienes. The n-6:n-3 PUFA ratio in serum TAG, phospholipids (PL), cholesteryl esters (CE) and heart TAG, PL and diacylglycerols (DAG) followed the ratio in the fed diet (in the sequence maize oil>lard>fish oil). In heart TAG, PL and DAG, 20 : 4n-6 and 18 : 2n-6 were replaced by 22 : 6n-3 in the fish oil group. The main fatty acid in CE was 20 : 4n-6 in the lard and maize oil groups whereas in the fish oil group, half of 20 : 4n-6 was replaced by 20 : 5n-3. CIH further increased 20 : 5n-3 in CE in the fish oil group. CIH decreased the n-6:n-3 PUFA ratio in serum CE, heart TAG, PL and DAG in all dietary groups and stimulated the activity of catalase in the maize and fish oil groups. In conclusion, PUFA diets and CIH, both interventions considered to be cardioprotective, distinctly modified the fatty acid profile in serum and heart lipids with specific effects on conjugated diene production and catalase activity.

Mitigation of methanogenesis in ruminants has been an important goal for several decades. Free lauric acid, known to suppress ruminal methanogenesis, has a low palatability; therefore, in the present study the aim was to evaluate the mitigation efficacy of its esterified form (monolaurin). Further, 13C-isotope abundance (δ13C) and 13C–12C fractionation during methanogenesis and fermentation were determined to evaluate possible microbial C-isotope preferences. Using the rumen simulation technique, four basal diets, characterised either by the C3 plants grass (hay) and wheat (straw and grain), or the C4 plant (13C excess compared with C3 plants) maize (straw and grain), and a mixture of the latter two, were incubated with and without monolaurin (50 g/kg dietary DM). Added to hay, monolaurin did not significantly affect methanogenesis. When added to the other diets (P < 0·05 for the wheat-based diet) methane formation was lowered. Monolaurin decreased fibre disappearance (least effect with the hay diet), acetate:propionate ratio, and protozoal counts. Feed residues and SCFA showed the same δ13C as the diets. Methane was depleted in 13C while CO2 was enriched in 13C compared with the diets. Monolaurin addition resulted in 13C depletion of CO2 and enrichment in CH4 (the latter only in the hay diet). In conclusion, monolaurin proved to effectively decrease methanogenesis in the straw–grain diets although this effect might partly be explained by the concomitantly reduced fibre disappearance. The influence on 13C-isotope abundance and fractionation supports the hypothesis that ruminal microbes seem to differentiate to some extent between C-isotopes during methanogenesis and fermentation.

A dog's nutrient requirements can theoretically be met from a properly balanced meat-free diet; however, proof for this is lacking. Exercise places additional demands on the body, and dogs fed a meat-free diet may be at increased risk of developing sports anaemia. We hypothesised that exercising dogs would remain in good health and not develop anaemia when fed a nutritionally balanced meat-free diet. To this end, twelve sprint-racing Siberian huskies were fed either a commercial diet recommended for active dogs (n 6), or a meat-free diet formulated to the same nutrient specifications (n 6). The commercial diet contained 43 % poultry meal, whereas soyabean meal and maize gluten made up 43 % of the meat-free diet, as the main protein ingredients. Dogs were fed these diets as their sole nutrient intake for 16 weeks, including 10 weeks of competitive racing. Blood samples were collected at weeks 0, 3, 8 and 16, and veterinary health checks were conducted at weeks 0, 8 and 16. Haematology results for all dogs, irrespective of diet, were within normal range throughout the study and the consulting veterinarian assessed all dogs to be in excellent physical condition. No dogs in the present study developed anaemia. On the contrary, erythrocyte counts and Hb values increased significantly over time (P < 0·01) in both groups of dogs. The present study is the first to demonstrate that a carefully balanced meat-free diet can maintain normal haematological values in exercising dogs.

We evaluated the effects of long-term daily cows' milk (CM) administration on insulin resistance induced by a high-sucrose diet. F344 rats, aged 3 weeks, were divided into two groups according to diet (dextrin-fed v. sucrose-fed). These groups were further divided into two groups receiving either CM or artificial milk (AM; isoenergetic emulsion of egg white protein, maltose, lard and minerals). Rats were fed a sucrose- or dextrin-based diet for 7 weeks and orally administered CM or AM at 25 ml/kg following an 8 h fast on a daily basis. Insulin sensitivity was evaluated via postprandial changes in serum glucose and insulin, oral glucose tolerance tests, and fasting serum insulin and fructosamine concentrations. The sucrose-fed rats showed an overall decrease in insulin sensitivity, but postprandial insulin levels were lower in the CM-treated subgroup than in the AM-treated subgroup. Peak serum glucose and insulin concentrations were highest in the sucrose-fed rats, but CM administration reduced peak glucose and insulin values in comparison with AM administration. By area under the curve analysis, insulin levels after feeding and glucose loads were significantly lower in the CM-treated groups than in the AM-treated groups. The CM-treated groups also demonstrated lower fasting insulin and fructosamine levels than the AM-treated groups. Improved insulin sensitivity due to CM administration seemed to be associated with reduced duodenal GLUT2 mRNA levels and increased propionate production within the caecum.

Measurement of fatty acids in biological fluids and cell membranes including leucocytes from multiple sclerosis patients is inconsistent. The objective of the present study was to investigate the fatty acid composition within the different membrane phospholipid fractions in peripheral blood mononuclear cells in multiple sclerosis patients, and correlate with severity of neurological outcome as measured by the Kurtzke Expanded Disability Status Scale and Functional System Scores. The fatty acid composition of phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, sphingomyelin and phosphatidylinositol phospholipids in the peripheral blood mononuclear cells of twenty-six multiple sclerosis and twenty-five control subjects were measured by GC, and C-reactive protein was measured in all subjects. The elongation product of 20 : 4n-6, 22 : 4n-6, was significantly decreased in membrane phosphatidylethanolamine and phosphatidylserine in multiple sclerosis patients (P = 0·01 and P = 0·03 respectively), and correlated inversely with severity of disease and C-reactive protein. Also an inverse correlation was observed between the C-reactive protein and membrane phosphatidylcholine and phosphatidylserine 20 : 4n-6. Cultural and ethnic differences, as well as dietary variability, especially in a diseased state have been implicated in the differences observed in the fatty acid composition in peripheral blood mononuclear cell membranes of patients with multiple sclerosis. The present results suggest that the disease state may in part explain the reported inconsistencies in fatty acid levels in multiple sclerosis patients.

Both K and Ca supplementation may have beneficial effects on bone through separate mechanisms. K in the form of citrate or bicarbonate affects bone by neutralising the acid load caused by a high protein intake or a low intake of alkalising foods, i.e. fruits and vegetables. Ca is known to decrease serum parathyroid hormone (S-PTH) concentration and bone resorption. We compared the effects of calcium carbonate, calcium citrate and potassium citrate on markers of Ca and bone metabolism in young women. Twelve healthy women aged 22–30 years were randomised into four controlled 24 h study sessions, each subject serving as her own control. At the beginning of each session, subjects received a single dose of calcium carbonate, calcium citrate, potassium citrate or a placebo in randomised order. The diet during each session was identical, containing 300 mg Ca. Both the calcium carbonate and calcium citrate supplement contained 1000 mg Ca; the potassium citrate supplement contained 2250 mg K. Markers of Ca and bone metabolism were followed. Potassium citrate decreased the bone resorption marker (N-terminal telopeptide of type I collagen) and increased Ca retention relative to the control session. Both Ca supplements decreased S-PTH concentration. Ca supplements also decreased bone resorption relative to the control session, but this was significant only for calcium carbonate. No differences in bone formation marker (bone-specific alkaline phosphatase) were seen among the study sessions. The results suggest that potassium citrate has a positive effect on the resorption marker despite low Ca intake. Both Ca supplements were absorbed well and decreased S-PTH efficiently.

Females perform better in certain memory-related tasks than males. Sex differences in cognitive performance may be attributable to differences in circulating oestrogen acting on oestrogen β receptors (ERβ) which are prevalent in brain regions such as the hippocampus, frontal lobe and cortex that mediate cognitive functions. Since soya isoflavones are known to activate ERβ, chronic isoflavone supplementation in males may improve cognitive performance in memory-related tasks. A 12-week double-blind, placebo-controlled cross-over trial was conducted in thirty-four healthy men to investigate the effect of isoflavone supplementation on cognitive function. Volunteers were randomised to take four capsules/d containing soya isoflavones (116 mg isoflavone equivalents/d: 68 mg daidzein, 12 mg genistein, 36 mg glycitin) or placebo for 6 weeks, and the alternate treatment during the following 6 weeks. Assessments of memory (verbal episodic, auditory and working), executive function (planning, attention, mental flexibility) and visual-spatial processing were performed at baseline and after each treatment period. Isoflavone supplementation significantly improved spatial working memory (P = 0·01), a test in which females consistently perform better than males. Compared with placebo supplementation, there were 18 % fewer attempts (P = 0·01), 23 % fewer errors (P = 0·02) and 17 % less time (P = 0·03) required to correctly identify the requisite information. Isoflavones did not affect auditory and episodic memory (Paired Associate Learning, Rey's Auditory Verbal Learning Task, Backward Digit Span and Letter-Number Sequencing), executive function (Trail Making and Initial Letter Fluency Task) or visual-spatial processing (Mental Rotation Task). Isoflavone supplementation in healthy males may enhance cognitive processes which appear dependent on oestrogen activation.

The risk of CHD has been linked to n-3 and trans-fatty acids. The purpose of the present study was to evaluate the hypothesis that lower n-3 fatty acids and higher trans-fatty acids in erythrocytes are associated with an increased risk of acute non-fatal myocardial infarction (MI), and that fatty acid profiles can discriminate MI cases from controls. Fifty cases with acute non-fatal MI and fifty age- and sex-matched controls without MI were recruited. The Omega-3 Index (the sum of EPA and DHA in erythrocytes) was significantly lower in cases than controls (9·57 (sem 0·28) v. 11·81 (sem 0·35) %; P < 0·001), while total trans-fatty acids were significantly higher (1·01 (sem 0·04) v. 0·56 (sem 0·03) %; P < 0·001). The Omega-3 Index was associated with decreased risk of MI (OR 0·08 (95 % CI 0·02, 0·38); P = 0·001), while total trans-fatty acids were associated with an increased risk of MI (OR 72·67 (95 % CI 6·68, 790·74); P < 0·001). The area under the receiver operating characteristic curve of fatty acid profiles was larger than that for traditional risk factors, suggesting that fatty acid profiles make a higher contribution to the discrimination of MI cases from controls compared with modified Framingham risk factors. In conclusion, a higher Omega-3 Index and lower trans-fatty acids in erythrocytes are associated with a decreased risk of MI. Furthermore, fatty acid profiles improve discrimination of acute non-fatal MI compared with established risk factors.

Adverse sensory changes prevent the addition of highly bioavailable ferrous sulfate (FeSO4) to most wheat flours. Poorly absorbable reduced Fe powders are commonly used. Encapsulation of FeSO4 can overcome these sensory changes, but the particle size of commercial compounds is too large to be used by flour mills. The first objective of the study was to measure the efficacy in wheat flour of two newly developed Fe compounds, an H-reduced Fe powder (NutraFine™ RS; North America Höganäs High Alloys LLC, Johnstown, PA, USA) and small particle-sized (40 μm) encapsulated FeSO4. As a second objective, the microcapsules were evaluated as a vehicle for iodine fortification. A randomised, double-blind controlled intervention trial was conducted in Kuwaiti women (n 279; aged 18–35 years) with low body Fe stores (serum ferritin (SF) < 25 μg/l) randomly assigned to one of three groups (20 mg Fe as NutraFine™ RS, 10 mg Fe as encapsulated FeSO4 and 150 μg iodine, or no fortification Fe) who consumed wheat-based biscuits 5 d per week. At baseline and 22 weeks, Hb, SF, transferrin receptor, urinary iodine and body Fe stores were measured. Relative to control, mean SF in the encapsulated FeSO4 group increased by 88 % (P < 0·001) and body Fe stores increased from − 0·96 to 2·24 mg/kg body weight (P < 0·001), while NutraFine™ RS did not significantly increase SF or body Fe stores. The median urinary iodine concentration increased from 140 to 213 μg/l (P < 0·01). NutraFine™ RS added at double the amount of Fe as FeSO4 was not efficacious in improving Fe status. The newly developed microcapsules were highly efficacious in improving both Fe stores and iodine status.

The objective of the present study was to investigate the relationship between plasma n-3 PUFA composition and weight status. A total of 124 adults, stratified by weight status: healthy weight (n 21), overweight (n 40) and obese (n 63) were recruited. Fasting blood samples, anthropometric measures and body composition were collected. Plasma fatty acid composition was determined by GC. BMI, waist circumference and hip circumference were inversely correlated with n-3 PUFA, EPA and DHA (P < 0·05 for all) in the obese group. Obese individuals had significantly lower plasma concentrations of total n-3 PUFA, compared with healthy-weight individuals (4·53 (sd 1·11) v. 5·25 (sd 1·43) %). When subjects were pooled and stratified into quartiles of total n-3 PUFA, a significant inverse trend was found for BMI (P = 0·002), waist circumference and hip circumference (P = 0·01 and P < 0·001 respectively). Higher plasma levels of total n-3 PUFA are associated with a healthier BMI, waist circumference and hip circumference. Our findings suggest that n-3 PUFA may play an important role in weight status and abdominal adiposity.

Taste is a major determinant of children's food preferences, but its development is incompletely known. Thus, exploring infants' acceptance of basic tastes is necessary. The first objective was to evaluate the acceptance of tastes and their developmental changes over the first year. The second objective was to compare acceptance across tastes. The third objective was to evaluate global taste reactivity (within-subject variability of acceptance across tastes). Acceptance of sweet, salty, bitter, sour and umami tastes was assessed in three groups of forty-five 3-, 6- and 12-month-old infants using observations based on ingestion and liking scored by the experimenter. For each taste, four bottles were presented (water, tastant, tastant, water). Acceptance of each taste relative to water was defined using proportional variables based on ingestion or liking. Acceptance over the first year only evolved for sweet taste (marginal decrease) and salty taste (clear increase). At each age, sweet and salty tastes were the most preferred tastes. Reactions to umami were neutral. Sour and bitter tastes were the least accepted ones but rejected only when considering liking data. Ingestion and liking were complementary to assess taste acceptance. However, congruency between these measures rose during the first year. Moreover, with increasing age, reactions were more and more contrasted across tastes. Finally, during the first year, inter-individual variability increased for all tastes except salty taste. By enhancing knowledge of the development of taste acceptance the present study contributes to understand better food behaviour in infancy, the foundation of food behaviour in adulthood.