The effect of wheat and rye breads made from white wheat flour with added refined fibre (WFL), whole-wheat grain, wheat aleurone flour (WAF) or rye aleurone flour (RAF) on digestion and fermentation processes in the gut was studied in a model experiment with pigs. The diets were similar in dietary fibre (DF) but differed in arabinoxylan (AX) content and composition. Twenty pigs were fed the breads three times daily (08.00, 13.00 and 18.00 hours) and the digesta collected through a T-cannula for two successive periods (breakfast: 8.00–13.00; lunch: 13.00–18.00 hours). Faeces were collected for 24 h and caecal and colonic contents at slaughter. The rigid nature of the aleurone cell walls encapsulated nutrients, which resulted in reduced (P < 0·01) digestibility of protein (WAF and RAF breads) and fat (RAF bread). For the RAF bread, the digestibility of starch was also lower (P < 0·001) than of the wheat-based diets primarily due to the higher intestinal viscosity. The DF composition had an impact on (P < 0·001) the site for fibre degradation in the large intestine. Thus, AX of the WAF bread, with the lowest degree of substitution, were fermented as much in the caecum as in the colon, whereas AX of the RAF bread, with an intermediary degree of substitution, were mainly fermented in the caecum. The WFL bread, rich in cellulose, was fermented more distally. Fermentation of experimental breads in the large intestine had no effect (P>0·05) on the production of metabolites, except for butyrate which was higher (P < 0·01) after the WAF bread consumption.

Extrusion is used to decrease leguminous seed protein degradability in the rumen in order to shift part of the dietary protein digestion towards the small intestine. The effect of such displacement of digestion site on the partitioning of nutrient net fluxes across the gastrointestinal tract was studied using four sheep fitted with catheters and blood-flow probes, allowing measurements across the rumen, the mesenteric-drained viscera (MDV) and the portal-drained viscera (PDV). Two diets containing 34 % of pea seeds were tested in a crossover design. They differed only according to pea treatment: raw pea (RP) or extruded pea (EP) diet. Rumen undegradable protein (RUP) accounted for 23 and 40 % of dietary crude protein for RP and EP diets, respectively. Across the rumen wall, ammonia net flux was lower with EP diet, whereas urea net flux was not different. Across the MDV, free amino acid (FAA) net flux was greater with EP diet, whereas peptide amino acid net flux was not different, accounting for 7 % of the non-protein amino acid net release. From RP to EP diet, PDV net flux of ammonia decreased by 23 %, whereas FAA net release increased by 21 %. The difference in dietary RUP did not affect the PDV net flux of SCFA, 3-hydroxybutyrate, lactate and glucose. In conclusion, the partial shift in pea protein digestion from the rumen to the small intestine did not affect the portal net balance of N, but decreased N loss from the rumen, and increased amino acid intestinal absorption and portal delivery.

Fe deficiency is a public-health problem worldwide, and effective measures for preventing Fe deficiency are needed. The aim of the present study was to determine the bioavailability of Fe in cocoa using the Hb regeneration efficiency (HRE) method. Thirty-five F344/N male weanling rats were fed a low-Fe diet for 4 weeks to deplete body Fe stores. Then, four groups of seven animals each were repleted for 20 d using a modified AIN-93G diet fortified with ferrous sulphate, ferric citrate or two brands of cocoa powder to provide a total dietary Fe concentration of 20 mg/kg. As a negative control, seven rats were maintained on the low-Fe diet. The HRE were 0·733, 0·350, 0·357 and 0·336 for ferrous sulphate, ferric citrate and the two brands of cocoa powder, respectively. The relative biological values (RBV), defined as the ratio of the sample HRE to that of ferrous sulphate, were 0·478, 0·488 and 0·459 for ferric citrate and the two brands of cocoa powder, respectively. The Fe bioavailability of cocoa was significantly less than that of ferrous sulphate and was similar to that of ferric citrate. The difference in Fe bioavailability between the two brands of cocoa powder was negligible. When the negative control was used to correct the data, estimates of the RBV derived from Hb gain were similar to those derived from the HRE. These results suggest that cocoa is a significant source of moderately bioavailable Fe.

The European micronutrient recommendations aligned (EURRECA) Network of Excellence seeks to establish clear guidelines for assessing the validity of reported micronutrient intakes among vulnerable population groups. A systematic literature review identified studies validating the methodology used in elderly people for measuring usual dietary micronutrient intake. The quality of each validation study selected was assessed using a EURRECA-developed scoring system. The validation studies were categorised according to whether the reference method applied reflected short-term intake ( < 7 d), long-term intake ( ≥ 7 d) or used biomarkers (BM). A correlation coefficient for each micronutrient was calculated from the mean of the correlation coefficients from each study weighted by the quality of the study. Thirty-three papers were selected, which included the validation of twenty-five different FFQ, six diet histories (DH), one 24-h recall (24HR) and a videotaped dietary assessment method. A total of five publications analysed BM, which were used to validate four FFQ, and one 24HR, presenting very good correlations only for vitamin E. The analysis of weighted correlation coefficients classified by FFQ or DH showed that most of the micronutrients had higher correlations when the DH was used as the dietary method. Comparing only FFQ results showed very good correlations for measuring short-term intakes of riboflavin and thiamin and long-term intakes of P and Mg. When frequency methods are used for assessing micronutrient intake, the inclusion of dietary supplements improves their reliability for most micronutrients.

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.

We evaluated the effects of partly substituting lard with marine n-3 fatty acids (FA) on body composition and weight, adipose tissue distribution and gene expression in five adipose depots of male Wistar rats fed a high-fat diet. Rats were fed diets including lard (19·5 % lard) or n-3 FA (9·1 % lard and 10·4 % Triomar™) for 7 weeks. Feed consumption and weight gain were similar, whereas plasma lipid concentrations were lower in the n-3 FA group. Magnetic resonance imaging revealed smaller visceral (mesenteric, perirenal and epididymal) adipose depots in the n-3 FA-fed animals (35, 44 and 32 % reductions, respectively). n-3 FA feeding increased mRNA expression of cytokines as well as chemokines in several adipose depots. Expression of Adipoq and Pparg was enhanced in the mesenteric adipose depots of the n-3 FA-fed rats, and fasting plasma insulin levels were lowered. Expression of the lipogenic enzymes Acaca and Fasn was increased in the visceral adipose depots, whereas Dgat1 was reduced in the perirenal and epididymal depots. Cpt2 mRNA expression was almost doubled in the mesenteric depot and liver. Carcass analyses showed similar body fat (%) in the two feeding groups, indicating that n-3 FA feeding led to redistribution of fat away from the visceral compartment.

Vitamin K contributes to bone health, probably through its role as cofactor in the carboxylation of osteocalcin. Intervention studies in adults have demonstrated that markedly higher osteocalcin carboxylation is obtained by intakes of vitamin K well above the current recommended dietary intake. However, the relationship between increased vitamin K2 intake and enhanced osteocalcin carboxylation has never been shown in healthy children. The objective was to study the effect of 45 μg menaquinone-7 (MK-7; one of the vitamin K2 species) on the circulating levels of undercarboxylated osteocalcin (ucOC) and carboxylated osteocalcin (cOC) in healthy prepubertal children. We hypothesised that MK-7 supplementation will reduce the ucOC:cOC ratio (UCR), indicating an improved vitamin K status. The present study is a double-blind randomised placebo-controlled trial examining the effect of 8 weeks MK-7 supplementation on the carboxylation of osteocalcin in healthy children (n 55). Serum levels of ucOC, cOC and MK-7 were measured at baseline and after 8 weeks, together with bone markers and coagulation parameters. The UCR was used as an indicator of vitamin K status. In the MK-7-supplemented group (n 28), the circulating concentration of inactive ucOC reduced and the UCR improved whereas the concentration of MK-7 increased. Within the placebo group, ucOC, cOC, UCR and MK-7 did not significantly change over time. In both groups, bone markers and coagulation parameters remained constant over time. These findings demonstrate that in healthy, prepubertal children, modest supplementation with MK-7 increases circulating concentrations of MK-7 and increases osteocalcin carboxylation.

Conjugated linoleic acid (CLA) has been reported to exert beneficial physiological effects on body composition and the immune system. However, little information is available on the influence of CLA on immune function during early life periods. The present study evaluates the effect of feeding an 80:20 mixture of cis-9, trans-11- and trans-10, cis-12-CLA isomers during gestation and suckling on the systemic immune response of weaned Wistar rats. Pups received dietary CLA from dams through the placental barrier and during suckling by breast milk (group A) or by oral administration (group B). Pups from group C only received CLA during suckling by oral administration. Group D constituted the reference group. Milk from dams fed the CLA diet had a high content of CLA and higher IgA and IgG concentrations than rats fed the standard diet. The plasma of pups from groups A, B and C showed six, twelve and nine times higher content of the cis-9, trans-11-CLA isomer than that of the group D pups. Rats from group A exhibited higher serum IgG concentrations than rats from the rest of the groups (22·14 (sem 2·14) v. about 5 mg/ml; P < 0·05), whereas rats from groups A and B showed approximately 2-fold higher splenocyte IgM production than rats from groups C and D. However, CLA supplementation did not influence significantly the splenocyte proliferative response or cytokine secretion. Supplementation during gestation and suckling with an 80:20 cis-9, trans-11–trans-10, cis-12 CLA mix enhances the production of the main in vivo and in vitro Ig isotypes in Wistar rats.

The present study investigated the effect of parenteral glutamine (Gln) supplementation on cellular adhesion molecule expression and release of chemokines responsible for inflammatory cell recruitment in rats undergoing a total gastrectomy. Normal rats with internal jugular catheters were assigned to one control group and two experimental groups and received total parenteral nutrition (TPN). A total gastrectomy was performed in the experimental groups, whereas the control group received a sham operation (Sham). The TPN solutions were isonitrogenous and identical in nutrient composition except that the Sham group and one of the experimental group received conventional (Conv) TPN solution, whereas the other experimental group received 25 % of the amino acid nitrogen as Gln. Half of the rats in each group were killed 1 or 3 d after surgery or the Sham to examine their immune response. The results showed that the surgery produced higher polymorphonuclear leucocyte CD11b/CD18 expressions, and Gln supplementation lowered CD11b/CD18 expressions compared with the Conv group post-operatively. The levels of monocyte chemotactic protein-1 and macrophage inflammatory protein-2 in peritoneal lavage fluid were higher in the Gln group than those in the Conv group 1 d post-operatively; these chemotactic proteins had returned to the levels comparable with those in the Sham group on post-operative day 3. These results suggest that Gln supplementation attenuated polymorphonuclear leucocyte integrin expression. In addition, Gln-enriched parenteral nutrition induced an earlier more intensive and rapid immune response to injury than the Conv parenteral nutrition after a total gastrectomy.

Gambian infants show growth faltering, but the underlying body composition is unknown. The present study aimed to compare body composition in Gambian and UK infants using 2H dilution; and to evaluate accuracy of bioelectrical impedance analysis (BIA) and creatinine excretion for estimating lean mass (LM), using 2H as the reference. Body composition was measured in thirty Gambian infants, aged 3–18 months, using (1) anthropometry, (2) 2H, (3) BIA (equation of Fjeld et al.Pediatr Res (1990), 27, 98–102) and (4) 5 h urinary creatinine excretion. Compared with UK reference data, Gambian infants were light, short and had reduced BMI and skinfolds. The subscapular skinfold standard deviation score (SDS) was greater than the triceps SDS (P < 0·01), indicating central fat preservation. Both LM and fat mass were reduced in Gambian infants, with or without adjustment for length. However, whereas the Gambia–UK difference in LM increased with age, that in fat mass decreased. Average creatinine excretion was similar to that expected (95·5 (sd 23·2) % recovery), but LM estimates showed unacceptable error in individuals. BIA using Fjeld's equation overestimated total body water and LM (P < 0·001), hence a new equation was developed, with standard error of 0·47 kg LM. In conclusion, Gambian infants characterised by growth faltering had LM deficits that increased with age. However, adiposity increased with age, and showed indications of a more central distribution than in the reference infants. A new BIA equation for LM prediction is presented; however, creatinine excretion is not recommended for LM estimation in this population.

Postprandial hyperglycaemia is thought to increase inflammation in leucocytes. In the present study, we examined whether sucrose loading in rats with moderate postprandial hyperglycaemia induces the expression of cytokines in peripheral leucocytes and whether these inductions are suppressed by inhibiting postprandial hyperglycaemia with the α-glucosidase inhibitor miglitol. One group of streptozotocin-treated rats and age-matched saline-treated rats were orally administered sucrose only, and another group of streptozotocin-treated rats was administered sucrose with miglitol, at a single daily dose for 4 d, under 4 h fasting conditions. Blood glucose levels at 0, 0·25, 0·5, 1, 2 and 3 h and cytokine mRNA in peripheral leucocytes at 0 and 3 h after sucrose loading on days 1 and 4 from the start of sucrose loading were determined. Streptozotocin-treated rats showed moderate postprandial hyperglycaemia (>2000 mg/l) at 0·25–1 h after sucrose loading on days 1 and 4. Postprandial hyperglycaemia was not observed in the miglitol-treated rats loaded with sucrose. Gene expression levels of IL-1β and TNF-α were higher in the streptozotocin-treated rats at fasting on day 1 than in saline-treated rats. Fasting IL-1β and TNF-α gene expression on day 1 were not only increased at 3 h on the same day of sucrose loading, but was also increased at the fasting period on day 4. These inductions on day 4 by intermittent sucrose administration were inhibited by miglitol. The present results suggest that miglitol decreases postprandial hyperglycaemia and intermittent sucrose-induced expression of the IL-1β and TNF-α genes in rat peripheral leucocytes.

d-chiro-inositol (DCI) and pinitol (1d-3-O-methyl-chiro-inositol) are distinctive inositols reported to possess insulin-mimetic properties. DCI-containing compounds are abundant in common laboratory animal feed. By GC–MS of 6 m-HCl hydrolysates, Purina Laboratory Rodent Diet 5001 (diet 5001) contained 0·23 % total DCI by weight with most found in the lucerne and soya meal components. In contrast, only traces of l-chiro-inositol were observed. The DCI moiety was present in a water-soluble non-ionic form of which most was shown to be pinitol. To measure the absorption of dietary inositols, rats were fed diet 5001 in a balance study or given purified pinitol or [2H6]DCI. More than 98 % of the total DCI fed to rats as diet 5001, purified pinitol or [2H6]DCI was absorbed from the gastrointestinal tract. Rats chronically on diet 5001 consumed 921 μmol total DCI/kg body weight per d but excreted less than 5·3 % in the stools and urine, suggesting that the bulk was metabolised. The levels of pinitol or DCI in plasma, stools or urine remained relatively stable in mice fed Purina PicoLab® Rodent Diet 20 5053 over a 5-week period, whereas these values declined to very low levels in mice fed a pinitol/DCI-deficient chemically defined diet. To test whether DCI was synthesised or converted from myo-inositol, mice were treated with heavy water or [2H6]myo-inositol. DCI was neither synthesised endogenously from 2H-labelled water nor converted from [2H6]myo-inositol. DCI and pinitol in rodents appear to be derived solely from the diet.

In consideration of economical and environmental concerns, fish oil (FO) substitution in aquaculture is the focus of many fish nutritionists. The most stringent drawback of FO replacement in aquafeeds is the consequential modification to the final fatty acid (FA) make-up of the fish fillet. However, it is envisaged that a solution may be achieved through a better understanding of fish FA metabolism. Therefore, the present study investigated the fate of individual dietary FA in rainbow trout (Oncorhynchus mykiss) fed a FO-based diet (rich in 20 : 5n-3) or a linseed oil-based diet (LO; rich in 18 : 3n-3). The study demonstrated that much of the 18 : 3n-3 content from the LO diet was oxidised and, despite the significantly increased accretion of Δ-6 and Δ-5 desaturated FA, a 2- and 3-fold reduction in the fish body content of 20 : 5n-3 and 22 : 6n-3, respectively, compared with the FO-fed fish, was recorded. The accretion of longer-chain FA was unaffected by the dietary treatments, while there was a greater net disappearance of FA provided in dietary surplus. SFA and MUFA recorded a net accretion of FA produced ex novo. In the fish fed the FO diet, the majority of dietary 20 : 5n-3 was accumulated (53·8 %), some was oxidised (14·7 %) and a large proportion (31·6 %) was elongated and desaturated up to 22 : 6n-3. In the fish fed the LO diet, the majority of dietary 18 : 3n-3 was accumulated (58·1 %), a large proportion was oxidised (29·5 %) and a limited amount (12·4 %) was bio-converted to longer and more unsaturated homologues.

An association between anorexia nerviosa (AN) and low bone mass has been demonstrated. Bone loss associated with AN involves hormonal and nutritional impairments, though their exact contribution is not clearly established. We compared bone mass in AN patients with women of similar weight with no criteria for AN, and a third group of healthy, normal-weight, age-matched women. The study included forty-eight patients with AN, twenty-two healthy eumenorrhoeic women with low weight (LW group; BMI < 18·5 kg/m2) and twenty healthy women with BMI >18·5 kg/m2 (control group), all of similar age. We measured lean body mass, percentage fat mass, total bone mineral content (BMC) and bone mineral density in lumbar spine (BMD LS) and in total (tBMD). We measured anthropometric parameters, leptin and growth hormone. The control group had greater tBMD and BMD LS than the other groups, with no differences between the AN and LW groups. No differences were found in tBMD, BMD LS and total BMC between the restrictive (n 25) and binge–purge type (n 23) in AN patients. In AN, minimum weight (P = 0·002) and percentage fat mass (P = 0·02) explained BMD LS variation (r2 0·48) and minimum weight (r2 0·42; P = 0·002) for tBMD in stepwise regression analyses. In the LW group, BMI explained BMD LS (r2 0·72; P = 0·01) and tBMD (r2 0·57; P = 0·04). We concluded that patients with AN had similar BMD to healthy thin women. Anthropometric parameters could contribute more significantly than oestrogen deficiency in the achievement of peak bone mass in AN patients.

Obesity during pregnancy has major consequences for maternal and neonatal health, but the long-term effects on the offspring are less clear. It is not known whether the effects observed in animal models are a result of maternal obesity per se or of the high-fat diets used to induce obesity. This investigation aimed to develop a model for the evaluation of the independent effects of cafeteria feeding and maternal obesity, considering their impact on plasma volume expansion, circulating metabolites, and fetal and placental growth. Wistar rats were fed a control or cafeteria diet from weaning. After 8 weeks, all animals were mated and half of the animals within each group were crossed-over to the alternative diet. This generated four treatment groups, differing in their pre-gestational and gestational diets. Half of the animals were culled at day 5 of gestation and the remainder at day 20. Maternal body composition, blood volume and circulating glucose, TAG and cholesterol were determined. Cafeteria feeding was effective in inducing obesity, as demonstrated by increased fat depot weights and total body fat, without impacting upon reproductive success or circulating lipid concentrations. The study successfully demonstrated that there were differential effects of maternal body fatness and diet upon fetal and placental growth, with pre-gestational obesity leading to lower fetal weight at day 20 of gestation (P < 0·001). The model will provide a useful vehicle for the investigation of the complex interactions between dietary- and obesity-related factors during pregnancy in their effects on fetal development and postnatal metabolic function.

25-Hydroxy vitamin D (25(OH)D) deficiency is linked with predisposition to autoimmune type 1 diabetes and multiple sclerosis. Our objective was to assess the relationship between serum 25(OH)D levels and thyroid autoimmunity. Subjects included students, teachers and staff aged 16–60 years (total 642, 244 males, 398 females). Serum free thyroxine, thyroid-stimulating hormone (TSH), and thyroid peroxidase autoantibodies (TPOAb), intact parathyroid hormone and 25(OH)D were measured by electrochemiluminescence and RIA, respectively. Thyroid dysfunction was defined if (1) serum TSH ≥ 5 μU/ml and TPOAb>34 IU/ml or (2) TSH ≥ 10 μU/ml but normal TPOAb. The mean serum 25(OH)D of the study subjects was 17·5 (sd 10·2) nmol/l with 87 % having values ≤ 25 nmol/l. TPOAb positivity was observed in 21 % of subjects. The relationship between 25(OH)D and TPOAb was assessed with and without controlling for age and showed significant inverse correlation (r − 0·08, P = 0·04) when adjusted for age. The prevalence of TPOAb and thyroid dysfunction were comparable between subjects stratified according to serum 25(OH)D into two groups either at cut-off of ≤ 25 or >25 nmol/l or first and second tertiles. Serum 25(OH)D values show only weak inverse correlation with TPOAb titres. The presence of such weak association and narrow range of serum 25(OH)D did not allow us to interpret the present results in terms of quantitative cut-off values of serum 25(OH)D. Further studies in vitamin D-sufficient populations with wider range of serum 25(OH)D levels are required to substantiate the findings of the current study.

Mitochondrial (mt) DNA deletions and low folate status, proposed characteristics of carcinogenesis, in relation to human hepatocellular carcinoma (HCC) susceptibility are not clearly understood. We hypothesised that low folate status may modify frequencies of mtDNA deletions in humans, both of which could predispose individuals to HCC development. Biochemical folate status of serum and lymphocytes, and frequencies of mtDNA deletions in lymphocytes were determined in ninety HCC cases and ninety cancer-free healthy controls, individually matched by age and sex. The data revealed that HCC patients had lower levels of serum folate (P = 0·0002), lymphocytic folate (P = 0·040) and accumulated higher frequency of lymphocytic mtDNA deletions (P < 0·0001) than the controls. In the total studied subjects, frequencies of lymphocytic mtDNA deletions were associated with hepatitic B infection (P = 0·004) and HCC incidents (P = 0·001), and were correlated with serum folate (r − 0·155; P = 0·041), lymphocyte folate (r − 0·314; P = 0·0001), levels of glutamate-oxaloacetate transaminase (GOT) (r 0·206; P = 0·006), glutamate-pyruvate transaminase (GPT) (r 0·163; P = 0·037) and α-fetal protein concentrations (r 0·212; P = 0·005). After adjustment for age, sex, lifestyle and one-carbon metabolite factors, individuals with low blood folate ( < 11·5 nmol/l) or high mtDNA deletions (Δ threshold cycle number (Ct)>5·3) had increased risks for HCC (OR 7·7, 95 % CI 1·9, 29·9, P = 0·003; OR 5·4; 95 % CI 1·7, 16·8, P = 0·003, respectively). When combined with folate deficiency (serum folate < 14 nmol/l), the OR of HCC in individuals with high levels of lymphocytic mtDNA deletions was enhanced (OR 13·3; 95 % CI 1·45, 122; P = 0·008). Further controlling for GOT and GPT levels, however, negated those effects on HCC risk. Taken together, the data suggest that biochemical folate status and liver injuries are important modulators to lymphocytic mtDNA deletions. The mt genetic instability that results from a high rate of mtDNA deletions and/or low folate status increased the risk for HCC, which is mediated by clinical hepatic lesions.

Cardiovascular complications are a major cause of morbidity and mortality in patients with diabetes, obesity and the metabolic syndrome. Recently, there has been an increasing interest in tea as a protective agent against CVD. Here, we compared the modulatory effects of two different doses (50 and 100 mg/kg body weight given orally for 28 consecutive days) of black tea aqueous extract (BTE, rich in theaflavins and thearubigins) and green tea aqueous extract (GTE, rich in catechins) on experimentally induced hyperglycaemia, hyperlipidaemia and liver dysfunction by alloxan (which destroys pancreatic β-cells and induces type 1 diabetes) and a cholesterol-rich diet (which induces obesity and type 2 diabetes) in male Wistar albino rats. Both tea extracts significantly alleviated most signs of the metabolic syndrome including hyperglycaemia (resulting from type 1 and 2 diabetes), dyslipidaemia and impairment of liver functions induced by alloxan or the cholesterol-rich diet in the animals. Also, the tea extracts significantly modulated both the severe decrease and increase in body weight induced by alloxan and the high-cholesterol diet, respectively. The modulatory effects obtained here were partial or complete, but significant and dose dependent, and slightly more in GTE in most cases. No harmful effects were detected for tea consumption on all parameters measured, except that the high dose of both tea extracts significantly decreased the spleen weight:body weight ratio and induced lymphopenia. The present study supports the hypothesis that both black and green teas may have beneficial effects against the risks of the metabolic syndrome and CVD as shown in rat models of human obesity and diabetes.

Arachidonic acid (AA) is considered essential in fetal development and some of its metabolites are thought to be important mediators of the immune responses. Therefore, we studied whether prenatal exposure to AA is associated with some immune-related clinical conditions and plasma markers in childhood. In 280 children aged 7 years, atopy, lung function and plasma inflammation markers were measured and their relationships with early AA exposure were studied by linear and logistic regression analyses. AA exposure was deduced from AA concentrations in plasma phospholipids of the mothers collected at several time points during pregnancy and at delivery, and in umbilical cord plasma and arterial and venous wall phospholipids. In unadjusted regression analyses, significant positive associations were observed between maternal AA concentrations at 16 and 32 weeks of pregnancy (proxies for fetal AA exposure) and peak expiratory flow decline after maximal physical exercise and plasma fibrinogen concentrations of their children, respectively. However, after correction for relevant covariables, only trends remained. A significant negative relationship was observed between AA concentrations in cord plasma (reflecting prenatal AA exposure) and the average daily amplitude of peak expiratory flow at rest, which lost significance after appropriate adjustment. Because of these few, weak and inconsistent relationships, a major impact of early-life exposure to AA on atopy, lung function and selected plasma inflammation markers of children at 7 years of age seems unlikely.