Curcumin has been used in Asian traditional medicine for its medicinal properties. Recent studies have demonstrated that curcumin has antioxidant, anti-tumour and anti-inflammatory activities. The aim of the present study is to investigate the effects of curcumin on established lupus nephritis (LN) in New Zealand Black/White (NZB/W) F1 female mice, in particular, its interaction with regulatory T (Treg) cells. Starting at 18 weeks of age, mice were fed a standard diet or a diet containing 1 % curcumin until the end of the study. The proteinuria level and the serum levels of IgG1, IgG2a and anti-double-stranded DNA (dsDNA) IgG antibodies were measured. Additionally, IgG immune complex deposition in the glomeruli and renal inflammation were compared between curcumin-treated mice and control mice. Curcumin decreased the proteinuria level and serum levels of IgG1, IgG2a and anti-dsDNA IgG antibodies in NZB/W F1 female mice. IgG immune complex deposition in the glomeruli was reduced in curcumin-treated mice. Furthermore, renal inflammation was also decreased after curcumin treatment. Interestingly, these therapeutic effects of curcumin disappeared after Treg depletion by anti-CD25 antibody injection. Curcumin exerted a protective effect against LN in NZB/W F1 mice. We speculate that the protective effects of curcumin in LN may involve, at least in part, its interaction with Treg cells.

SCFA resulting from the microbial fermentation of carbohydrates have been linked to increased glucagon-like peptide-1 (GLP-1) secretion from the gastrointestinal tract in cell and animal models; however, there is little direct evidence in human subjects to confirm this. The present study was designed to investigate whether endogenous plasma GLP-1 concentrations increase following acute consumption of 48 g dietary fibre (as resistant starch (RS) from high-amylose maize type 2 RS (HAM-RS2)) compared with a matched placebo. A total of thirty healthy males participated in the present randomised cross-over study where HAM-RS2 or placebo was consumed as part of standardised breakfast and lunch meals. Changes to GLP-1, glucose, insulin and C-peptide were assessed half hourly for 7 h. Following the breakfast meal, plasma GLP-1 concentrations were lower with HAM-RS2 compared with the placebo (P =0·025). However, there was no significant difference between the supplements following the lunch meal. Plasma insulin concentrations were significantly lower following the lunch meal (P =0·034) with HAM-RS2 than with the placebo, but were not different after breakfast. Plasma glucose and C-peptide concentrations did not differ at any point. These results suggest that increased dietary fibre intake, in the form of HAM-RS2, does not acutely increase endogenous GLP-1 concentrations in human subjects. Further fibre feeding studies are required to determine whether GLP-1 concentrations may increase following longer-term consumption.

The H+-coupled transporter, peptide transporter 1 (PepT1), is responsible for the uptake of dietary di- and tripeptides in the intestine. Using an in vivo continuously perfused gut loop model in Yucatan miniature pigs, we measured dipeptide disappearance from four 10 cm segments placed at equidistant sites along the length of the small intestine. Pigs were studied at 1, 2, 3 (suckling) and 6 weeks (post-weaning) postnatal age. Transport capability across the PepT1 transporter was assessed by measuring the disappearance of 3H-glycylsarcosine; real-time RT-PCR was also used to quantify PepT1 mRNA. Each of the regions of intestine studied demonstrated the capacity for dipeptide transport. There were no differences among age groups in transport rates measured in the most proximal intestine segment. Transport of 3H-glycylsarcosine was significantly higher in the ileal section in the youngest age group (1 week) compared with the other the suckling groups; however, all suckling piglet groups demonstrated lower ileal transport compared with the post-weaned pigs. Colonic PepT1 mRNA was maximal in the earliest weeks of development and decreased to its lowest point by week 6. These results suggest that peptide transport in the small intestine may be of importance during the first week of suckling and again with diet transition following weaning.

2-Oxoglutaric acid (2-Ox), a precursor to hydroxyproline – the most abundant amino acid in bone collagen, exerts protective effects on bone development during different stages of organism development; however, little is known about the action of 2-Ox on cartilage. The aim of the present study was to elucidate the influence of dietary 2-Ox supplementation on the growth plate, articular cartilage and bone of growing rats. A total of twelve male Sprague–Dawley rats were used in the study. Half of the rats received 2-oxoglutarate at a dose of 0·75 g/kg body weight per d in their drinking-water. Body and organ weights were measured. Histomorphometric analyses of the cartilage and bone tissue of the femora and tibiae were conducted, as well as bone densitometry and peripheral quantitative computed tomography (pQCT). Rats receiving 2-Ox had an increased body mass (P< 0·001) and absolute liver weight (P= 0·031). Femoral length (P= 0·045) and bone mineral density (P= 0·014), overall thickness of growth plate (femur P= 0·036 and tibia P= 0·026) and the thickness of femoral articular cartilage (P< 0·001) were also increased. 2-Ox administration had no effect on the mechanical properties or on any of the measured pQCT parameters for both bones analysed. There were also no significant differences in histomorphometric parameters of tibial articular cartilage and autofluorescence of femoral and tibial growth plate cartilage. Dietary supplementation with 2-Ox to growing rats exerts its effects mainly on cartilage tissue, having only a slight influence on bone. The effect of 2-Ox administration was selective, depending on the particular bone and type of cartilage analysed.

In the present study, the effect of long-term fructose feeding on skeletal muscle mitochondrial energetics was investigated. Measurements in isolated tissue were coupled with the determination of whole-body energy expenditure and insulin sensitivity. A significant increase in plasma NEFA, as well as in skeletal muscle TAG and ceramide, was found in fructose-fed rats compared with the controls, together with a significantly higher plasma insulin response to a glucose load, while no significant variation in plasma glucose levels was found. Significantly lower RMR values were found in fructose-fed rats starting from week 4 of the dietary treatment. Skeletal muscle mitochondrial mass and degree of coupling were found to be significantly higher in fructose-fed rats compared with the controls. Significantly higher lipid peroxidation was found in fructose-fed rats, together with a significant decrease in superoxide dismutase activity. Phosphorylated Akt levels normalised to plasma insulin levels were significantly lower in fructose-fed rats compared with the controls. In conclusion, a fructose-rich diet has a deep impact on a metabolically relevant tissue such as skeletal muscle. In this tissue, the consequences of high fructose feeding are altered glucose tolerance, elevated mitochondrial biogenesis and increased mitochondrial coupling. This latter modification could have a detrimental metabolic effect by causing oxidative stress and energy sparing that contribute to the high metabolic efficiency of fructose-fed rats.

High fructose consumption is commonly associated with insulin resistance, disturbed glucose homeostasis and low-grade inflammation. Increased glucocorticoid production within adipose tissue has been implicated in the pathogenesis of fructose-induced metabolic syndrome. Immunosuppressive actions of glucocorticoids can be counter-regulated by macrophage migration inhibitory factor (MIF), which is recognised as a key molecule in metabolic inflammation. In the present study, we hypothesised that coordinated action of glucocorticoids and MIF can mediate the effects of a high-fructose diet on adipose tissue and liver inflammation. We examined the effects of long-term consumption of a 10 % fructose solution on corticosterone (CORT) and MIF levels in rat blood plasma, liver and adipose tissue, as well as MIF and TNF-α mRNA expression and NF-κB activation in the same tissues. The high-fructose diet led to an increase in both CORT and MIF in the adipose tissue, and a highly significant positive correlation between their levels was observed. The attenuated NF-κB activation and unaltered TNF-α mRNA expression noticed in the adipose tissue could be interpreted as an outcome of the opposing actions of CORT and MIF. In contrast to adipose tissue, inflammation in the liver was characterised by NF-κB activation, an increased TNF-α mRNA level and unchanged levels of MIF protein, MIF mRNA and CORT. Overall, these findings suggest that a high-fructose diet differently affects the levels of glucocorticoids and MIF in the adipose tissue and liver, implicating that fructose over-consumption has tissue-specific effects on regulation of metabolic inflammation.

The aim of the present study was to investigate the effects of oil extracted from the zooplankton Calanus finmarchicus (Calanus oil) on diet-induced obesity and obesity-related disorders in mice. C57BL/6J mice fed a high-fat diet (HFD, 45 % energy from fat) exhibited increased body weight and abdominal fat accumulation as well as impaired glucose tolerance compared with mice fed a normal chow diet (10 % energy from fat). Supplementing the HFD with 1·5 % (w/w) Calanus oil reduced body-weight gain, abdominal fat accumulation and hepatic steatosis by 16, 27 and 41 %, respectively, and improved glucose tolerance by 16 %. Calanus oil supplementation reduced adipocyte size and increased the mRNA expression of adiponectin in adipose tissue. It also reduced macrophage infiltration by more than 70 %, accompanied by reduced mRNA expression of pro-inflammatory cytokines (TNF-α, IL-6 and monocyte chemotactic protein-1). The effects of Calanus oil were not only preventive, but also therapeutic, as the oil proved to be beneficial, regardless of whether the supplementation was started before or after the onset of obesity and glucose intolerance. Although the present study cannot pinpoint the active component(s) of the oil, there is reason to believe that the n-3 fatty acids EPA and DHA and/or antioxidants are responsible for its beneficial effects. It should be noted that the concentration of n-3 fatty acids in the Calanus oil diet was considerably lower than the concentrations used in similar studies reporting beneficial effects on obesity and obesity-related abnormalities.

There are several studies in which a correlation between maternal vitamin D deficiency and serum mineral disorders in the mother and the newborn has been reported. The present randomised clinical trial was designed to investigate the effect of vitamin D administration on maternal and fetal Ca and vitamin D status. The trial was carried out on 160 pregnant women. Vitamin D-deficient (25-hydroxyvitamin D (25(OH)D) < 30 ng/ml) pregnant women were recruited at 26–28 weeks of pregnancy. In the control group, a multivitamin supplement containing 400 IU vitamin D3/d was given. Patients in the treatment group were treated with 50 000 IU vitamin D3 weekly for a total duration of 8 weeks. At delivery, maternal and fetal Ca and 25(OH)D levels in both groups were compared. In total, 81 % of pregnant women were vitamin D deficient. At the time of delivery, Ca and vitamin D levels were higher in the treatment group compared with the control group (92 (sd 3) v. 85 (sd 4) mg/l, respectively, P= 0·001 for serum Ca; 47·8 (sd 11·1) v. 15·9 (sd 6·6) ng/ml, respectively, P< 0·001 for vitamin D). At the time of delivery, 32·7 % of women in the control group had hypocalcaemia, while no hypocalcaemic case was detected in the vitamin D-treated group. Mean neonatal serum 25(OH)D was higher in the treatment group compared with the control group (27·7 (sd 5·2) v.10·9 (sd 4·4) ng/ml, respectively, P< 0·01). The neonatal Ca level in the treatment group was significantly higher than that of the control group (99 (sd 3) v. 91 (sd 3) mg/l, respectively, P< 0·001). The administration of vitamin D to pregnant women with vitamin D deficiency improves both maternal and neonatal Ca levels.

The effects of conjugated linoleic acid (CLA) on growth performance, non-specific immunity, antioxidant capacity, lipid deposition and related gene expression were investigated in the large yellow croaker (Larmichthys crocea). Fish (7·56 (sem 0·60) g) were fed soyabean oil-based diets with graded levels of CLA (0, 0·42, 0·83, 1·70 %) for 70 d. Quantitative PCR was used to assess the effects of CLA on the transcription of inflammation- and fatty acid oxidation-related genes. Growth in fish fed the diet with 0·42 % CLA was significantly higher. Also, phagocytic index and respiratory burst activity were significantly higher in fish fed the diets containing 0·42 and 0·83 % CLA, respectively. Hepatic total antioxidative capacity and catalase activities increased significantly when CLA increased from 0 to 0·83 %, and then decreased with further increase of CLA. However, hepatic malondialdehyde content decreased significantly as dietary CLA increased. Lipid concentration in the whole body and muscle increased significantly with increasing dietary CLA. Transcription of genes related to inflammation (cyclo-oxygenase-2 and IL-β) in the liver and kidney and fatty acid oxidation (carnitine palmitoyl transferase I and acyl CoA oxidase) in the kidney decreased significantly as dietary CLA increased. PPARα and acyl CoA oxidase expression in the liver decreased significantly as CLA increased from 0·42 to 1·70 %. These results strongly suggest that dietary CLA could significantly affect growth performance, non-specific immunity, antioxidant capacity, lipid deposition and transcription of inflammation- and fatty acid oxidation-related genes of the large yellow croaker. This may contribute to our understanding of the mechanisms related to the physiological effects of dietary CLA in fish.

The present study aimed at (1) describing age-related changes in faecal bacterial functional groups involved in carbohydrate degradation and in their activities in foals (n 10) from birth (day (d) 0) to 6 months (d180) and (2) investigating the effect of maternal supplementation (five mares per treatment) from d − 45 to d60 with fermented feed products on response trends over time of the foal bacterial carbohydrate-degrading capacity. Maternal supplementation with fermented feed products stimulated foal growth from d0 to d60 and had an impact on the establishment of some digestive bacterial groups and their activities in foals from d0 to d5 but not in the longer term. Irrespective of the maternal treatment, total bacteria, total anaerobic, lactate-utilising and amylolytic bacteria were established immediately after birth (P< 0·05) and were active as shown by the significant increase in total volatile fatty acids. In the foals of supplemented mares, total anaerobes and lactate utilisers were established rapidly between d0 and d2 (P= 0·021 and 0·066, respectively) and the increase in the percentage of propionate occurred earlier (P= 0·013). Maternal supplementation had no effect on the establishment of fibrolytic bacteria and their activity. Cellulolytic bacteria and Fibrobacter succinogenes first appeared at d2 and d5, and increased progressively, reaching stable values at d30 and d60, respectively. From the second week of life, the increase in the molar percentage of acetate and the ratio (acetate+butyrate):propionate (P< 0·05) suggested that fibrolytic activity had begun. From d60, only minor changes in bacterial composition and activities occurred, showing that the bacterial carbohydrate-degrading capacity was established at 2 months of age.

The present study was conducted to evaluate the immune-enhancing effects of dietary l-glutamine supplementation in porcine circovirus type 2 (PCV2)-infected mice, and to examine the clearance effects of glutamine against PCV2 in experimentally infected mice. A total of sixty Kunming female mice were infected with PCV2 at a dose of 100 TCID50 (50 % tissue culture infection dose) by intraperitoneal injection after 2 weeks of dietary l-glutamine supplementation or l-alanine supplementation (as the control (isonitrogenous) group). The measured variables on 3rd, 5th, 7th, 9th and 11th d post-infection (dpi) included: (1) PCV2 virus loaded in the liver, spleen, heart, lung, kidney, ovary and serum was determined by real-time PCR; (2) IL-2, IL-6, IL-10, interferon (IFN)-α, IFN-γ and C-reactive protein levels in serum were measured by ELISA; (3) serum total superoxide dismutase activity was measured spectrophotometrically at 550 nm absorbance. Dietary l-glutamine supplementation significantly increased serum IL-2 levels on the 3rd (P< 0·01), 5th (P< 0·01), 7th (P< 0·05) and 9th dpi, significantly (P< 0·05) increased serum IL-6 levels on 3rd dpi, significantly (P< 0·05) increased serum IFN-γ levels on the 9th and 11th dpi and significantly decreased (P< 0·01) serum IL-10 levels on the 9th and 11th dpi, compared with those in the control group. Meanwhile, the PCV2 virus genome was detected sporadically throughout the experimental period in both groups. Taken together, the present results suggest that dietary l-glutamine supplementation enhances immune function in PCV2-infected mice.

Human milk (HM) is rich in oligosaccharides (HMO) that exert prebiotic and anti-infective activities. HM feeding reduces the incidence of rotavirus (RV) infection in infants. Herein, the anti-RV activity of oligosaccharides was tested in an established in vitro system for assessing cellular binding and viral infectivity/replication, and also tested in a newly developed, acute RV infection, in situ piglet model. For the in vitro work, crude HMO isolated from pooled HM, neutral HMO (lacto-N-neotetraose, LNnT; 2′-fucosyllactose) and acidic HMO (aHMO, 3′-sialyllactose, 3′-SL; 6′-sialyllactose, 6′-SL) were tested against the porcine OSU strain and human RV Wa strain. The RV Wa strain was not inhibited by any oligosaccharides. However, the RV OSU strain infectivity was dose-dependently inhibited by sialic acid (SA)-containing HMO. 3′-SL and 6′-SL concordantly inhibited 125I-radiolabelled RV cellular binding and infectivity/replication. For the in situ study, a midline laparotomy was performed on 21-d-old formula-fed piglets and six 10 cm loops of ileum were isolated in situ. Briefly, 2 mg/ml of LNnT, aHMO mixture (40 % 6′-SL/10 % 3′-SL/50 % SA) or media with or without the RV OSU strain (1 × 107 focus-forming units) were injected into the loops and maintained for 6 h. The loops treated with HMO treatments+RV had lower RV replication, as assessed by non-structural protein-4 (NSP4) mRNA expression, than RV-treated loops alone. In conclusion, SA-containing HMO inhibited RV infectivity in vitro; however, both neutral HMO and SA with aHMO decreased NSP4 replication during acute RV infection in situ.

Lactic acid bacteria confer a variety of health benefits. Here, we investigate the mechanisms by which Lactobacillus brevis KB290 (KB290) enhances cell-mediated cytotoxic activity. Female BALB/c mice aged 9 weeks were fed a diet containing KB290 (3 × 109 colony-forming units/g) or starch for 1 d. The resulting cytotoxic activity of splenocytes against YAC-1 cells was measured using flow cytometry and analysed for gene expression using DNA microarray technology. KB290 enhanced the cell-mediated cytotoxic activity of splenocytes. DNA microarray analysis identified 327 up-regulated and 347 down-regulated genes that characterised the KB290 diet group. The up-regulated genes were significantly enriched in Gene Ontology terms related to immunity, and, especially, a positive regulation of T-cell-mediated cytotoxicity existed among these terms. Almost all the genes included in the term encoded major histocompatibility complex (MHC) class I molecules involved in the presentation of antigen to CD8+ cytotoxic T cells. Marco and Signr1 specific to marginal zone macrophages (MZM), antigen-presenting cells, were also up-regulated. Flow cytometric analysis confirmed that the proportion of MZM was significantly increased by KB290 ingestion. Additionally, the over-represented Kyoto Encyclopedia of Genes and Genomes pathways among the up-regulated genes were those for natural killer (NK) cell-mediated cytotoxicity and antigen processing and presentation. The results for the selected genes associated with NK cells and CD8+ cytotoxic T cells were confirmed by quantitative RT-PCR. These results suggest that enhanced cytotoxic activity could be caused by the activation of NK cells and/or of CD8+ cytotoxic T cells stimulated via MHC class I presentation.

Low maternal vitamin D status during pregnancy may have negative consequences for both mother and child. There are few studies of vitamin D status and its determinants in pregnant women living at northern latitudes. Thus, the present study investigates vitamin D status and its determinants during the third trimester of women living in Sweden (latitudes 57–58°N). A total of ninety-five fair-skinned pregnant women had blood taken between gestational weeks 35 and 37. The study included a 4 d food diary and questionnaires on dietary intake, supplement use, sun exposure, skin type, travels to southern latitudes and measure of BMI. Serum 25-hydroxyvitamin D (25(OH)D) was analysed using the chemiluminescence immunoassay. In the third trimester of pregnancy, mean serum concentration of 25(OH)D was 47·4 (sd 18·1) nmol/l (range 10–93 nmol/l). In total, 65 % of women had serum 25(OH)D < 50 nmol/l and 17 % < 30 nmol/l. During the winter, 85 % of the pregnant women had serum 25(OH)D < 50 nmol/l and 28 % < 30 nmol/l. The main determinants of vitamin D status were as follows: season; use of vitamin D supplements; travels to southern latitudes. Together, these explained 51 % of the variation in 25(OH)D. In conclusion, during the winter, the majority of fair-skinned pregnant women had serum 25(OH)D < 50 nmol/l in their third trimester and more than every fourth woman < 30 nmol/l. Higher vitamin D intake may therefore be needed during the winter for fair-skinned pregnant women at northern latitudes to avoid vitamin D deficiency.

Few epidemiological studies have examined the association between an overall fatty acid (FA) profile and CHD risk. The aim of the present study was to examine a novel index that summarises individual FA levels based on FA affinity and fluidity in relation to CHD risk in men. In a prospective nested case–control study, FA in plasma and erythrocytes were measured in 459 CHD cases and 879 matched controls. Lipophilic index (LI) was computed by summing the products between FA levels and melting point of each FA to reflect the overall FA lipophilicity. Among controls, higher plasma LI was significantly correlated with adverse profiles of blood lipids, inflammatory markers and adiponectin. After multivariate adjustment for age, smoking, BMI and other CHD risk factors, plasma LI was significantly associated with an increased risk of CHD: the relative risk was 1·61 (95 % CI 1·03, 2·53; P for trend = 0·04) comparing extreme quintiles. This association was attenuated to 1·21 (95 % CI 0·48, 3·09; P for trend = 0·77) after adjusting for plasma levels of total trans-FA, long-chain n-3 FA and polyunsaturated:saturated fat ratio. Erythrocyte LI was not significantly associated with CHD risk. The present data indicate that a novel LI is associated with an adverse profile of cardiovascular risk markers and increased risk of CHD in men; its usefulness as a complement of individual FA in assessing disease risk needs to be elucidated in future studies.

Cuminum cyminum, a commonly used spice, is known to have anti-diabetic action. The present study aims towards the isolation of bioactive components from C. cyminum and the evaluation of their insulin secretagogue potential with the probable mechanism and β-cell protective action. The anti-diabetic activity was detected in the petroleum ether (pet ether) fraction of the C. cyminum distillate and studied through in vivo and in vitro experiments. Bioactive components were identified through GC–MS, Fourier transform infrared spectroscopy and NMR analysis. The isolated components were evaluated for their insulin secretagogue action using rat pancreatic islets. Further, the probable mechanism of stimulation of islets was evaluated through in vitro studies using diazoxide, nifedipine and 3-isobutyl-1-methylxanthine. β-Cell protection was evaluated using the (1-(4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan) (MTT) assay, the alkaline comet assay and nitrite production. The administration of the pet ether fraction for 45 d to streptozotocin-induced diabetic rats revealed an improved lipid profile. Cuminaldehyde and cuminol were identified as potent insulinotrophic components. Cuminaldehyde and cuminol (25 μg/ml) showed 3·34- and 3·85-fold increased insulin secretion, respectively, than the 11·8 mm-glucose control. The insulinotrophic action of both components was glucose-dependent and due to the closure of the ATP-sensitive K (K+-ATP) channel and the increase in intracellular Ca2+ concentration. An inhibitor of insulin secretion with potent β-cell protective action was also isolated from the same pet ether fraction. In conclusion, C. cyminum was able to lower blood glucose without causing hypoglycaemia or β-cell burn out. Hence, the commonly used spice, C. cyminum, has the potential to be used as a novel insulinotrophic therapy for prolonged treatment of diabetes.

Maternal dietary Zn deficiency during fetal development induces substantial cognitive dysfunctions in the resultant offspring. The mechanism underlying this effect is unclear. The present study evaluated whether the impairments caused by gestational and lactational Zn deficiency are mediated by the hippocampal calmodulin-dependent protein kinase II α (α-CaMKII)/brain-derived neurotrophic factor (BDNF) signalling pathway as well as whether they can be restored by postnatal Zn supplementation. Rats were randomly divided into four groups on the first day of pregnancy (n 12): control (CO) group; pair-fed (PF) group; Zn-deprived (ZD) group; orally Zn-supplemented group. The spatial memory of the offspring was tested at postnatal day 35 using the Morris water maze. Long-term potentiation (LTP) in the rat hippocampal medial perforant path–dentate gyrus pathway was evaluated simultaneously, and α-CaMKII and BDNF protein levels were examined by Western blot analysis. The results demonstrated that the ZD group exhibited a significantly longer latency period in the Morris water maze as well as a significantly decreased LTP amplitude compared with the CO and PF groups. α-CaMKII and BDNF protein expression in the hippocampus was significantly reduced in the ZD group. Postnatal Zn supplementation restored the cognitive dysfunction induced by gestational Zn deficiency but could not completely reverse the decreased LTP and α-CaMKII/BDNF protein levels. Our findings suggest that the α-CaMKII/BDNF signalling pathway may be involved in Zn deficiency-induced cognitive and synaptic impairments.

Intra-uterine growth-retarded (IUGR) neonates have shown an impairment of postnatal intestinal development and function. We hypothesised that the immune function of IUGR neonates might be affected by increased nutrient intake (NI) during the suckling period. Therefore, we investigated the effects of high NI (HNI) on the growth performance, intestinal morphology and immunological response of IUGR and normal-birth weight (NBW) piglets. A total of twelve pairs of IUGR and NBW piglets (7 d old) were randomly assigned to two different nutrient-level formula milk groups. After 21 d of rearing, growth performance, the composition of peripheral leucocytes, serum cytokines and intestinal innate immune-related genes involved in the Toll-like receptor (TLR)-4–myeloid differentiation factor 88–NF-κB pathway were determined. The results indicated that IUGR decreased the average daily DM intake (ADMI) and the average daily growth (ADG). However, the ADMI and ADG were increased by HNI, irrespective of body weight. Likewise, serum cytokines (TNF-α and IL-1β) and ileal gene expressions (TLR-4, TLR-9, TRAF-6 and IL-1β) were lower in IUGR piglets, whereas HNI significantly increased blood lymphocyte percentage and serum IL-10 concentrations, but decreased neutrophil percentage, serum IL-1β concentrations and ileal gene expressions (NF-κB and IL-1β). Furthermore, IUGR piglets with HNI exhibited lower serum concentrations of TNF-α and IL-1β than NBW piglets, and these alterations in the immune traits of IUGR piglets receiving HNI were accompanied by decreasing ileal gene expressions of TLR-4, TLR-9, NF-κB and IL-1β that are related to innate immunity. In conclusion, the present findings suggest that increased NI during the suckling period impaired the immune function of neonatal piglets with IUGR.

Earlier studies in animals have suggested an essential role for Si in connective tissues, but such works have not been replicated per se. Nonetheless, a study conducted in 2000 has reported that Si may be essential during pregnancy for the growing fetus, since serum Si concentrations in infants were approximately 300 % higher than those in older children and adults and serum Si concentrations in pregnant women were approximately 300 % lower than those in age-matched non-pregnant controls. To reproduce these potentially important findings, in the present study, serum Si concentrations were measured in fourteen pregnant women (15–24 weeks of gestation) and compared with those of seventeen non-pregnant, non-lactating female controls. Serum Si concentrations were also measured in fourteen full-term mothers at the time of delivery and in the umbilical cord (UC) vein and artery where possible. Fasting serum Si concentrations in pregnant women were not significantly different from those of the female controls and showed little change with advancing gestation (r 0·2). Mean serum Si concentrations in the UC vein samples were 52 % higher, while those in the UC artery samples were 235 % higher than those in the maternal forearm vein samples, although data were widely spread and differences were not significant. Mean maternal forearm vein Si concentrations at delivery were 50 % lower than those of pregnant women and female controls, but, again, these were not significant. Overall, we note that there are significant analytical challenges in comparing baseline Si levels between different groups; notwithstanding, our findings cannot confirm a reduction in fasting serum Si levels during pregnancy, but, equally, we cannot rule out higher serum Si levels in newborns than in their mothers, and further work is required.