We aimed to systematically review available data on the association between vitamin C intake and bone mineral density (BMD), as well as risk of fractures and osteoporosis, and to summarise this information through a meta-analysis. Previous studies on vitamin C intake in relation to BMD and risk of fracture and osteoporosis were selected through searching PubMed, Scopus, ISI Web of Science and Google Scholar databases before February 2017, using MeSH and text words. To pool data, either a fixed-effects model or a random-effects model was used, and for assessing heterogeneity, Cochran’s Q and I2 tests were used. Subgroup analysis was applied to define possible sources of heterogeneity. Greater dietary vitamin C intake was positively associated with BMD at femoral neck (pooled r 0·18; 0·06, 0·30) and lumbar spine (pooled r 0·14; 95 % CI 0·06, 0·22); however, significant between-study heterogeneity was found at femoral neck: I2=87·6 %, Pheterogeneity<0·001. In addition, we found a non-significant association between dietary vitamin C intake and the risk of hip fracture (overall relative risk=0·74; 95 % CI 0·51, 1·08). Significant between-study heterogeneity was found (I2=79·1 %, Pheterogeneity<0·001), and subgroup analysis indicated that study design, sex and age were the main sources of heterogeneity. Greater dietary vitamin C intake was associated with a 33 % lower risk of osteoporosis (overall relative risk=0·67; 95 % CI 0·47, 0·94). Greater dietary vitamin C intake was associated with a lower risk of hip fracture and osteoporosis, as well as higher BMD, at femoral neck and lumbar spine.

Non-exercise physical activity (NEPA) and/or non-exercise activity thermogenesis (NEAT) reductions may occur from diet and/or exercise-induced negative energy balance interventions, resulting in less-than-expected weight loss. This systematic review describes the effects of prescribed diet and/or physical activity (PA)/exercise on NEPA and/or NEAT in adults. Studies were identified from PubMed, web-of-knowledge, Embase, SPORTDiscus, ERIC and PsycINFO searches up to 1 March 2017. Eligibility criteria included randomised controlled trials (RCT), randomised trials (RT) and non-randomised trials (NRT); objective measures of PA and energy expenditure; data on NEPA, NEAT and spontaneous PA; ≥10 healthy male/female aged>18 years; and ≥7 d length. The trial is registered at PROSPERO-2017-CRD42017052635. In all, thirty-six articles (RCT-10, RT-9, NRT-17) with a total of seventy intervention arms (diet, exercise, combined diet/exercise), with a total of 1561 participants, were included. Compensation was observed in twenty-six out of seventy intervention arms (fifteen studies out of thirty-six reporting declines in NEAT (eight), NEPA (four) or both (three)) representing 63, 27 and 23 % of diet-only, combined diet/exercise, and exercise-only intervention arms, respectively. Weight loss observed in participants who decreased NEAT was double the weight loss found in those who did not compensate, suggesting that the energy imbalance degree may lead to energy conservation. Although these findings do not support the hypothesis that prescribed diet and/or exercise results in decreased NEAT and NEPA in healthy adults, the underpowered trial design and the lack of state-of-the-art methods may limit these conclusions. Future studies should explore the impact of weight-loss magnitude, energetic restriction degree, exercise dose and participant characteristics on NEAT and/or NEPA.

Leucine, one of the branched-chain amino acids, is the only amino acid to regulate protein turnover in skeletal muscle. Leucine not only increases muscle protein synthesis, but also decreases muscle protein degradation. It is well documented that leucine plays a positive role in differentiation of murine muscle cells. However, the role of leucine on porcine myoblast differentiation and its mechanism remains unclear. In this study, porcine myoblasts were induced to differentiate with differentiation medium containing different concentrations of leucine, and wortmannin was used to interdict the activity of protein kinase B (Akt). We found that leucine increased the number of myosin heavy chain-positive cells and creatine kinase activity. Moreover, leucine increased the mRNA and protein levels of myogenin and myogenic determining factor (MyoD). In addition, leucine increased the levels of phosphorylated Akt/Akt and phosphorylated Forkhead box O1 (P-FoxO1)/FoxO1, as well as decreased the protein level of FoxO1. However, wortmannin, a specific repressor of PI3K/Akt signalling pathway, attenuated the positive role of leucine on porcine myoblast differentiation. Our results suggest that leucine promotes porcine myoblast differentiation through the Akt/FoxO1 signalling pathway.

A previous study showed that flesh quality of large yellow croaker (LYC) was improved by feeding dietary hydroxyproline (Hyp, 0·69 %). The aim of the present study was to explore the underlying mechanisms using transcriptomics and metabolomics analysis. The metabolomics analysis showed that muscle metabolite profiles could be clearly separated between the basal diet and Hyp supplementation diet. Metabolites including betaine, Hyp, lactate, glucose-6-phosphate, trimethylamine N-oxide, taurine, creatine, inosine monophosphate, histamine and serine made significant contribution to the separation. Compared with the control diet, the transcriptomics analysis identified a total of 334 different expressed genes, of which 298 genes were up-regulated and thirty-six genes were down-regulated in the Hyp supplementation group. The altered genes of the Hyp supplementation group were involved in collagen metabolism, lipid metabolism and energy metabolism. The integrated results revealed that the increased muscle collagen content in the Hyp supplementation diet was partly because of its enhancement of biosynthesis and the reduction of degradation. The improvement of muscle quality by dietary Hyp supplementation could also be related to a good utilisation of glucose through enhancement of glycolysis. It was concluded that dietary Hyp supplementation could improve flesh quality because of comprehensive metabolism changes including elevated collagen content, glycolysis, lipid metabolism and flesh flavour of LYC. The present study provided a novel strategy to understand the underlying molecular mechanism of flesh quality of LYC fed diet with Hyp supplementation.

The purpose of this study was primarily to evaluate the association of total fibre intake with the risk of incident chronic kidney disease (CKD). We also evaluated the association of dietary fibre from fruits, vegetables, cereals and legumes with the incidence of CKD in a population-based prospective study. We followed up 1630 participants of the Tehran Lipid and Glucose Study for 6·1 years, who were initially free of CKD. Baseline diet was assessed by a valid and reliable FFQ. Estimated glomerular filtration rate (eGFR) was calculated, using the Modification of Diet in Renal Disease Study equation, and CKD was defined as eGFR <60 ml/min per 1·73 m2. OR using multivariable logistic regression was reported for the association of incident CKD with tertiles of dietary fibre intake. After adjustment for age, sex, smoking, total energy intake, physical activity, diabetes and using angiotensin-converting-enzyme inhibitor, the OR for subjects in the highest compared with the lowest tertile of total fibre intake was 0·47 (95 % CI 0·27, 0·86). In addition, for every 5 g/d increase in total fibre intake, the risk of incident CKD decreased by 11 %. After adjusting for potential confounders, OR for participants in the highest compared with the lowest tertile of fibre from vegetables was 0·63 (95 % CI 0·43, 0·93) and from legumes it was 0·68 (95 % CI 0·47, 0·98). We observed inverse associations between total fibre intake and risk of incident CKD, which demonstrate that high fibre intake, mainly from legumes and vegetables, may reduce the occurrence of CKD.

Ca digestibility and utilisation in growing pigs are not well understood, and are usually neglected in diet formulation. This has implications not only for the accurate determination of its requirements but also for its interactions with other nutrients. A systematic review and meta-analysis (meta-regression) of published trials was carried out to quantify factors affecting Ca absorption and utilisation, and to derive an estimate of Ca endogenous excretion. The analysis was carried out on the data from forty studies, corresponding to 201 treatments performed on 1204 pigs. The results indicated that although Ca absorption and retention (g/kg of body weight per d) increased with increasing Ca intake (P<0·001), non-phytate-P intake (P<0·001) and exogenous phytase supplementation (P<0·001), these values decreased with increasing phytate-P intake (P<0·05). Interactions between exogenous phytase and Ca intake, indicating reduced efficacy of this enzyme (P<0·001), and between phytate-P intake and exogenous phytase, counteracting the direct negative effect of phytate-P (P<0·05) on Ca absorption and retention, were also detected. There were no effects of animal-related characteristics, such as pig genotype in Ca absorption and retention. The large amount of variance explained in Ca absorption (90 %) and retention (91 %) supported our choice of independent variables. Endogenous Ca losses obtained via linear regression were 239 mg/kg of DM intake (95 % CI 114, 364). These outcomes advance the current understanding of Ca digestibility and utilisation, and should contribute towards establishing requirements for digestible Ca. Consequently, pig diets will be more correctly formulated if digestible Ca values are used in estimating requirements for Ca.

n-3 Fatty acids, flavonoids and resveratrol are well publicised for their beneficial effects on human health and wellbeing. Identifying common, underlying biological mechanisms targeted by these functional foods would therefore be informative for the public health sector for advising on nutritional health and disease, food and drug product development and consumer interest. The aim of this study was to explore the potential effects of gene expression changes associated with n-3 fatty acids EPA and DHA, flavonoids and resveratrol on modifying biological systems and disease pathways. To test this, publicly available human microarray data for significant gene expression changes associated with dietary intervention with EPA/DHA, flavonoids and resveratrol was subjected to pathway analysis and significance testing for overlap with signals from genome-wide association studies (GWAS) for common non-communicable diseases and biological functions. There was an enrichment of genes implicated in immune responses and disease pathways which was common to all of the treatment conditions tested. Analysis of biological functions and disease pathways indicated anti-tumorigenic properties for EPA/DHA. In line with this, significance testing of the intersection of genes associated with these functional foods and GWAS hits for common biological functions (ageing and cognition) and non-communicable diseases (breast cancer, CVD, diabesity, neurodegeneration and psychiatric disorders) identified significant overlap between the EPA/DHA and breast cancer gene sets. Dietary intervention with EPA/DHA, flavonoids and resveratrol can target important biological and disease pathways suggesting a potentially important role for these bioactive compounds in the prevention and treatment of dietary-related diseases.

Findings from observational studies investigating the association between fruit and vegetable consumption and risk of depression were inconsistent. We conducted a systematic review and meta-analysis to summarise available data on the association between fruit and vegetable intake and depression. A systematic literature search of relevant reports published in Medline/PubMed, ISI (Web of Science), SCOPUS and Google Scholar until Oct 2017 was conducted. Data from 27 publications (sixteen cross-sectional, nine cohort and two case–control studies) on fruit, vegetables and/or total fruit and vegetable consumption in relation to depression were included in the systematic review. A total of eighteen studies that reported relative risks (RR), hazard ratios or OR for the relationship were included in the meta-analysis. The pooled RR for depression in the highest v. the lowest category of fruit intake was 0·83 (95 % CI 0·71, 0·98) in cohort studies and 0·76 (95 % CI 0·63, 0·92) in cross-sectional studies. Consumption of vegetables was also associated with a 14 % lower risk of depression (overall RR=0·86; 95 % CI 0·75, 0·98) in cohort studies and a 25 % lower risk of depression (overall RR=0·75; 95 % CI 0·62, 0·91) in cross-sectional studies. Moreover, an inverse significant association was observed between intake of total fruit and vegetables and risk of depression (overall RR=0·80; 95 % CI 0·65, 0·98) in cross-sectional studies. In a non-linear dose–response association, we failed to find any significant association between fruit or vegetable intake and risk of depression (fruit (cross-sectional studies): Pnon-linearty=0·12; vegetables (cross-sectional studies): Pnon-linearty<0·001; (cohort studies) Pnon-linearty=0·97). Meta-regression of included observational studies revealed an inverse linear association between fruit or vegetable intake and risk of depression, such that every 100-g increased intake of fruit was associated with a 3 % reduced risk of depression in cohort studies (RR=0·97; 95 % CI 0·95, 0·99). With regard to vegetable consumption, every 100-g increase in intake was associated with a 3 % reduced risk of depression in cohort studies (RR=0·97; 95 % CI 0·95, 0·98) and 5 % reduced odds in cross-sectional studies (RR=0·95; 95 % CI 0·91, 0·98). This meta-analysis of observational studies provides further evidence that fruit and vegetable intake was protectively associated with depression. This finding supports the current recommendation of increasing fruit and vegetable intake to improve mental health.

The aim of the study was to investigate how the dietary sterol composition, including cholesterol, phytosterol:cholesterol ratio and phytosterols, affect the absorption, biliary excretion, retention, tissue storage and distribution of cholesterol and individual phytosterols in Atlantic salmon (Salmo salar L.). A feeding trial was conducted at two different temperatures (6 and 12°C), using nine different diets with varying contents of phytosterols, cholesterol and phytosterol:cholesterol ratio. Cholesterol retention values were clearly dependent on dietary cholesterol, and showed that fish fed cholesterol levels <1000 mg/kg feed produced considerable quantities of cholesterol de novo. Despite this production, cholesterol content increased with increasing dietary cholesterol in liver, plasma, bile, muscle, adipose tissue and whole fish at 12°C, and in plasma, bile and whole fish at 6°C. The tissue sterol composition generally depended on the dietary cholesterol content and on the dietary phytosterol:cholesterol ratio, but not on the dietary phytosterol content in itself. Campesterol and brassicasterol appeared to be the phytosterols with the highest intestinal absorption in Atlantic salmon. There was a high biliary excretion of campesterol, but not of brassicasterol, which accumulated in tissues and particularly in adipose tissue, with 2-fold-higher retention at 12°C compared with 6°C. Campesterol had the second highest retention of the phytosterols in the fish, but with no difference between the two temperatures. Other phytosterols had very low retention. Although brassicasterol retention decreased with increasing dietary phytosterols, campesterol retention decreased with increasing dietary cholesterol, indicating differences in the uptake mechanisms for these two sterols.

To investigate the P absorption and gene expression levels of related co-transporters, type IIb sodium-dependent phosphate co-transporter (NaPi-IIb), inorganic phosphate transporter 1 (PiT-1) and inorganic phosphate transporter 2 (PiT-2) in the small intestine of broilers, 450 1-d-old Arbor Acres male broilers were randomly allocated to one of three treatments with ten replicate cages of fifteen birds per cage for each treatment in a completely randomised design. Chickens were fed a diet with no added inorganic P (containing 0·06 % non-phytate P (NPP)) or with either 0·21 or 0·44 % NPP for 21 d. Plasma P concentration in the hepatic portal vein, mRNA and protein expression levels of NaPi-IIb, PiT-1 and PiT-2 were determined at 7, 14 and 21 d of age. The results showed that the concentration of P in plasma in the hepatic portal vein increased as dietary NPP increased (P<0·0001). At 14 and 21 d of age, the increase in dietary NPP inhibited (P<0·003) NaPi-IIb mRNA expression level in the duodenum, as well as PiT-1 mRNA and protein expression levels in the ileum, but promoted NaPi-IIb protein expression level (P<0·002) and PiT-2 mRNA and protein expression levels (P<0·04) in the duodenum. These results suggest that NaPi-IIb, PiT-1 and PiT-2 might be important P transporters in the small intestine of broilers. Higher intestinal P absorption may be achieved by up-regulating the protein expression levels of NaPi-IIb and PiT-2 and down-regulating the protein expression of PiT-1.

This study systematised and synthesised the results of observational studies that were aimed at supporting the association between dietary patterns and cardiometabolic risk (CMR) factors among adolescents. Relevant scientific articles were searched in PUBMED, EMBASE, SCIENCE DIRECT, LILACS, WEB OF SCIENCE and SCOPUS. Observational studies that included the measurement of any CMR factor in healthy adolescents and dietary patterns were included. The search strategy retained nineteen articles for qualitative analysis. Among retained articles, the effects of dietary pattern on the means of BMI (n 18), waist circumference (WC) (n 9), systolic blood pressure (n 7), diastolic blood pressure (n 6), blood glucose (n 5) and lipid profile (n 5) were examined. Systematised evidence showed that an unhealthy dietary pattern appears to be associated with poor mean values of CMR factors among adolescents. However, evidence of a protective effect of healthier dietary patterns in this group remains unclear. Considering the number of studies with available information, a meta-analysis of anthropometric measures showed that dietary patterns characterised by the highest intake of unhealthy foods resulted in a higher mean BMI (0·57 kg/m²; 95 % CI 0·51, 0·63) and WC (0·57 cm; 95 % CI 0·47, 0·67) compared with low intake of unhealthy foods. Controversially, patterns characterised by a low intake of healthy foods were associated with a lower mean BMI (−0·41 kg/m²; 95 % CI −0·46,−0·36) and WC (−0·43 cm; 95 % CI −0·52,−0·33). An unhealthy dietary pattern may influence markers of CMR among adolescents, but considering the small number and limitations of the studies included, further studies are warranted to strengthen the evidence of this relation.

Osteoporosis and adipose tissue are closely related with many contradictions. Visfatin is an adipokine that is related to osteoporosis and adiposity. This nutrigenomics study examined the interaction between visfatin genotypes and dietary fat intake, with regard to bone mineral density (BMD) among an obese population. In this cross-sectional study, 336 subjects were enrolled; the mean age was 38·25 (sd 11·69) years and the mean BMI was 31·79 (sd 4·77) kg/m2. Laboratory measurements were lipid profile, insulin and fasting blood sugar. Bone density measurements were assessed by dual-energy X-ray absorptiometry. Dietary data were collected through a 3-d 24-h dietary recall. Genotyping for visfatin gene SNP (rs2110385) was performed by the PCR-restriction fragment length polymorphism method. The frequency of GG, GT and TT genotypes were 33·92 48·51 and 17·54 %, respectively, and 86·6 % of participants were women. The results showed that subjects with TT genotypes had significantly higher lumbar BMD, T score and z score (P<0·0001). After categorisation by percentage of fat intake (30 % of total energy content as a cut-off point), no interaction was found, but when categorised by fat types, we found an interaction between visfatin genotypes and dietary PUFA intake in terms of the hip T score and z score (P=0·043, B= −0·08; P=0·04, B= −0·078, respectively). There was a significant relationship between high PUFA intake and lower energy and protein intake. When participants were categorised by median PUFA intake (22·8 g), it was concluded that subjects with GG genotype who had high PUFA-intake diets had lower hip z scores and T scores, unlike the other genotypes.

Whole-grain highland hull-less barley (WHLB) contains high amounts of bioactive compounds that potentially exhibit cholesterol-lowering effects. This study investigated the hypocholesterolaemic effect of WHLB. A total of seventy-two male Sprague–Dawley rats were divided into four groups and were fed with the normal control diet, high-fat diet (HFD) and HFD containing low or high dose (10 or 48·95 %) of WHLB. High dose of WHLB significantly decreased the organ indexes of liver and abdominal fat and lipid levels of plasma and liver in HFD rats. The lipid regulation effect of WHLB, which was reconfirmed through hepatocyte morphologic observation, was accompanied by a large excretion of bile acids in the small intestinal contents and the faeces. Real-time PCR analyses, which were further reconfirmed through Western blot analyses, revealed that a high dose of WHLB significantly enhanced the hepatic expressions of AMP-activated protein kinase α, cholesterol 7α-hydroxylase, LDL receptor, liver X receptor, and PPARα and decreased the expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase. It also enhanced the ileal expression of farnesoid X receptor and resulted in the decrease of expression of apical sodium-dependent bile acid transporter. WHLB exhibited hypocholesterolaemic effects mainly by inhibiting cholesterol synthesis, cholesterol accumulation in peripheral tissue, and bile acid reabsorption and by stimulating bile acid synthesis.

Diabetes mellitus is a metabolic disease spreading worldwide that has been reported to worsen the development and progression of other diseases (cancer, vascular diseases and dementia). To establish functional rice lines with anti-postprandial hyperglycaemic effects, we developed mutant rice lines, which lack one or two gene(s) related to starch synthesis, and evaluated their effects. Powder of mutant rice lines or other grains was loaded to rats fasted overnight (oral grain powder loading test). Incremental area under time-concentration curves (iAUC) were calculated with monitored blood glucose levels. Rice lines with anti-postprandial hyperglycaemic effects were separated by cluster analysis with calculated iAUC. A double mutant rice #4019 (starch synthase IIIa (ss3a)/branching enzyme IIb (be2b)), one of the screened mutant rice lines, was fed to Goto-Kakizaki (GK) rats, an animal model for type 2 diabetes, for 5 weeks. Plasma levels of C-peptide, a marker of pancreatic insulin secretion, were measured with ELISA. For in vitro study, a rat pancreatic cell line was cultured with a medium containing rat serum which was sampled from rats fed #4019 diet for 2 d. After 24-h of incubation, an insulin secretion test was performed. Through the oral rice powder loading test, seven rice lines were identified as antidiabetic rice lines. The intake of #4019 diet increased plasma C-peptide levels of GK rats. This result was also observed in vitro. In rat serum added to cell medium, ornithine was significantly increased by the intake of #4019. In conclusion, the mutant rice #4019 promoted pancreatic insulin secretion via elevation of serum ornithine levels.

At birth, when immune responses are insufficient, there begins the development of the defence capability against pathogens. Leptin and adiponectin, adipokines that are present in breast milk, have been shown to play a role in the regulation of immune responses. We report here, for the first time, the influence of in vivo adipokine supplementation on the intestinal immune system in early life. Suckling Wistar rats were daily supplemented with leptin (0·7 μg/kg per d, n 36) or adiponectin (35 μg/kg per d, n 36) during the suckling period. The lymphocyte composition, proliferation and cytokine secretion from mesenteric lymph node lymphocytes (on days 14 and 21), as well as intestinal IgA and IgM concentration (day 21), were evaluated. At day 14, leptin supplementation significantly increased the TCRαβ+ cell proportion in mesenteric lymph nodes, in particular owing to an increase in the TCRαβ+ CD8+ cell population. Moreover, the leptin or adiponectin supplementation promoted the early development CD8+ cells, with adiponectin being the only adipokine capable of enhancing the lymphoproliferative ability at the end of the suckling period. Although leptin decreased intestinal IgA concentration, it had a trophic effect on the intestine in early life. Supplementation of both adipokines modulated the cytokine profile during (day 14) and at the end (day 21) of the suckling period. These results suggest that leptin and adiponectin during suckling play a role in the development of mucosal immunity in early life.

The incidence of obesity and its metabolic complications are rapidly increasing and become a major public health issue. This trend is associated with an increase in the prevalence of non-alcoholic fatty liver disease (NAFLD), insulin resistance and diabetes. The sequence of events leading to NAFLD progression and mitochondrial dysfunction and their interrelation remains to be elucidated. This study aimed to explore the installation and progression of NAFLD and its association with the liver mitochondrial structure and activity changes in rats fed an obesogenic diet up to 20 weeks. Male Wistar rats were fed either a standard or high-fat–high-fructose (HFHFR) diet and killed on 4, 8, 12, 16 and 20 weeks of diet intake. Rats fed the HFHFR diet developed mildly overweight, associated with increased adipose tissue weight, hepatic steatosis, hyperglycaemia and hyperinsulinaemia after 8 weeks of HFHFR diet. Hepatic steatosis and many biochemical modifications plateaued at 8–12 weeks of HFHFR diet with slight amelioration afterwards. Interestingly, several biochemical and physiological parameters of mitochondrial function, as well as its phospholipid composition, in particular cardiolipin content, were tightly related to hepatic steatosis installation. These results showed once again the interrelation between hepatic steatosis development and mitochondrial activity alterations without being able to say whether the mitochondrial alterations preceded or followed the installation/progression of hepatic steatosis. Because both hepatic steatosis and mitochondrial alterations occurred as early as 4 weeks of diet, future studies should consider these four 1st weeks to reveal the exact interconnection between these major consequences of obesogenic diet intake.

Mammalian neonates undergo rapid transitions from a sterile uterine environment with a continuous intravenous supply of nutrients to a microbe-rich environment with intermittent ingesting of colostrum/milk via the gut. Currently, little is known about the colostrum-induced alterations of intestinal mucosal proteins in piglets with intra-uterine growth restriction (IUGR). In this study, we sought to investigate the innate differences and effects of colostrum on alterations in small-intestinal proteomes of IUGR piglets. Two IUGR (approximately 0·9 kg) and two normal-birth weight (NBW; approximately 1·3 kg) piglets were obtained from each of six sows at birth. One half (n 12; 6 IUGR v. 6 NBW) of the selected newborn piglets were killed to obtain jejunum samples, and the other half (n 12; 6 IUGR v. 6 NBW) of the newborn piglets were allowed to suckle colostrum from their own mothers for 24 h before jejunum sample collection. On the basis of proteomic analysis, we identified thirty-one differentially expressed proteins in the jejunal mucosa between IUGR and normal neonates before or after colostrum consumption. The intestinal proteins altered by colostrum feeding play important roles in the following: (1) increasing intestinal integrity, transport of nutrients, energy metabolism, protein synthesis, immune response and, therefore, cell proliferation; and (2) decreasing oxidative stress, and therefore cell apoptosis, in IUGR neonates. However, colostrum only partially ameliorated the inferior status of the jejunal mucosa in IUGR neonates. These findings provide the first evidence in intestinal protein alterations of IUGR neonates in response to colostrum ingestion, and thus render new insights into the mechanisms responsible for impaired growth in IUGR neonates and into new nutritional intervention strategies.