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.

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.

Aplastic anaemia (AA) is characterised by pancytopenia resulting from a marked reduction in haemopoietic stem cells (HSC). The regulation of haemopoiesis depends on the interaction between HSC and various cells of the bone marrow (BM) microenvironment, including BM-derived mesenchymal stromal cells (BMSC). The purpose of this study was to analyse the biological effect of nutritional supplement (NS), a dietary supplement consisting of thirty-six compounds: amino acids, nucleotides, vitamins and micronutrients on the BMSC of AA rats. The AA rat model was established by irradiating X-ray (2·5 Gy) and intraperitoneal injections of cyclophosphamide (35 mg/kg; Sigma) and chloramphenicol (35 mg/kg; Sigma). Then AA rats were fed with NS in a dose-dependent manner (2266·95, 1511·3, 1057·91 mg/kg d) by intragastric administration. The effect of NS on the BMSC of AA rats was analysed. As compared with AA rats, NS treatment significantly improved these peripheral blood parameters and stimulated the proliferation of total femoral nucleated cells. NS treatment affected proliferative behaviour of BMSC and suppressed BMSC differentiation to adipocytes. Furthermore, NS treatment of AA rats accelerated osteogenic differentiation of BMSC and enhanced bone mineral density. Co-incubation of HSC with mesenchymal stromal cells and serum from AA rats subjected to high-dose NS markedly improved the yield of CD34+cells. Protein microarray analysis revealed that there were eleven differentially expressed proteins in the NS group compared with the AA rat group. The identified specific NS might be implicated in rehabilitation of BMSC in AA rats, suggesting their potential of nutritional support in AA treatment.

Balanced vegetarian diets are popular, although they are nearly absent in creatine and carnosine and contain considerably less carnitine than non-vegetarian diets. Few longitudinal intervention studies investigating the effect of a vegetarian diet on the availability of these compounds currently exist. We aimed to investigate the effect of transiently switching omnivores onto a vegetarian diet for 6 months on muscle and plasma creatine, carnitine and carnosine homeostasis. In a 6-month intervention, forty omnivorous women were ascribed to three groups: continued omnivorous diet (control, n 10), vegetarian diet without supplementation (Veg+Pla, n 15) and vegetarian diet combined with daily β-alanine (0·8–0·4 g/d) and creatine supplementation (1 g creatine monohydrate/d) (Veg+Suppl, n 15). Before (0 months; 0M), after 3 months (3M) and 6 months (6M), a fasted venous blood sample and 24-h urine was collected, and muscle carnosine content was determined by proton magnetic resonance spectroscopy (1H-MRS). Muscle biopsies were obtained at 0M and 3M. Plasma creatine and muscle total creatine content declined from 0M to 3M in Veg+Pla (P=0·013 and P=0·009, respectively), whereas plasma creatine increased from 0M in Veg+Suppl (P=0·004). None of the carnitine-related compounds in plasma or muscle showed a significant time×group interaction effect. 1H-MRS-determined muscle carnosine content was unchanged over 6M in control and Veg+Pla, but increased in Veg+Suppl in soleus (P<0·001) and gastrocnemius (P=0·001) muscle. To conclude, the body creatine pool declined over a 3-month vegetarian diet in omnivorous women, which was ameliorated when accompanied by low-dose dietary creatine supplementation. Carnitine and carnosine homeostasis was unaffected by a 3- or 6-month vegetarian diet, respectively.

To investigate the effects of heat stress on broiler metabolism, we assigned 144 broilers to normal control (NC), heat stress (HS) or pair-fed (PF) groups and then monitored the effects using growth performance, carcass characteristics, biochemical assays and GC-MS-based metabolomics. The up-regulation of cloacal temperature confirmed that our experiment was successful in inducing chronic heat stress. The average daily gain and average daily feed intake of the HS group were significantly lower than those of the NC group, by 28·76 and 18·42 %, respectively (P<0·001), whereas the feed:gain ratio was significantly higher, by 14·49 % (P=0·003), and heat stress also increased leg proportion (P=0·027) and intramuscular fat proportion (P<0·001) and decreased breast proportion (P=0·009). When comparing the HS and NC groups and HS and PF groups, our metabolomics approach identified seventy-eight and thirty-four metabolites, respectively, with significantly different levels (variable importance in the projection values >1 and P<0·05). The greater feed:gain ratio of the HS group was significantly positively correlated with the leg, abdominal fat, subcutaneous fat and intramuscular fat proportions and levels of some free amino acids (proline, l-cysteine, methionine and threonine) but was negatively correlated with breast proportion and levels of some NEFA (stearic acid, arachidonic acid, palmitic acid and oleic acid). These findings indicated that the heat-stressed broilers were in negative energy balance and unable to effectively mobilise fat, thereby resulting in protein decomposition, which subsequently affected growth performance and carcass characteristics.

Currently, energy evaluation of fish feeds is performed on a digestible energy basis. In contrast to net energy (NE) evaluation systems, digestible energy evaluation systems do not differentiate between the different types of digested nutrients regarding their potential for growth. The aim was to develop an NE evaluation for fish by estimating the energy efficiency of digestible nutrients (protein, fat and carbohydrates) and to assess whether these efficiencies differed between Nile tilapia and rainbow trout. Two data sets were constructed. The tilapia and rainbow data set contained, respectively, eight and nine experiments in which the digestibility of protein, fat and energy and the complete energy balances for twenty-three and forty-five diets was measured. The digestible protein (dCP), digestible fat (dFat) and digestible carbohydrate intakes (dCarb) were calculated. By multiple regression analysis, retained energy (RE) was related to dCP, dFat and dCarb. In tilapia, all digestible nutrients were linearly related to RE (P<0·001). In trout, RE was quadratically related to dCarb (P<0·01) and linearly to dCP and dFat (P<0·001). The NE formula was NE=11·5×dCP+35·8×dFAT+11·3×dCarb for tilapia and NE=13·5×dCP+33·0×dFAT+34·0×dCarb–3·64×(dCarb)2 for trout (NE in kJ/(kg0·8×d); dCP, dFat and dCarb in g/(kg0·8×d)). In tilapia, the energetic efficiency of dCP, dFat and dCarb was 49, 91 and 66 %, respectively, showing large similarity with pigs. Tilapia and trout had similar energy efficiencies of dCP (49 v. 57 %) and dFat (91 v. 84 %), but differed regarding dCarb.

There is much epidemiological evidence suggesting a reduced risk of development of type 2 diabetes (T2D) in habitual coffee drinkers, however to date there have been few longer-term interventions, directly examining the effects of coffee intake on glucose and lipid metabolism. Previous studies may be confounded by inter-individual variation in caffeine metabolism. Specifically, the rs762551 SNP in the CYP1A2 gene has been demonstrated to influence caffeine metabolism, with carriers of the C allele considered to be of a ‘slow’ metaboliser phenotype. This study investigated the effects of regular coffee intake on markers of glucose and lipid metabolism in coffee-naïve individuals, with novel analysis by rs762551 genotype. Participants were randomised to either a coffee group (n 19) who consumed four cups/d instant coffee for 12 weeks or a control group (n 8) who remained coffee/caffeine free. Venous blood samples were taken pre- and post-intervention. Primary analysis revealed no significant differences between groups. Analysis of the coffee group by genotype revealed several differences. Before coffee intake, the AC genotype (‘slow’ caffeine metabolisers, n 9) displayed higher baseline glucose and NEFA than the AA genotype (‘fast’ caffeine metabolisers, n 10, P<0·05). Post-intervention, reduced postprandial glycaemia and reduced NEFA suppression were observed in the AC genotype, with the opposite result observed in the AA genotype (P<0·05). These observed differences between genotypes warrant further investigation and indicate there may be no one-size-fits-all recommendation with regard to coffee drinking and T2D risk.

The effectiveness of salt iodisation in improving the mental development of young children has not been assessed. We implemented a community-based cluster-randomised effectiveness trial in sixty randomly selected districts in the Amhara region of Ethiopia. We randomly allocated each district to treatment and randomly selected one of its villages. In parallel to national salt iodisation efforts, iodised salt was brought early into the markets of the thirty intervention villages before it became widely available in the thirty control villages 4–6 months later. The primary outcome was children’s mental development scores on the Bayley Scales. This was an intention-to-treat analysis using mixed linear models adjusted for covariates and clusters. The trial was registered at ClinicalTrials.gov, NCT013496. We assessed 1835 infants aged 5–11 months at baseline. The same children (85 % of the sample) were re-assessed at 20–29 months when all villages had iodised salt. At endline, urinary iodine concentration was higher in children in the intervention group compared with those in the control group (median 228·0 v. 155·1 µg/l, P=0·001). The intervention group had higher scores compared with the control group on the Bayley composite score (raw scores:130·60 v. 128·51; standardised scores: 27·8 v. 26·9; d=0·13; 95 % CI 0·02, 0·23) and three of the four subscales: cognitive (53·27 v. 52·54, d=0·13; 95 % CI 0·03, 0·23), receptive language (20·71 v. 20·18, d=0·13; 95 % CI 0·03, 0·24) and fine motor (35·45 v. 34·94, d=0·15; 95 % CI 0·04, 0·25). The introduction of iodised salt contributes to children’s higher urinary iodine concentration and mental development.

In 2011, the Committee on Nutrition of the European Society for Paediatric Gastroenterology, Hepatology and Nutrition systematically reviewed published evidence related to the safety and health effects of the administration of formulae supplemented with pro- and/or prebiotics compared with unsupplemented formulae. We updated evidence on the effects of the administration of prebiotic-supplemented infant formulae (IF) compared with unsupplemented IF. Five databases were searched up to March 2017 for randomised controlled trials. In all, forty-one publications were identified, including twenty-five new publications. The administration of currently evaluated prebiotic-supplemented formulae to healthy infants does not raise safety concerns with regard to growth and adverse effects. Some favourable clinical effects are possible, primarily stool softening, which may be beneficial in some infants. Currently, there is no existing robust evidence to recommend the routine use of prebiotic-supplemented formulae. The latter conclusion may reflect the small amount of data on specific prebiotics and outcomes, rather than a genuine lack of an effect. The efficacy and safety should be considered for each prebiotic(s)-supplemented formula.

Malnutrition is a common feature of chronic and acute diseases, often associated with a poor prognosis, including worsening of clinical outcome, owing, among other factors, to dysfunction of the most internal organs and systems affecting the absorption, metabolism and elimination of drugs and nutrients. Taurine is involved in numerous biological processes and is required in increased amounts in response to pathological conditions. The aim of this study was to describe the behaviour of taurine in well-nourished (WN) rats and to analyse the influence of protein–energy undernutrition on the pharmacokinetic (PK) parameters of taurine, using a PK model. Wistar rats were randomly distributed into two groups, WN and undernourished (UN), and taurine was administered intravenously or orally at different doses: 1, 10 and 100 mg. Population pharmacokinetic modelling of plasma levels was performed using the NONMEM 7.2 program. Several distribution and absorption models were explored in combination with dose and/or time covariate effects. Covariates such as nutritional status, serum albumin, body weight and score of undernutrition were used. A two-compartment population pharmacokinetic model with zero-order endogenous formation, passive absorption, first-order kinetics distribution and non-linear elimination with parallel Michaelis–Menten excretion and reabsorption processes best described taurine pharmacokinetics. Undernutrition acted as a covariate reducing the Vmax of the active elimination process. Data analysis showed linear absorption and distribution, and non-linear elimination processes for taurine. Elimination of taurine was reduced in UN animals, suggesting that the reabsorption process via the secretion transporter was modified in that group.

High adherence to healthy diets has the potential to prevent disease and prolong life span, and healthy dietary pattern scores have each been associated with disease and mortality. We studied two commonly promoted healthy diet scores (modified Mediterranean diet score (mMED) and the Healthy Nordic Food Index (HNFI)) and the combined effect of the two scores in association with all-cause and cause-specific mortality (cancer, CVD and ischaemic heart disease). The study included 38 428 women (median age of 61 years) from the Swedish Mammography Cohort. Diet and covariate data were collected in a questionnaire. mMED and HNFI were generated and categorised into low-, medium- and high-adherence groups, and in nine combinations of these. Multivariable-adjusted hazard ratios (HR) of register-ascertained mortality and 95 % CI were calculated in Cox proportional hazards regression analysis. During follow-up (median: 17 years), 10 478 women died. In the high-adherence categories compared with low-adherence categories, the HR for all-cause mortality was 0·76 (95 % CI 0·70, 0·81) for mMED and 0·89 (95 % CI 0·83, 0·96) for HNFI. Higher adherence to mMED was associated with lower mortality in each stratum of HNFI in the combined analysis. In general, mMED, compared with HNFI, was more strongly associated with a lower cause-specific mortality. In Swedish women, both mMED and HNFI were inversely associated with all-cause and cardiovascular mortality. The combined analysis, however, indicated an advantage to be adherent to the mMED. The present version of HNFI did not associate with mortality independent of mMED score.