Rice bran (RB) consumption has been shown to reduce colorectal cancer (CRC) growth in mice and modify the human stool microbiome. Changes in host and microbial metabolism induced by RB consumption was hypothesised to modulate the stool metabolite profile in favour of promoting gut health and inhibiting CRC growth. The objective was to integrate gut microbial metabolite profiles and identify metabolic pathway networks for CRC chemoprevention using non-targeted metabolomics. In all, nineteen CRC survivors participated in a parallel randomised controlled dietary intervention trial that included daily consumption of study-provided foods with heat-stabilised RB (30 g/d) or no additional ingredient (control). Stool samples were collected at baseline and 4 weeks and analysed using GC-MS and ultra-performance liquid chromatography-MS. Stool metabolomics revealed 93 significantly different metabolites in individuals consuming RB. A 264-fold increase in β-hydroxyisovaleroylcarnitine and 18-fold increase in β-hydroxyisovalerate exemplified changes in leucine, isoleucine and valine metabolism in the RB group. A total of thirty-nine stool metabolites were significantly different between RB and control groups, including increased hesperidin (28-fold) and narirutin (14-fold). Metabolic pathways impacted in the RB group over time included advanced glycation end products, steroids and bile acids. Fatty acid, leucine/valine and vitamin B6 metabolic pathways were increased in RB compared with control. There were 453 metabolites identified in the RB food metabolome, thirty-nine of which were identified in stool from RB consumers. RB consumption favourably modulated the stool metabolome of CRC survivors and these findings suggest the need for continued dietary CRC chemoprevention efforts.

Legume consumption plays a pivotal role in the prevention and treatment of the metabolic syndrome (MetS). This systematic review aimed to highlight the beneficial effects of legume interventions for the prevention and/or improvement of parameters related to the MetS and the implicated metabolic pathways so far reported. The methodology involved a search in four electronic databases (Medline, Web of Science, Scopus, Cochrane Library) from January 2007 to December 2014, considering as descriptors ‘Metabolic Syndrome’ and ‘Fabaceae’ and adequately adjusting the equation in each one of them. In total, forty-one studies were finally included. The majority of the studies described a regulating effect on glucose and lipid metabolism due to legume administration, whereas effects on blood pressure and renal parameters are not fully described. Regarding the metabolic pathways involved, they include the up-regulation of genes related to β-oxidation and acetyl-CoA degradation and the down-regulation of glycolytic and lipogenesis genes, as well as those associated with the acetyl-CoA synthesis. The ameliorating effects of legume consumption on the alterations associated with the MetS are clearly reported and coincide with changes in the expression of protein and genes involved in lipid and glucose metabolism. More research needs to be conducted including more legume species that are highly consumed as part of a healthy dietary pattern.

Hyperglycemia, dyslipidemia and hyperhomocysteinemia are associated with both adult cardiovascular disease (CVD) and having a child with a congenital heart disease (CHD). We investigated associations between CVD in grandparents and the risk of CHD in grandchildren. In a case–control family study, we obtained detailed questionnaire information on CVD and CHD in 247 families with a CHD child and 203 families without a CHD child. Grandparents with CVD or intermittent claudication (IC) were significantly associated with an increased risk for CHD in grandchildren [OR 1.39 (95% CI 1.03–1.89) and OR 2.77 (95% CI 1.02–7.56), respectively]. The risk of CHD grandchildren was particularly increased in paternal grandfathers with CVD [OR 1.85 (95% CI 1.01–3.37)]. Overall, having a grandparent with CVD increased the risk for CHD in the grandchild by 1.65 (95% CI 1.12–2.41). After adjustment for potential maternal confounders, this risk was 1.44 (95% CI 0.94–2.21). Having two or more grandparents with CVD was associated with an approximately threefold risk for CHD grandchildren [OR adjusted 2.72 (95% CI 1.08–6.89)]. Our data suggest that CVD and IC in grandparents are associated with an increased risk of having a CHD grandchild. These first findings may be explained by shared causality of derangements in metabolic pathways and are in line with the fetal origins of health and disease.

Following identification of essential micronutrients, there has been a continuum of research aimed at revealing their absorption, transport, utilization as cofactors, and excretion and secretion. Among those cases that have received our attention are vitamin B6, riboflavin, biotin, lipoate, ascorbate, and certain metal ions. Circulatory transport and cellular uptake of the water-soluble vitamins exhibit relative specificity and facilitated mechanisms at physiological concentrations. Isolation of enzymes and metabolites from micro–organisms and mammals has provided information on pathways involved in cofactor formation and metabolism. Kinases catalysing phosphorylation of B6 and riboflavin have a preference for Zn2+ in stereospecific chelates with adenosine triphosphate. The synthetase for flavin adenine dinucleotide prefers Mg2+. The flavin mononucleotide-dependent oxidase that converts the 5′–phosphates of pyridoxine and of pyridoxamine to pyridoxal phosphate is a connection between B6 and riboflavin and is a primary control point for conversion of B6 to its coenzyme. Sequencing and cloning of a side–chain oxidase for riboflavin was achieved. Details on binding and function have been delineated for some cofactor systems, especially in several flavoproteins. There is both photochemical oxidation and oxidative catabolism of B6 and riboflavin. Both biotin and lipoate undergo oxidation of their acid side chains with redox cleavage of the rings. Applications from our findings include the development of affinity absorbents, enhanced drug delivery, delineation of residues in biopolymer modification, pathogen photoinactivation in blood components, and input into human dietary recommendations. Ongoing and future research in the cofactor arena can be expected to add to this panoply. At the molecular level, the way in which the same cofactor can participate in diverse catalytic reactions resides in interactions with surrounding enzyme structures that must be determined case by case. At the level of human intake, more knowledge is desirable for making micronutrient recommendations based on biochemical indicators, especially for the span between infancy and adulthood.

Giardia lamblia, a protozoan parasite, infects a wide variety of vertebrates, including humans. Studies indicate that this anaerobic protist possesses a limited ability to synthesize lipid molecules de novo and depends on supplies from its environment for growth and differentiation. It has been suggested that most lipids and fatty acids are taken up by endocytic and non-endocytic pathways and are used by Giardia for energy production and membrane/organelle biosynthesis. The purpose of this article is to provide an update on recent progress in the field of lipid research of this parasite and the validation of lipid metabolic pathways through recent genomic information. Based on current cellular, biochemical and genomic data, a comprehensive pathway has been proposed to facilitate our understanding of lipid and fatty acid metabolism/syntheses in this waterborne pathogen. We envision that the current review will be helpful in identifying targets from the pathways that could be used to design novel therapies to control giardiasis and related diseases.

This review describes some of the developments in helminth biochemistry that have taken place over the last 40 years. Since the early 1970s the main anabolic and catabolic pathways in parasitic helminths have been worked out. The mode of action of the majority of anthelmintics is now known, but in many cases the mechanisms of resistance remain elusive. Developments in helminth biochemistry have depended heavily on developments in other areas. High throughput methods such as proteomics, transcriptomics and genome sequencing are now generating vast amounts of new data. The challenge for the future is to interpret and understand the biological relevance of this new information.

Growth performance and meat yield of commercial broilers and turkeys has improved linearly each year during the past four decades (Havenstein et al., 2003b; Havenstein et al., 2003a; Havenstein et al., 2007), and this trend is likely to continue in the future as new technologies in genetics, biotechnology and developmental biology are adopted by the poultry industry. As the time it takes meat birds to achieve market size decreases, the period of embryonic development becomes a greater proportion of a bird's productive life. Therefore, incubation and embryonic development towards hatch is of greater relative importance to the successful rearing of meat poultry than ever before (Hulet 2007; Foye et al., 2007b). Consequently, anything that supports or limits growth and development during the incubation period will have a marked effect on overall growth performance and health of modern strains of meat poultry. Many poultry researchers now realize that future gains in genetic and production potential of poultry will come from advancements made during the incubation period and embryogenesis (Elibol et al., 2002; Peebles et al., 2005; Christensen et al., 2007; Collin et al., 2007; Leksrisompong et al., 2007). The urgent need to explore and understand the biology of incubation has been emphasised by several symposia: two held at the annual conference of the U.S. Poultry Science Society (July 2006-Edmonton, Alberta, Canada “Managing the embryo for performance”, and July 2007-San Antonio, TX Informal Nutrition Meeting “The impact of imprinting on biological and economical performance in animals”), and one held by the European Federation of World Poultry Science Society (October 2007-Berlin, Germany “Fundamental physiology and perinatal development in poultry), which were specifically devoted to demonstrating the importance of the embryonic period on poultry performance. This review will summarise the metabolic events and pathways in four of the most active tissues of embryos during the period just prior to hatch, and the hormonal control that coordinates the marked changes as the embryo prepares for its post-hatch life.

Rumen nitrogen metabolism values were estimated by the use of a single injection of 15(NH4)2SO4 into the rumen of sheep and consecutive 15N enrichment measurements in the rumen ammonia pool, rumen non-NH3-N (NAN) pool, rumen purine pool and blood urea-N (BUN) pool for a period of 24 h. Synthesis and degradation of N compounds in the rumen and passage of N to and from the rumen were evaluated on a chemical rather than a microbial basis; microbial fractions were not separated. This model was examined in two experiments. In Expt 1 a ram (55 kg) was given a semi-synthetic diet (1067 g dry matter (DM), 22.8 g N) in which soya-bean meal provided over 90% of the N. In Expt 2, two rams (45 kg) were given in three consecutive periods a semi-synthetic basal diet containing: (1) roasted soya-bean meal (SBM, 725 g DM, 14.8 g N/d); or (2) fishmeal (FM, 728 g DM, 15.5 g N/d); or (3) raw soya-bean meal (RSBM, 724 g DM, 13.8 g N/d). In all these rations, the main protein source provided over 90% of the N. In Expt 1, 68.3% of N intake was degraded directly to NH3 in the rumen, 21.2% escaped rumen degradation and 10.5% was incorporated into stable N compounds in the rumen. Net NH3 transfer to the blood was 30.4%, NH3 flow from the rumen was 6.6% and rumen NAN output was 63% of N intake. In Expt 2, rumen NAN output was larger (7.67, 14.36 and 8.89 g N/d for diets containing SBM, FM and RSBM respectively; P < 0.05) and net NH3 loss to the blood was smaller (6.1, 0.39 and 4.17 g N/d for diets SBM, FM and RSBM respectively; P < 0.05) for diet FM as compared with the soya-bean diets. The percentage of rumen NAN that was synthesized from NH3 was larger for diet RSBM (36.4, 40.3 and 49.1 for diets SBM, FM and RSBM respectively; P < 0.05) than for the other two rations. NH3 pool sizes (g N) were 0.463, 0.385 and 0.301 for diets SBM, FM and RSBM respectively (P < 0.05), while their hourly turnover rates were 15.8, 26.1 and 5.12 for diets SBM, FM and RSBM respectively (P < 0.01), indicating no correlation between pool size and its turnover rate. The existence of a small and rapidly turning over NAN pool to which NH3 is first bound (SNAN1) was indicated by the difference in the shape of the NAN and purines 15N-enrichment curves in the first 3 h after label injection. The fact that the rate of NH3 initial binding to SNAN1 pool was related neither to ammonia pool size nor to SNAN1 pool size suggests the existence of an unknown control mechanism at this site.