The Importance of B Vitamins in Enhanced Precision Nutrition of Dairy Cows: The Case of Folates and Vitamin B12

Dairy cow diets are generally balanced for energy and major nutrients with B vitamins generally assumed not to be limiting, in spite of their role as coenzymes, essential to many metabolic reactions in protein, carbohydrate and lipid metabolism. Assuming adequacy of B-vitamin supply may explain some of the discrepancies between the outcomes of metabolic prediction models and measured cow performance. In lactating dairy cow, the amount of B vitamins from the diet and synthesized by the ruminal microbiota is generally sufficient to prevent deficiency symptoms and, as such, is assumed to fulfill requirements. However, reports of beneficial effects of B-vitamin supplementation on dairy cow performance suggest that B-vitamin supply is sometimes lower than its needs, as an insufficient B-vitamin supply decreases metabolic efficiency by driving a shift towards alternative metabolic pathways with greater energy cost. Using information on folates and vitamin B12 illustrated how meeting dairy cow needs for B vitamins should not be overlooked in formulation of rations for lactating dairy cattle. The present review discusses current knowledge and indicates areas presently impeded by the lack of research results, especially the limitations on the ability to estimate B vitamin need and supply.

Comparison of Feed Digestibility between Ponies, Standardbreds and Andalusian Horses Fed Three Different Diets

Ponies and some horse breeds such as Andalusians exhibit an ‘easy keeper’ phenotype and tend to become obese more readily than other breeds such as Standardbreds. Various hypotheses have been proposed, including differences in appetite or metabolic efficiency. This study aimed to investigate the effect of breed on nutrient digestibility. Ponies, Standardbreds and Andalusian horses were adapted to consuming either a control fibre-based diet (n = 9), a hypercaloric cereal-rich diet (n = 12) or a hypercaloric fat-rich diet (n = 12) over 20 weeks. Total faecal collection was performed over 24 h to determine apparent total tract digestibility of gross energy, dry matter (DM), neutral detergent fibre (NDF), starch, crude protein and crude fat. There was no effect of breed on apparent digestibility for any of the nutrients studied (all p > 0.05). However, there was a significant effect of diet, with animals consuming the cereal-rich or fat-rich diets demonstrating higher digestibility of gross energy, DM, NDF and crude protein compared with those consuming the control diet (all p < 0.05). Animals adapted to the cereal-rich diet demonstrated higher digestibility of starch (p < 0.001) and animals adapted to the fat-rich diet demonstrated higher digestibility of fat (p < 0.001). This study found that horses and ponies had similar nutrient digestibility when adapted to the same diets and management conditions. Limitations included the relatively small number of animals from each breed per diet group and the short period of total faecal collection. The tendency towards increased adiposity in ponies and Andalusian-type horse breeds is more likely to reflect differences in metabolism, rather than differences in feed digestibility.

The Donor-Dependent and Colon-Region-Dependent Metabolism of (+)-Catechin by Colonic Microbiota in the Simulator of the Human Intestinal Microbial Ecosystem

The intestinal absorption of dietary catechins is quite low, resulting in most of them being metabolized by gut microbiota in the colon. It has been hypothesized that microbiota-derived metabolites may be partly responsible for the association between catechin consumption and beneficial cardiometabolic effects. Given the profound differences in gut microbiota composition and microbial load between individuals and across different colon regions, this study examined how microbial (+)-catechin metabolite profiles differ between colon regions and individuals. Batch exploration of the interindividual variability in (+)-catechin microbial metabolism resulted in a stratification based on metabolic efficiency: from the 12 tested donor microbiota, we identified a fast- and a slow-converting microbiota that was subsequently inoculated to SHIME, a dynamic model of the human gut. Monitoring of microbial (+)-catechin metabolites from proximal and distal colon compartments with UHPLC-MS and UPLC-IMS-Q-TOF-MS revealed profound donor-dependent and colon-region-dependent metabolite profiles with 5-(3′,4′-dihydroxyphenyl)-γ-valerolactone being the largest contributor to differences between the fast- and slow-converting microbiota and the distal colon being a more important region for (+)-catechin metabolism than the proximal colon. Our findings may contribute to further understanding the role of the gut microbiota as a determinant of interindividual variation in pharmacokinetics upon (+)-catechin ingestion.

Short term effects of restricted food availability and peripheral leptin injections in redheaded bunting, Emberiza bruniceps

Migratory birds need continued food supply and efficient metabolic machinery to meet high energy demands of the magnanimous feat of flight. Two questions are important i.e. as to 1) how a bird adapts to a temporary food constrain on a daily basis, and 2) how peripheral leptin, an anorectic hormone, impacted feeding and migratory behaviour in buntings? The aim of this study was to induce a non-photoperiodic tweak in the physiology of redheaded buntings through exogenous leptin administration and study its effect on their food intake and migratory behaviour. Groups of male redheaded buntings, Emberiza bruniceps (n=17) were transferred from short (8L: 16D) to long (16L: 8D) days and presented with food only either for first (morning food presence, MFP) or second (evening food presence, EFP) half of the 16h lighted phase, while control group received food ad libitum. Total daily food intake (FI) did not differ significantly between the MFP, EFP and controls, but hourly FI in MFP and EFP indicated increased activity differences based on time of food availability and bird’s tendency to cache food/ recompense for food scarcity during migration. In another experiment, a chemical tweak in bird’s FI was induced by peripheral administration of leptin, to add to current understanding of transition in buntings’ metabolic efficiency during high energy demanding migratory journey. Exogenous leptin appeared to safeguard cadaveric effect of exogenous injection in migrating buntings through promoting blood cholesterol and reduced liver fibrosis. Food restriction in the morning was better responded by buntings than that in evening. Therefore, migratory buntings exhibited diurnal variation in response to food scarcity.

Phosphorus Supplementation Mitigates Perivascular Adipose Inflammation–Induced Cardiovascular Consequences in Early Metabolic Impairment

Background The complexity of the interaction between metabolic dysfunction and cardiovascular complications has long been recognized to extend beyond simple perturbations of blood glucose levels. Yet, structured interventions targeting the root pathologies are not forthcoming. Growing evidence implicates the inflammatory changes occurring in perivascular adipose tissue (PVAT) as early instigators of cardiovascular deterioration. Methods and Results We used a nonobese prediabetic rat model with localized PVAT inflammation induced by hypercaloric diet feeding, which dilutes inorganic phosphorus (Pi) to energy ratio by 50%, to investigate whether Pi supplementation ameliorates the early metabolic impairment. A 12‐week Pi supplementation at concentrations equivalent to and twice as much as that in the control diet was performed. The localized PVAT inflammation was reversed in a dose‐dependent manner. The increased expression of UCP1 (uncoupling protein1), HIF‐1α (hypoxia inducible factor‐1α), and IL‐1β (interleukin‐1β), representing the hallmark of PVAT inflammation in this rat model, were reversed, with normalization of PVAT macrophage polarization. Pi supplementation restored the metabolic efficiency consistent with its putative role as an UCP1 inhibitor. Alongside, parasympathetic autonomic and cerebrovascular dysfunction function observed in the prediabetic model was reversed, together with the mitigation of multiple molecular and histological cardiovascular damage markers. Significantly, a Pi‐deficient control diet neither induced PVAT inflammation nor cardiovascular dysfunction, whereas Pi reinstatement in the diet after a 10‐week exposure to a hypercaloric low‐Pi diet ameliorated the dysfunction. Conclusions Our present results propose Pi supplementation as a simple intervention to reverse PVAT inflammation and its early cardiovascular consequences, possibly through the interference with hypercaloric‐induced increase in UCP1 expression/activity.

Soil microbial trait-based strategies drive metabolic efficiency along an altitude gradient

Trait-based approaches provide a candidate framework for linking soil microbial community to ecosystem processes, yet how the trade-offs in different microbial traits regulate the community-level metabolic efficiency remains unknown. Herein we assessed the roles of the microbial taxa with particular trait strategies in mediating soil microbial metabolic efficiency along an altitude gradient on the Tibetan Plateau. Results showed that soil microbial metabolic efficiency declined with increasing altitude, as indicated by the increasing metabolic quotient (microbial respiration per unit biomass, qCO2) and decreasing carbon use efficiency (CUE). Both qCO2 and CUE were predominantly predicted by microbial physiological and taxonomic attributes after considering key environmental factors including soil pH, substrate quantity and quality. Specifically, the reduced metabolic efficiency was associated with higher investment into nutrient (particularly for phosphorus) acquisitions via enzymes. Furthermore, we identified key microbial assemblies selected by harsh environments (low substrate quality and temperature) as important predictors of metabolic efficiency. These results suggest that particular microbial assemblies adapted to nutrient limited and cold habitats, but at the expense of lower metabolic efficient at higher altitude. Our findings provide a candidate mechanism underlying community-level metabolic efficiency, which has important implications for microbial-mediated processes such as carbon dynamics under global climate changes.

Sensory coding and contrast invariance emerge from the control of plastic inhibition over emergent selectivity

Visual stimuli are represented by a highly efficient code in the primary visual cortex, but the development of this code is still unclear. Two distinct factors control coding efficiency: Representational efficiency, which is determined by neuronal tuning diversity, and metabolic efficiency, which is influenced by neuronal gain. How these determinants of coding efficiency are shaped during development, supported by excitatory and inhibitory plasticity, is only partially understood. We investigate a fully plastic spiking network of the primary visual cortex, building on phenomenological plasticity rules. Our results suggest that inhibitory plasticity is key to the emergence of tuning diversity and accurate input encoding. We show that inhibitory feedback (random and specific) increases the metabolic efficiency by implementing a gain control mechanism. Interestingly, this led to the spontaneous emergence of contrast-invariant tuning curves. Our findings highlight that (1) interneuron plasticity is key to the development of tuning diversity and (2) that efficient sensory representations are an emergent property of the resulting network.

Polymorphisms of the AS3MT gene are associated with arsenic methylation capacity and damage to the P21 gene in arsenic trioxide plant workers

Epidemiological evidence suggests that the metabolic profiles of each individual exposed to arsenic (As) are related to the risk of cancer, coronary heart disease, and diabetes. The arsenite methyltransferase ( AS3MT) gene plays a key role in As metabolism. Several single nucleotide polymorphisms in the AS3MT gene may affect both enzyme activity and gene transcription. AS3MT polymorphisms are associated with the proportions of monomethylarsenic acid (MMA) and dimethylarsenic acid (DMA) in urine as well as the incidence of cancer. P21 protein is a cyclin-dependent kinase inhibitor. Mutations of the P21 gene have been found in cancer patients. In our study, we investigate whether polymorphisms of the AS3MT gene alter As methylation capacity and adversely affect the P21 gene in arsenic trioxide plant workers. The DNA damage was examined by the quantitative polymerase chain reaction. Restriction fragment length polymorphism was used to analyze the genotype of the AS3MT gene. The results showed that DNA damage in P21 gene fragments was greater in those individuals exposed to high levels of As. There was a strong positive correlation between the DNA damage to P21 gene fragments and the percentage of MMA in urine. However, DNA damage in P21 gene fragments was negatively associated with the percentage of DMA in urine (%uDMA), primary methylation index (PMI), and secondary methylation index. We found that subjects with the rs7085104 GG or GA allele were associated with higher %uDMA and PMI and less DNA damage. The subjects with the rs11191454 GG+GA or GA allele were also associated with higher %uDMA and PMI and less DNA damage. Our results suggest that rs1191454 and rs7085104 in the AS3MT gene affect the As-induced DNA damage by altering individual metabolic efficiency.

Angiotensin II inhibition: a potential treatment to slow the progression of sarcopenia

Sarcopenia is defined as the progressive and generalized loss of skeletal muscle mass and strength, which is associated with increased likelihood of adverse outcomes including falls, fractures, physical disability, and mortality. The etiology of sarcopenia has been postulated to be multifactorial with genetics, aging, immobility, nutritional deficiencies, inflammation, stress, and endocrine factors all contributing to the imbalance of muscle anabolism and catabolism. The prevalence of sarcopenia is estimated to range from 13 to 24% in adults over 60 years of age and up to 50% in persons aged 80 and older. As the population continues to age, the prevalence of sarcopenia continues to increase and is expected to affect 500 million people by the year 2050. Sarcopenia impacts the overall health of patients through limitations in functional status, increase in hospital readmissions, poorer hospital outcomes, and increase in overall mortality. Thus, there exists a need to prevent or reduce the occurrence of sarcopenia. Here, we explore the potential mechanisms and current studies regarding angiotensin receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors on reducing the development of sarcopenia through the associated changes in cardiovascular function, renal function, muscle fiber composition, inflammation, endothelial dysfunction, metabolic efficiency, and mitochondrial function.

Mitochondrial Uncoupling Proteins (UCPs) as Key Modulators of ROS Homeostasis: A Crosstalk between Diabesity and Male Infertility?

Uncoupling proteins (UCPs) are transmembrane proteins members of the mitochondrial anion transporter family present in the mitochondrial inner membrane. Currently, six homologs have been identified (UCP1-6) in mammals, with ubiquitous tissue distribution and multiple physiological functions. UCPs are regulators of key events for cellular bioenergetic metabolism, such as membrane potential, metabolic efficiency, and energy dissipation also functioning as pivotal modulators of ROS production and general cellular redox state. UCPs can act as proton channels, leading to proton re-entry the mitochondrial matrix from the intermembrane space and thus collapsing the proton gradient and decreasing the membrane potential. Each homolog exhibits its specific functions, from thermogenesis to regulation of ROS production. The expression and function of UCPs are intimately linked to diabesity, with their dysregulation/dysfunction not only associated to diabesity onset, but also by exacerbating oxidative stress-related damage. Male infertility is one of the most overlooked diabesity-related comorbidities, where high oxidative stress takes a major role. In this review, we discuss in detail the expression and function of the different UCP homologs. In addition, the role of UCPs as key regulators of ROS production and redox homeostasis, as well as their influence on the pathophysiology of diabesity and potential role on diabesity-induced male infertility is debated.