Journal of Animal Science and Biotechnology最新文献

Poultry is a major nutritional source providing food for large human populations. Infectious diseases threaten the productivity of poultry flocks and diminish animal welfare. Recent advances in genome editing have significantly contributed to our understanding of various physiological aspects and have helped elucidate the interaction between the chicken host and pathogens. Several chicken lines were generated, including those with Type I and Type III interferon receptor knockouts, those lacking specific T cell populations, and those missing contributing factors to V(D)J recombination, such as the recombination-activating gene 1 (RAG1). In addition, researchers achieved resistance to the avian influenza virus (AIV) by targeting acidic nuclear phosphoproteins. Finally, reinstating retinoic acid-inducible gene I (RIG-I) and RING finger protein 135 (RNF135) in the chicken revealed new insights into their evolutionary role, particularly during host-pathogen interactions with AIV. This review provides an update about recent achievements in genome editing of chickens, particularly in immunology and disease resistance.

Background: Food by-products, such as corn germ meal from starch processing, are increasingly used as sustainable feed supplements, reducing competition between food and feed and supporting the valorisation of food waste. However, their effects on gut microbial metabolism and host health remain unclear. This study aimed to determine how corn germ meal fermentation influences microbial community structure and metabolite production using an ex vivo pig faecal culture system.

Results: Corn germ meal supplementation significantly altered the microbial composition, increasing diversity and enriching fibre-degrading Prevotellaceae, a key bacterial family involved in complex carbohydrate metabolism. Metabolomic analysis revealed marked increases in tryptophan-derived metabolites, including indoleacrylic acid, indolepropionic acid, and indolelactic acid, which act as ligands for the aryl hydrocarbon receptor and have anti-inflammatory properties. Prevotella-mediated catabolite repression reduced Escherichia coli-derived indole formation, redirecting microbial tryptophan metabolism toward the production of these bioactive compounds. Microbial and metabolic responses differed among farms, reflecting farm-specific microbiome structures.

Conclusions: Corn germ meal supplementation reshapes gut microbial communities, enhances metabolic activity, and promotes the generation of bioactive tryptophan metabolites with potential immunomodulatory effects. These findings highlight the value of corn by-products as dietary fibres that can drive beneficial microbial cross-feeding and influence host intestinal homeostasis. Although demonstrated in an ex vivo setting, this study provides a mechanistic basis and preclinical evidence for future in vivo studies, supporting the sustainable utilisation of food industry by-products to improve gut health and resource efficiency in livestock production.

Background: Iron deficiency (ID) poses a significant health burden to both human infants and suckling piglets. In piglets, ID leads to substantial economic losses for the industry by compromising growth performance, health, and survival. However, current research has predominantly concentrated on hematological abnormalities, whereas the mechanisms underlying ID-associated hepatic inflammatory injury remain inadequately elucidated. Our study employed the iron-deficient suckling piglet model to address this knowledge gap and to establish a molecular theoretical foundation.

Results: To investigate the underlying mechanisms, this study conducted in vivo and in vitro models. In piglets, ID triggered hepatic oxidative stress by inducing a redox imbalance and suppressing the core Nrf2/HO-1 antioxidant signaling pathway. Histopathological examination revealed structural abnormalities in ID piglet livers, including disorganized hepatic cords, cytoplasmic vacuolation, hydropic degeneration, and mononuclear inflammatory cell infiltration. Transmission electron microscopy further showed shrunk nuclear envelopes, reduced numbers of rough endoplasmic reticulum (RER), and dilated RER cisternae in hepatocytes of ID piglets. Mechanistically, ID activated endoplasmic reticulum stress (ERS) and the PERK/IRE1α branches of the unfolded protein response (UPR). RNA-seq transcriptomic analysis demonstrated significant dysregulation of immune-related pathways, accompanied by elevated pro-inflammatory cytokines (e.g., IL1B, TNF) and decreased anti-inflammatory cytokines (e.g., IL4, IL10). Central to this inflammatory response was the activation of the TLR4/NF-κB pathway, evidenced by upregulation of MyD88 and increased phosphorylation of IκBα and NF-κB p65. In vitro, deferoxamine (DFO)-induced ID in AML12 hepatocytes consistently recapitulated the key features of this phenotype, including the activation of ERS/ UPR and the TLR4/NF-κB signaling pathway. Pharmacological inhibition of ERS by 4-phenylbutyric acid (4-PBA) attenuated DFO-induced NF-κB activation and ameliorated the imbalance between pro- and anti-inflammatory cytokines.

Conclusions: ID exacerbated hepatic inflammation through ERS-mediated activation of the NF-κB pathway, providing novel mechanistic insights into liver injury associated with ID.

Background: Intramuscular fat (IMF) deposition determines beef marbling quality, with current industry practices relying on vitamin A (VA) restriction throughout fattening to enhance marbling development. This study challenges the conventional approach by investigating late-fattening vitamin A supplementation effects on marbling formation in Woking black cattle.

Results: Initial in vitro experiments using bovine skeletal muscle cells (BSMCs) demonstrated that all-trans-retinoic acid (ATRA) treatment during late differentiation (0.1-1 μmol/L) enhanced lipid accumulation with upregulated PPARγ and FABP4 expression. In vivo trials with late-fattening VA supplementation (3,000 IU/kg DM) significantly improved marbling grades, achieving 75% high-grade marbling (A3 or above) with enhanced nutritionally beneficial fatty acids including EPA and DHA levels. Large-scale analysis using 336 genetically homogeneous cattle revealed that superior marbling development correlated with serum VA depletion after VA supplementation, indicating active utilization rather than restriction. A4-grade cattle showed significantly lower serum VA levels than A1-grade cattle, with coordinated upregulation of lipogenic proteins (FASN, SCD, ACACA, PPARγ, FABP4). Transcriptomic analysis unexpectedly revealed significant AMPK pathway activation alongside enhanced marbling development, contradicting conventional understanding of AMPK as an adipogenesis inhibitor. Functional validation using AMPK modulators in BSMCs confirmed that while AMPK inhibition (Compound C) dramatically enhanced VA-induced adipogenesis, AMPK activation (AICAR) suppressed lipogenesis, demonstrating AMPK functions as a negative feedback regulator during VA-mediated adipogenesis rather than preventing intramuscular fat accumulation.

Conclusions: Strategic late-fattening VA supplementation enhances marbling development through PPARγ-mediated transcriptional networks, with AMPK serving as a metabolic sensor and negative feedback regulator rather than an absolute inhibitor. This stage-specific intervention achieved superior marbling quality and improved fatty acid composition in Woking black cattle, suggesting potential for optimization of premium beef production. Validation across diverse genetic backgrounds and production systems will be essential for broader industry implementation.

Background: The phenomenon where excessive activation of branched-chain amino acid (BCAA) degrading enzymes caused by high concentrations of leucine (Leu) leads to a decrease in the overall concentration of BCAA [including isoleucine (Ile) and valine (Val)] is called BCAA antagonism. Although this phenomenon has long been widely studied, the specific mechanism of its occurrence is still poorly understood. In this study, we investigated the specific mechanism by which Val and Ile alleviate the antagonistic effect caused by high concentrations of Leu through influencing insulin function. First, the ratios of Ile and Val in the low-protein diet were adjusted up and down by 15% to observe the metabolic status of broilers at the end of the experiment (the experiment period was from 0 to 42 d). Subsequently, the physiological and biochemical changes related to antagonism were determined using transcriptome and lipid metabolome analyses.

Results: When fed with a high concentration of Leu, restricting Ile or supplementing Val can effectively alleviate antagonism. Under conditions of excessive dietary Val supplementation, insulin levels remained stable, whereas blood glucose levels increased (P < 0.05), and liver fat accumulated predominantly as ceramides rather than triglycerides, thereby disrupting the insulin-mediated phosphatidylinositol 3-kinase/protein kinase B signaling pathway (P < 0.05). Excessive dietary Ile promoted liver inflammation and interleukin-6 release (P < 0.05), which acted on the pancreas to enhance insulin secretion. Additionally, the glucagon content in the pancreas decreased (P < 0.05), while insulin and glucagon-like peptide-1 levels increased (P < 0.05).

Conclusion: Supplementation of Val or restriction of Ile in low-protein diets could alleviate the BCAA antagonism caused by high Leu, which mainly achieved by influencing insulin function. These findings provide new insights in revealing the BCAA antagonism.

Background: Nicotinamide riboside (NR) supplementation has been demonstrated efficacy in enhancing female reproductive outcomes, but its regulatory role in sow performance and gut microbiome remains undefined. This study systematically evaluated the impacts of dietary NR supplementation during late gestation and lactation on sow performance and gut microbiome remodeling. A total of 280 sows were randomized assigned to one of four groups: a control group fed basal diet or one of three groups receiving NR-supplemented diets (2, 4, or 8 g/d; n = 70/group). Sow reproductive performance, blood metabolic parameters, milk metabolome, and fecal 16S rRNA sequencing were measured.

Results: Maternal NR supplementation linearly shortened farrowing duration (P < 0.01) and tended to decrease the incidence of intrauterine growth restriction and the number of late gestation mummies (P < 0.1), while concurrently increasing the within-litter uniformity (P = 0.1). Litter weaning weight and average daily gain increased quadratically with NR dosage (P < 0.05). NR supplementation orchestrated plasma metabolite regulation (triglycerides and total cholesterol; P < 0.05), enhanced antioxidant biomarkers (T-AOC, GSH-Px, T-SOD; P < 0.05), and reduced inflammatory cytokines (TNF-α; P < 0.05) across gestation and lactation. Milk yield, colostrum/milk dry matter, crude protein, and crude fat were increased (P < 0.05), together with higher levels of NAD⁺ metabolites (NAD⁺, NR, nicotinamide) and beneficial bioactive factors (milk polar lipids, 3-aminosalicylic acid, fenugreekine; P < 0.05). Gut microbiota analyses at lactation day 14 revealed NR-enriched beneficial taxa (Bifidobacterium, Ruminococcus, Lachnospiraceae, Subdoligranulum, Clostridium butyricum, Succiniclasticum) across sow-offspring dyads, which was associated with the activation of microbial NAD⁺ enzymes (NadR/NAMPT; P < 0.05) and enhancement of systemic short-chain fatty acid flux, notably an increase in plasma butyrate acid (P < 0.05).

Conclusion: Maternal supplementation of NR during late gestation and lactation increases sow performance and promotes gut NAD⁺ metabolic-associated microbiome remodeling. These findings propose maternal NR intervention as a novel strategy to enhance mammary lactogenesis and lactation metabolism in swine production, with potential applications for therapeutic strategies for lactation insufficiency.

Background: This study was conducted to investigate the impact of varying degrees of heat stress on milk protein synthesis in dairy cows using comprehensive analyses of metabolomics and proteomics. Eighteen dairy cows were subjected to no heat stress (No-HS), mild heat stress (Mild-HS), and moderate heat stress (Mod-HS). Blood and milk samples were collected to determine the content and composition of amino acids (AA), and milk samples were used for metabolomic and proteomic analyses.

Results: Milk protein yield was significantly lower under Mild-HS and Mod-HS than No-HS (P < 0.001). During Mild-HS, no significant difference was found in total AA concentration in both arterial (P = 0.545) and venous blood (P = 0.057), but arterial AA supply to the mammary gland significantly increased (P = 0.045) when compared with No-HS. Under Mod-HS, the supply (P < 0.001) and uptake (P = 0.001) of total AA in the mammary gland decreased significantly, affecting the availability of precursors necessary for milk protein synthesis. Milk metabolomic analysis revealed that Mod-HS significantly impacted nucleotide metabolism, energy metabolism, and protein synthesis processes including translation, folding, and transport. Milk proteomic analysis showed significant downregulation of ribosomal and heat shock proteins which are crucial for protein synthesis and folding.

Conclusions: These findings suggest that heat stress disrupts AA utilization and energy metabolism in the mammary gland, leading to the reduced efficiency in milk protein synthesis and lowered milk protein yield. This study offers valuable insights into the metabolic and proteomic changes in dairy cows under heat stress, highlighting potential strategies to mitigate the adverse effects of heat stress on dairy production and milk quality.

Background: Tibetan sheep grazing on the Qinghai-Tibet Plateau require dietary protein supplementation; however, they face economic constraints due to the high cost of feed transportation in this region. Given that the leucine metabolite β-hydroxy-β-methyl butyrate (HMB) enhances both protein synthesis and intestinal nutrient absorption, this study employed metagenomics and untargeted metabolomics to systematically evaluate HMB's effects on antioxidant capacity, immune response, microbiota, metabolites, and the health of the small intestine in Tibetan sheep. A total of 120 healthy weaned 60-day-old male Tibetan lambs were assigned to diets containing 0 mg/kg (control group, CON), 430 mg/kg (low HMB, L-HMB), 715 mg/kg (medium HMB, M-HMB), or 1,000 mg/kg (high HMB, H-HMB) for 90 d. At the end of the experiment, 6 lambs from each group were slaughtered for intestinal tissue and content sampling.

Results: The M-HMB treatment significantly increased average daily gain of the lambs without affecting feed intake, thereby improving feed utilization efficiency. M-HMB promoted the development of small intestinal morphological and elevated villus height, while also enhancing the activities of digestive enzyme and disaccharidase activities. Furthermore, M-HMB enhanced the antioxidant capacity, immune response, and barrier function of the small intestine. Metagenomic analysis revealed that M-HMB supplementation improved the composition of the small intestinal microbiota in Tibetan sheep, specifically increasing the relative abundance of Ruminococcus bacterium P7 and R. bromii, and enhanced microbial carbohydrate degradation capacity. Metabolomic analysis demonstrated that M-HMB supplementation significantly altered the small intestinal metabolite profile, enhancing carbohydrate metabolic pathways and increased the production of short-chain fatty acids (SCFAs). M-HMB upregulated PLCβ1 and ERK1/2 protein expression levels in small intestinal tissue and elevated the proportion of Ki67-positive cells at the basal crypt region of small intestinal crypts, suggesting enhanced proliferative activity of intestinal epithelial cells.

Conclusions: In summary, dietary supplementation with M-HMB (715 mg/kg) promoted small intestinal growth and development, enhanced digestive and absorptive functions, optimized the microbial composition, improved carbohydrate degradation, and increased the production of SCFAs, ultimately improving the growth performance of Tibetan sheep lambs.

Background: Nutritional strategies aimed at augmenting growth performance remain a central focus in poultry science. The liver, as a pivotal metabolic organ, exerts profound influence on skeletal muscle development. Nevertheless, the mechanistic interplay between hepatic metabolism and myogenesis has not been fully delineated. Here, by integrating multi-omics analyses with functional validation, we identified xanthosine, a metabolic derivative of hepatic caffeine catabolism, as a previously unrecognized regulator of broiler muscle growth. We further elucidated its mechanistic role in promoting myoblast proliferation.

Results: Comparative phenotypic assessment of high- and low-body-weight broilers revealed substantial differences in breast muscle mass. Metagenomic profiling of cecal microbiota demonstrated only a limited association between microbial composition and body weight. In contrast, untargeted plasma metabolomics uncovered a systemic upregulation of amino acid metabolism in high-body-weight broilers, concomitant with a pronounced activation of caffeine metabolism. Consistently, hepatic transcriptomic profiling revealed marked induction of cytochrome P450 family 1 subfamily A member 2 (CYP1A2), encoding a key enzyme catalyzing caffeine catabolism. Integrated KEGG pathway enrichment across metabolomic and transcriptomic datasets highlighted caffeine metabolism as a significantly perturbed pathway. Among its downstream metabolites, plasma xanthosine was robustly elevated in high-body-weight broilers. Functional validation via in ovo injection demonstrated that xanthosine administration significantly augmented post-hatch growth performance by increasing skeletal muscle mass. Mechanistic investigations further established that xanthosine drives myoblast proliferation through activation of the ERK/GSK3β/β-catenin signaling cascade.

Conclusions: Together, these findings delineate a liver-muscle metabolic axis in which hepatic CYP1A2-driven caffeine metabolism elevates circulating xanthosine, which in turn acts as a pivotal molecular effector of myogenic growth. This study uncovers a previously unappreciated metabolic mechanism by which hepatic activity orchestrates skeletal muscle development. It also highlights targeted modulation of xanthosine metabolism as a promising strategy to enhance broiler growth performance and production efficiency.