Journal of Animal Science and Biotechnology最新文献

The primary role of the gastrointestinal tract in broiler chickens is nutrient assimilation, with transporter proteins facilitating the uptake of amino acids, peptides, monosaccharides, fatty acids, and minerals across the intestinal epithelium. Among these nutrient transporters, members of the solute carrier family are particularly important, and gene expression analyses targeting these transporters have provided informative insights into how birds adapt to diverse dietary, environmental, and physiological challenges to maintain nutrient homeostasis. These transporters are expressed either at the brush border membrane, where they facilitate the absorption of nutrients from the gut lumen into enterocytes, or at the basolateral membrane, where they mediate the transfer of nutrients from the enterocytes into the bloodstream. The expression of these transporters is influenced by a range of factors, including bird age, sex, intestinal segment, dietary substrate availability and source, as well as external stressors such as heat stress and pathogen exposure. While upregulation of transporter genes often suggests an enhanced capacity for nutrient uptake, it does not always correlate with improved growth performance, due to compensatory physiological responses and fluctuations in nutrient bioavailability. Understanding the regulation and functional dynamics of nutrient transporters presents valuable opportunities to develop targeted dietary and management strategies aimed at optimizing nutrient utilization and improving bird performance. This review summarizes current knowledge on the classification, function, and regulation of key nutrient transporters in broilers, highlights factors influencing their expression, and explores their implications for nutrition and production efficiency.

Skeletal muscle accounts for approximately 40% of body mass and 50%-75% of whole-body protein, playing a central role in meat production and quality. Efficient protein synthesis in skeletal muscle relies on an adequate supply of nutrient substrates and a balanced amino acid profile. Branched-chain amino acids (BCAA), including leucine (Leu), isoleucine (Ile), and valine (Val), are the most abundant essential amino acids in skeletal muscle and contribute to both protein synthesis and oxidative energy production. Additionally, BCAA function as signaling molecules that regulate gene expression and protein phosphorylation cascades, which significantly influence physiological processes, such as protein synthesis and degradation, glucose and lipid metabolism, and cell apoptosis and autophagy. These processes are primarily mediated through the PI3K/AKT/AMPK/mTOR signaling pathways. This review summarizes BCAA transporters and catabolic metabolism, their role as signaling molecules in regulating protein metabolism and glucose and lipid equilibrium, and applications in animal production. These findings offer both theoretical insights and practical guidelines for the precise regulation of feed efficiency and production performance through tailored dietary BCAA supplementations.

Background: Low dietary energy levels can disrupt energy balance, causing metabolic disorders, particularly those involving in hepatic lipid metabolism. Betaine (BET), an important methyl donor, has demonstrated protective effects against liver diseases. However, its effects on hepatic lipid metabolism in pigs fed a low-net energy (NE) diet and the underlying mechanisms remain unclear. Thirty-two pigs (85.52 ± 2.27 kg) were randomly assigned to four treatments: N-NE group (normal NE diet, 2,475 kcal/kg NE), N-NEB group (normal NE diet + 1,500 mg/kg BET, 2,475 kcal/kg NE), R100-NE group (low-NE diet, 2,375 kcal/kg NE), and R100-NEB group (low-NE diet + 1,500 mg/kg BET, 2,375 kcal/kg NE). The experiment lasted 35 d.

Results: There was no significant difference in growth performance among the groups (P > 0.05). Reducing dietary NE levels caused liver dysfunction and increased total glyceride concentration, accompanied by lipid metabolism disorders. BET supplementation in a low-NE diet exhibited hepatoprotective roles, as evidenced by increased TP concentration and reduced ALT level in serum (P < 0.05), as well as decreased fat content, adipocyte size, and total glyceride concentration in the liver (P < 0.05). Meanwhile, dietary BET alleviated low-NE diet-induced hepatic lipid metabolism disorder by downregulating mRNA expressions of genes related to fatty acid transport (FABP3 and CD36) and lipogenesis (SREBP1c and FASN), while upregulating mRNA expressions involved in lipolysis (CPT1 and HSL) (P < 0.05). Furthermore, dietary BET increased serum SAM concentration and the SAM/SAH ratio in pigs fed low-NE diets (P < 0.05), thereby providing sufficient methyl groups through regulating the activities of enzymes participated in BET metabolism. Mechanistically, BET increased m⁶A modification level and regulated mRNA and protein expressions of m⁶A modified proteins including METTL3, METTL14, WTAP, YTHDF1, and ALKBH5. Correlation analysis showed a significant association between m⁶A RNA methylation and hepatic lipid metabolism, suggesting that m⁶A RNA methylation may play a critical role in mediating hepatic lipid metabolism.

Conclusions: Dietary BET supplementation in low-NE diets alleviated hepatic lipid metabolism disorders by regulating m⁶A RNA methylation, ultimately reducing hepatic lipid accumulation in finishing pigs.

Background: The enteric methane inhibitor 3-nitrooxypropanol (3-NOP) inhibits the key enzyme in ruminal methanogenesis, but whether short-term (ST) and long-term (LT) dietary supplementation has similar effects on rumen microbiota in beef cattle and how microbes change after 3-NOP withdrawal have not been studied. This study investigated changes in rumen bacteria, archaea, and protozoa after ST and LT dietary supplementation and removal of 3-NOP using metataxonomic analysis.

Results: A total of 143 rumen samples were collected from two beef cattle studies with 3-NOP supplementation. The ST study (95 samples) used eight ruminally cannulated beef cattle in a 4 × 4 Latin square design with four 28-d of 3-NOP treatments [mg/kg of dry matter (DM)]: control: 0, low: 53, med: 161, and high: 345. The LT study (48 samples) was a completely randomized design with two 3-NOP treatments [control: 0, and high: 280 mg/kg of DM) fed for 112-d followed by a 16-d withdrawal (without 3-NOP). Bacterial and archaeal communities were significantly affected by 3-NOP supplementation but limited effects on protozoal communities were observed. Under ST supplementation, the relative abundances of Prevotella, Methanobrevibacter (Mbb.) ruminantium, Methanosphaera sp. ISO3-F5, and Entodinium were increased (Q < 0.05), whereas those of Mbb. gottschalkii and Epidinium were decreased (Q < 0.05) with 3-NOP supplementation. In LT study, relative abundances of Mbb. ruminantium, and Methanosphaera sp. Group5 were increased (Q < 0.05), while those of Saccharofermentans and Mbb. gottschalkii were decreased (Q < 0.05) with 3-NOP supplementation. Comparison between 3-NOP supplementation and the withdrawal revealed increased relative abundances of Clostridia UCG-014 and Oscillospiraceae NK4A214 group and decreased those of Eubacterium nodatum group and Methanosphaera sp. Group5 (P < 0.05) after 3-NOP withdrawal. Further comparison of rumen microbiota between control and 3-NOP withdrawal showed significantly higher (P = 0.029) relative abundances of Eggerthellaceae DNF00809, p-1088-a5 gut group, and Family XII UCG-001 in control group while no significant differences were detected for archaea and protozoa. Microbial network analysis revealed that microbial interactions differed by both 3-NOP dose and durations.

Conclusions: Both ST and LT supplementation affected overall rumen microbial profile, with individual microbial groups responded to 3-NOP supplementation differently. After 3-NOP withdrawal, not all microbes showed recovery, indicating that the 3-NOP driven shifts were only partially reversible. These findings provide an understanding of the effects of 3-NOP on rumen microbial communities and their adaptability to methane mitigation strategies.

Background: As probiotics, Bacillus strains may regulate some physiological functions in animals. This study aimed to evaluate whether dietary supplementation with a Bacillus-based probiotic could alleviate gut damage induced by rotavirus (RV) infection in piglets. Twenty-four piglets were randomly assigned into 2 groups fed with the basal diet (n = 16) and the diet containing 10⁹ colony-forming unit Bacillus spores/kg (n = 8). On d 8, 8 piglets fed with the diet supplemented with Bacillus-based probiotic and 8 piglets fed with basal diet were orally infused with RV, while the residue piglets had oral gavage of sterile essential medium. The trial duration was 12 d.

Results: RV challenge induced diarrhea, significantly destroyed the morphology of jejunal mucosa (P < 0.05), significantly increased RV-antibody and RV non-structural protein 4 of jejunal mucosa (P < 0.05), significantly impaired antioxidant capacity (including malondialdehyde level, total antioxidant capacity and catalase activity), immunity (such as interleukin 2, interleukin 4 and secreted immunoglobulin A levels), mucins and the mRNA expression of tight-junction-related (such as Zonula occludens 1, occludin) and apoptotic-related (including B-cell lymphoma/leukaemia-2-associated X protein, B cell lymphoma/leukaemia-2, cysteinyl aspartate specific proteinases) genes of jejunal mucosa (P < 0.05), and, to some extents, affected the bacteria community structure and abundance of ileal digesta in piglets. However, Bacillus-based probiotic administration could significantly attenuate the negative effects of RV infection on gut health of piglets (P < 0.05).

Conclusions: These findings suggested that supplementing Bacillus-based probiotic in the diet could decrease diarrhea rate, and improve gut health in weaned piglets, which was associated with regulating intestinal antioxidant capacity, apoptosis, and microbiota.

Background: Inflammatory bowel disease causes intestinal structural damage, impairs gut function, hinders animal growth and development, and reduces farming efficiency. Previous studies demonstrated that lactate alleviates dextran sulfate sodium (DSS)-induced inflammation and mitigates weight loss by enhancing intestinal barrier functions. However, ‌the mechanisms underlying‌ lactate-mediated protection of the intestinal epithelial barrier ‌remain unclear‌. This study aimed to explore the protective effect of lactate on intestinal barrier damage in colitis piglets and the possible underlying mechanisms through in vivo and in vitro experiments.

Methods: A total of 60 21-day-old weaned female piglets were randomly assigned into three groups based on weight: the control group (basal diet with physiological saline gavage), the DSS group (basal diet with 5% DSS gavage), and the DSS + LA group (2% lactate diet with 5% DSS gavage). There were 10 replicates per treatment, with 2 piglets per replicate. Jejunal morphology was assessed via hematoxylin and eosin staining, while Western blotting quantified the protein levels of proliferation markers, including cluster of differentiation 24 (CD24), cyclin D1, and wingless/integrated (Wnt)/β-catenin signaling components. In vitro, 0.08% DSS and 2-32 mmol/L sodium lactate-treated intestinal porcine epithelial cell line-J2 (IPEC-J2) cells (n = 4) were assessed for viability (Cell Counting Kit-8 assay), apoptosis (flow cytometry), and proliferation parameters, including cell cycle analysis and Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5⁺) stem cell quantification.

Results: In vivo, DSS administration induced jejunal villus shortening (P < 0.05), downregulated protein levels of CD24, cyclin D1, casein kinase 1 (CK1), and dishevelled-2 (DVL2) (P < 0.05). In vitro, DSS promoted apoptosis, inhibited proliferation, diminished the Lgr5⁺ cell populations (P < 0.05), and reduced S-phase cell proportions (P < 0.05). Conversely, lactate supplementation ameliorated DSS-induced villus atrophy (P < 0.05), restored CD24, cyclin D1, CK1, and DVL2 protein levels (P < 0.05). Furthermore, in vitro, sodium lactate attenuated DSS-induced apoptosis (P < 0.05), enhanced IPEC-J2 proliferation (P < 0.05), expanded Lgr5⁺ cells (P < 0.05), and increased S-phase progression (P < 0.05).

Conclusions: In summary, lactate ameliorated intestinal barrier damage in DSS-induced colitis by activating the Wnt/β-catenin pathway and restoring the balance between epithelial cell proliferation and apoptosis. This study provides novel mechanistic evidence supporting lactate's therapeutic potential for IBD management.

Gut-brain communication via the peripheral neural network is vital for regulating local digestive function and systemic physiology. Gut microbiota, which produces a wide array of neuroactive compounds, is a critical modulator in this bidirectional dialog. Perturbations in the gut microbiota have been implicated in neurological disorders such as depression and stress. Distinct from humans and other monogastric animals, ruminants possess a unique, microbially dense gastrointestinal compartment, the rumen, that facilitates the digestion of fibrous plant materials. These ruminal microbes are likely key contributors to rumen-brain crosstalk. Unlike certain microbe-derived neuroactive compounds produced in the hindgut that are minimally absorbed and primarily excreted in feces, those generated in rumen can reach the small intestine, where they are largely absorbed and affect central nervous system through systemic regulation in addition to the vagal pathway. Notably, emerging evidence suggests that rumen microbiota dysbiosis under stress is associated with abnormal behavior, altered hormonal and neurotransmitter levels. In this review, we introduce the concept of the rumen-microbiome-brain axis by comparing the anatomical structures and microbial characteristics of the intestine and the rumen, emphasizing the neuroactive potential of rumen microbiome and underlying mechanisms. Advances in this frontier hold tremendous promise to reveal a novel dimension of the gut-microbiome-brain axis, providing transformative opportunities to improve ruminant welfare, productivity, and agricultural sustainability.

Background: The rapid development of intensive layer breeding has intensified odor pollution that must be paid attention to for the green transformation of the industry. This study used Jingfen No.6 laying hens as the model to systematically evaluate the regulatory effect of compound microalgal powder (Chlorella vulgaris:Spirulina platensis:Haematococcus pluvialis = 3:1:1, 1:3:1, 1:1:3) on ammonia (NH₃) emissions from laying hen manure.

Results: Through analysis of the static NH₃ production in manure, it was found that the NH₃ emissions within 24 h in the experimental group with 0.50% compound microalgal powder added were reduced to 6.27-16.84 mg (vs.

Control: 28.29 mg), achieving a 40.47%-77.84% reduction. GC/MS and 16S rRNA sequencing analyses indicated that the compound microalgal powder intervened in the remodeling of the microbial community and nitrogen metabolism network in manure, driving the transformation from inorganic nitrogen to organic nitrogen, mitigated the proliferation of NH₃-producing bacteria (such as Escherichia coli, Klebsiella pneumoniae, Kurthia, and Proteus), and increased the abundance of acid-producing bacteria (such as Leuconostocaceae and Lactobacillaceae). The Spirulina platensis powder group had the best emission reduction effect (reduced by 77.84%), and its mechanism was closely related to the mitigation of Gram-negative bacteria activity by phycocyanin and increased synthesis of aromatic compounds, such as 2,3,5-trimethyl-6-ethylpyrazine.

Conclusions: This study revealed the mechanism by which the compound microalgal powder reduces NH₃ emissions by regulating the proliferation of acid-producing bacteria, reshaping the nitrogen metabolism network, and mitigating the activity of NH₃-producing bacteria, while providing theoretical and data support for the development of environmentally friendly feed.

Mastitis is one of the most significant diseases affecting the development of the dairy industry and has traditionally been associated with pathogenic infections. However, emerging evidence highlights that ruminal microbial homeostasis also plays a crucial role in the pathogenesis of mastitis. Specifically, cows with mastitis exhibit reduced alpha diversity and altered microbial composition in the rumen. Inducing ruminal dysbiosis through a high-concentrate diet has been shown to trigger mastitis in cows, and transplantation of ruminal microbiota from mastitis-affected cows to recipient mice can induce mastitis in mice. Mechanistically, ruminal dysbiosis increases gastrointestinal inflammation and compromises the integrity of the gastrointestinal barrier, thereby facilitating the translocation of harmful bacterial components, metabolites, and pathobionts into the bloodstream. This disruption impairs blood-milk barrier function, leading to systemic inflammation and the development of mastitis. In this review, we summarize recent advances in understanding how ruminal dysbiosis induces mastitis and explore potential prevention and control strategies targeting the modulation of ruminal microbiota.

Background: The deposition of intramuscular fat (IMF) in livestock can enhance the flavor and tenderness of meat products, significantly increasing consumer satisfaction. To achieve this industrial trait, this study investigated the regulatory effects of 20 dietary nutrients on sheep IMF deposition using a 3D organoid culture model.

Results: Key nutrients enhancing angiogenesis, adipocyte differentiation, and lipid accumulation were identified through assessments of capillary sprouts development, mRNA expression, and Oil Red O staining. Vitamins C (VC), E (VE), and K₁ (VK1), guanidinoacetic acid (GAA), leucine (Leu), lysine (Lys), methionine (Met), N-carbamylglutamate (NCG), tryptophan (Trp), α-linolenic acid (ALA), linoleic acid (LA), cis-9, trans-11 conjugated linoleic acid (c9, t11-CLA), acetic acid (HAc), and sodium acetate (NaAc) stimulated while vitamins B₉ (VB9), D (VD), K₂ (VK2), taurine (Tau), and sodium butyrate (NaBu) inhibited angiogenesis (P < 0.05). Furthermore, VC, VE, VK1, VK2, GAA, Leu, NCG, Trp, ALA, LA, and HAc enhanced adipocyte differentiation, with VE, VK1, GAA, Leu, LA, and HAc additionally elevating lipid accumulation (P < 0.05).

Conclusions: Various nutrients play distinct regulatory roles in angiogenesis, adipocyte differentiation, and lipid accumulation. These findings provide a roadmap for further optimizing the production of marbled meat through nutritional intervention in actual livestock breeding production.