Journal of Animal Science and Biotechnology最新文献

Microalgae are photosynthetic microorganisms capable of synthesizing diverse high-value bioactive compounds, including premium proteins, polyunsaturated fatty acids, pigments, and vitamins. These natural products exhibit significant potential in enhancing livestock growth and health, offering biological activity and nutritional benefits that surpass chemically synthesized alternatives. Nevertheless, the commercial production of microalgae-derived natural products remains insufficient to meet escalating market demands. Utilizing synthetic biology strategies, especially the CRISPR system, to increase productivity of microalgae cell factories is crucial for scaling up high-value product biosynthesis. This article reviews the current applications, construction strategies, and critical pathway nodes in microalgae cell factory, with emphasis on CRISPR-based genome editing breakthroughs for optimizing microalgae nutritional profiles, and recent progress in microalgae utilization for livestock production, providing a forward-looking perspective on future developments.

Background: Eating speed is a key eating behavior trait that influences energy intake and fat deposition, yet its regulation by host genetics and gut microbiota remains poorly understood in birds.

Results: We systematically investigated the interplay among host genetics, gut microbiota, eating speed, and fat deposition in chickens. Phenotypic analyses revealed a positive association between eating speed and abdominal fat, and Mendelian randomization (MR) analysis identified a bidirectional feedback loop in which fat deposition promotes faster eating, which in turn exacerbates fat accumulation. Microbiome and MR analyses highlighted the ileal genus Bradyrhizobium as a causal regulator of both eating speed and fat deposition, with higher abundance reducing abdominal fat, triglyceride levels, and inflammatory markers. Microbiome genome-wide association studies (mGWAS) further identified host genetic variants and candidate genes, including convergent signals at RECK, influencing Bradyrhizobium abundance. Mediation analyses indicated that Bradyrhizobium modulates eating speed partially through its effects on abdominal fat, emphasizing a host-microbe-behavior feedback axis.

Conclusions: Our findings reveal a complex interplay among host genetics, gut microbes, and eating behavior, providing mechanistic insights and potential targets for precision interventions to optimize growth and metabolic health in poultry.

Periparturient metabolic stress or pathogen infections leading to inflammation reduce milk yield and cause mammary dysfunction, thus, causing severe economic losses to dairy farming. As the primary organelle for cellular energy production, calcium regulation, cell death, and metabolism, mitochondrial homeostasis plays a crucial role in maintaining normal mammary gland function. This review focuses on the regulatory mechanisms of mitochondrial homeostasis and the effect of mitochondrial dysfunction on homeostatic mechanisms in bovine mammary gland. Furthermore, we summarize several potential therapeutic strategies targeting mitochondrial metabolic dysfunction to alleviate mammary tissue damage.

Background: The objective of this study was to investigate the effect of L-tryptophan (L-Trp) and its metabolite kynurenine (Kyn) on the regulation of porcine intestinal epithelial cell proliferation.

Results: Dietary supplementation of L-Trp significantly increased villus height and decreased crypt depth in the jejunum and ileum of weaned pigs. mRNA sequencing data and qPCR analysis found that L-Trp activated the expression of cell proliferative genes and the AHR (aryl hydrocarbon receptor)-MST1 (mammalian STE20-like kinase 1)-YAP1 (Yes-associated protein 1) axis in the ileum. Further in vitro analysis revealed that L-Trp treatment significantly enhanced cell proliferation of intestinal porcine epithelial cells-jejunum 2 (IPEC-J2) cells by activating the MST1-YAP1 signaling pathway. Further targeted metabolomics analysis identified Kyn as the core Trp metabolite involved in promoting IPEC-J2 cell proliferation. Mechanistically, Kyn interacted with AHR, which in turn bound to the upstream promote region of MST1 to initiate the transcription of downstream target gene YAP1 to activate intestinal epithelial cell proliferation. Furthermore, porcine intestinal organoid model also demonstrated that Kyn promoted intestinal organoid-budding efficiency and intestinal stem cell proliferation. Importantly, by using the AHR- or YAP1-specific inhibitors, the data confirmed that the Kyn-induced intestinal epithelial cell proliferation in IPEC-J2 cells and intestinal organoids was dependent on the activation of the AHR-MST1-YAP1 axis.

Conclusions: Together, this study has revealed a regulatory mechanism of Trp metabolism-derived Kyn in promoting porcine intestinal epithelial cell proliferation, offering insights into the connection between nutrient metabolism and intestinal epithelial homeostasis.

Background: Mycotoxin contamination poses a major challenge to public health and has garnered increasing attention across the world in recent decades. Zearalenone (ZEA), as one of the most prevalent contaminants, induces reproductive toxicity and then poses potential threats to animal health. Autophagy/beclin-1 regulator 1 (AMBRA1) is a protein critical for autophagy induction, and can enhance mitophagy by co-localizing with LC3. However, the potential health risk caused by ZEA in male germ cells of animals is unclear. This study aimed to investigate the underlying mechanisms of ZEA-induced swine testicular (ST) cell injury and to clarify the role of AMBRA1 in this process.

Methods: We established ST cell models to explore the effects of AMBRA1 on ferroptosis induced by ZEA. Multiple experimental approaches were applied to assess cell viability, mitochondrial dysfunction, oxidative stress, iron accumulation, and mitophagy. Mechanistic insights were further validated using AMBRA1 overexpression, RNA-seq, molecular docking, western blotting, immunofluorescence, and qRT-PCR analyses.

Results: In this study, ZEA induced mitochondrial structural damage and impaired mitochondrial function, leading to excessive ROS generation and loss of mitochondrial membrane potential. We also found that ZEA disrupted the iron homeostasis and thus led to the accumulation of ferrous iron, which further induce ferroptosis. In addition, ZEA reduced autophagy activity and autophagic flux, ultimately suppressing mitophagy. Of note, AMBRA1 overexpression effectively relieved ZEA-induced ferroptosis through restoration of mitophagy in ST cells.

Conclusions: In conclusion, our study demonstrated that ZEA targeted the AMBRA1, leading to down-regulation of AMBRA1 expression, which in turn inhibited mitophagy and thus resulted in ferroptosis in ST cells. Given the potential role of AMBRA1 in ST cells, our results uncover a previously unrecognized mechanism in which AMBRA1-mediated mitophagy functions as a crucial defense target against ferroptosis in testicular cells. Importantly, our results propose a unique insight which AMBRA1 as a promising therapeutic target for counteracting mycotoxin-induced testicular injury in animals.

Circadian rhythms are endogenous oscillations with a period of approximately 24 h. They enable organisms to anticipate and adapt to daily environmental changes, such as light and temperature. As the largest metabolic and motor organ in the body, skeletal muscle plays a decisive role in determining meat production efficiency in ruminants. Skeletal muscle development is largely governed by the proliferation and myogenic differentiation capacity of skeletal muscle satellite cells (SMSCs). More than 2,300 genes in skeletal muscle exhibit circadian oscillatory expression and are extensively involved in myogenesis, transcriptional regulation, and metabolic processes. The rhythmic expression of these genes is modulated by external factors including the photoperiod, feeding behavior, gut microbiota, and physical activity. Disruption of the endogenous circadian timing system can inhibit SMSC proliferation and myogenic differentiation, thereby impairing normal muscle development. Therefore, this review focuses on key management aspects of ruminant production-such as environmental control, nutritional regulation, and exercise management-and systematically elaborates on how these husbandry strategies may influence SMSC fate by modulating the circadian clock, along with the underlying molecular mechanisms.

Background: Rosemary-derived triterpene acids (TAs), primarily composed of ursolic acid, oleanolic acid, and betulinic acid, exhibit multiple bioactive properties. However, their effects on lipid metabolism and the underlying regulatory pathways remain unclear. This study investigated the effects of dietary supplementation with TAs on the growth performance, digestive and absorptive function, and hepatic lipid metabolism in juvenile grass carp (Ctenopharyngodon idella).

Methods: In this trial, 2,160 juvenile grass carp (average weight 13.04 ± 0.02 g) were randomly allocated to six dietary treatments, each comprising six replicates with 60 fish per replicate. Fish were fed diets supplemented with increasing concentrations of TAs (0, 58.80, 179.30, 261.90, 312.00, and 390.00 mg/kg) for 70 d. At the end of the trial, relevant samples were collected for subsequent analyses.

Results: The results demonstrated that dietary supplementation with TAs significantly increased specific growth rate (SGR), whole-body crude protein (CP) levels, and protein retention value (PRV) in juvenile grass carp, while reducing whole-body ether extract (EE) levels. Moreover, dietary supplementation with TAs significantly enhanced the activities of intestinal digestive enzymes and brush-border enzymes, thereby improving the digestive and absorptive capacity of juvenile grass carp. In the liver, dietary supplementation with TAs markedly inhibited lipid synthesis while promoting lipid utilization. The effects of TAs on lipid metabolism were associated with activation of the hepatic farnesoid X receptor (FXR) pathway, involving peroxisome proliferator-activated receptor alpha (PPARα) and sterol regulatory element-binding protein 1 (SREBP-1). Furthermore, TAs modulated the gut-liver axis by inhibiting the intestinal FXR-sphingomyelin phosphodiesterase 3 (SMPD3)-ceramide pathway, which may contribute to reduced hepatic lipid deposition. Quadratic regression analysis showed that the optimal dietary TAs supplementation levels were 245.00 mg/kg (SGR), 218.33 mg/kg (intestinal lipase activity), and 267.64 mg/kg (hepatic hormone-sensitive lipase activity).

Conclusions: The addition of TAs to the diet improved growth performance, digestive and absorptive capacity, and liver lipid utilization in juvenile grass carp. This work reveals the potential application of TAs in aquaculture and provides a theoretical basis for the development of functional feed additives.

Background: Fat metabolism in pigs is controlled by tissue-specific molecular mechanisms that ultimately affect growth performance and meat quality. Understanding how epigenetic modifications interact with gene expression across key metabolic and fat-depositing tissues is essential for identifying regulatory processes and potential biomarkers to improve pork quality traits. Therefore, this study aimed to elucidate tissue specific epigenetic regulation of fat metabolism by integrating DNA methylation and gene expression profiles from liver, backfat, and loin (longissimus dorsi) tissues at two physiologically developmental stages (10 and 26 weeks), representing the early post-weaning growth phase and near-market weight, respectively. By explicitly comparing these ages and tissues, the study was designed to capture the transition from muscle-dominated growth to increased lipid deposition and to identify tissue- and stage-specific regulatory signatures that may serve as biomarkers for pork quality.

Results: Genome-wide DNA methylation exhibited weak clustering by tissue, whereas gene expression showed clear tissue separation. The liver harbored fewer genes with differential methylation across stage and tissue but a greater number of genes with differential expression than backfat and loin, suggesting distinct regulatory modes. Integrative analysis of the overlap genes between methylation and expression signals highlighted epigenetically mediated regulation of extracellular matrix organization, lipid metabolism, and muscle development pathways. Furthermore, weighted gene co-expression network analysis revealed distinct tissue-specific correlations between co-methylated and co-expressed modules, with enrichment in cholesterol biosynthesis, muscle contractility, and extracellular matrix remodeling. Together, these findings suggest that methylation changes are more subtle than transcriptional shifts, yet they are aligned with key functional pathways, consistent with a role for methylation as a fine-tuning mechanism that shapes tissue-specific transcriptional networks during growth.

Conclusions: Across liver, backfat, and loin, DNA methylation modulates transcriptional programs in a tissue-dependent manner, prioritizing pathways central to lipid handling, extracellular matrix remodeling, and muscle function. This integrated multi-omics framework highlights candidate epigenetic markers and regulatory modules with potential utility for improving pork quality traits through selection or management strategies.

Background: Colostrum is recognised as the "golden elixir of health" due to its optimal chemical, immunological and nutraceutical properties for newborns, but little is known about its nature in the pig. This study aims to provide a multi-omics characterisation of pig colostrum from different parities (gilts, n = 7, second, n = 7 and mature, n = 6 sows) to identify the most relevant bioactive compounds associated with piglet survival and average daily gain (ADG) and faecal microbiota till d 6 and d 24.

Results: Nine hundred and fifty metabolites (108 chemically confirmed) and 71 fatty acids (FAs) were characterised in colostrum. Parity class was the main driver for piglet survivability (P < 0.001; highest in second parity), metabolomics (R² = 0.97; Q² = 0.52; > 200 discriminated metabolites) and lipidomic profile (22 discriminated FAs) and piglet faecal microbiota (beta diversity P < 0.05 at d 6 and d 24). Colostrum composition allowed clustering for piglet mortality from d 0 to d 6 (Q² > 0.50). Mortality classes at d 6 were discriminated by 177 metabolites and 2 FAs and 248 metabolites and 21 FAs at d 24. At both timepoints a higher abundance of C18:2 8trans,10cis discriminated for lower mortality (importance = 1 for d 6 and 0.34 for d 24). Pathway analysis at d 6 and d 24 indicated arginine biosynthesis and alpha-linoleic acid metabolism as most enriched metabolism in swine colostrum related to higher survivability. The multi-omics integration analysis revealed that a higher faecal abundance of Lachnospiraceae_FCS020, Holdemania, Roseburia, and a higher colostrum abundance of C18:2 8trans,10cis, and the C18:1 5trans and salicylic acid as metabolites were the most associated with a lower mortality. The ADG classes d 0-24 were discriminated by 151 metabolites and 33 FAs. Higher ADG (240 g/d) was discriminated by colostrum vitamin E, histidine, and branched-chain amino acids (VIP score > 1), while L-kynurenine and gamma-aminobutyric acid were linked to lower growth, suggesting maternal stress.

Conclusion: This study confirms the importance of parity order in shaping colostrum composition and identifies several bioactive compounds, some parity-dependent and others parity-independent, that may be associated with improved piglet survival and gut microbiota maturation. The findings may also support the development of next-generation artificial colostrum supplements.

Background: The transition period is a critical phase for the sow due to physiological changes and nutritional requirements. A diet balanced in energy and amino acid (AA) content could improve reproductive performance, colostrum quality and piglets' growth. This study evaluated the efficacy of a transition diet (TRT) with higher energy (12.97 MJ/kg of metabolizable energy (ME)) and SID lysine (Lys; 0.85%), compared to a standard (CO) diet (12.33 MJ/kg of ME and 0.70% SID Lys), on the composition and quality of colostrum and on sow and piglet performance. The AA/SID Lys ratio was maintained in both diets. Sows (50 sows/group) were fed the CO or TRT diet from 6 d prepartum to d 4 postpartum. At farrowing, sow performance (50 sows/group) and piglet vitality (12 sows/group) were recorded, and colostrum (20 sows/group) was collected to analyze its composition and microRNAs. Piglet performances were collected d 6 and weaning (d 24).

Results: The diet did not affect sow feed intake, body condition score, backfat and muscle loss, nor farrowing duration and time interval between piglets. The TRT group had fewer stillbirths (P = 0.002). Piglets of TRT litters had higher body weight at d 24 (P = 0.032) and tended to have higher average daily gain from d 0 to d 24 (P = 0.080). Colostrum from the TRT group tended to be higher in somatic cell count (P = 0.07), higher in fat percentage (P = 0.036), and higher in C18:2 9cis,12cis, C18:4 6cis,9cis,12cis,15cis, C20:0, UDP-glucuronate and carnitine (P < 0.05); moreover, it had a lower concentration of citrate (P < 0.05). The 208 microRNAs were detected in colostrum, 13 of which were differentially expressed (P < 0.05). The TRT group had a higher ssc-miR-143-3p expression, which is associated with increased phagocytosis and reduced inflammation and oxidative stress. This, together with the increase in fat and specific metabolites related to energy metabolism, could potentially benefit piglet performance.

Conclusion: These results suggest that the TRT diet improves sow parturition and lactation performance by modifying sow energy metabolism and colostrum quality. This highlights the importance of a properly designed transition diet for sows.