Pub Date : 2025-05-24DOI: 10.1186/s40104-025-01203-y
Fengdong Zhang, Yongchang Han, Fan Li, Boya Guo, Jian Chen, Wenchuan Zhou, Pan Xiao, Hui Ma, Yongyan Jin, Jia Feng, Yuna Min
Higher embryonic mortality, especially in aged breeding hens, is associated with insufficient hepatic functionality in maintaining redox homeostasis. Our previous study demonstrated that egg exosome-derived miRNAs may play a key role in modulating embryonic oxidation-reduction process, whereas the exact function and mechanism were still poorly understood. The present study aimed to investigate the roles of egg exosome miRNAs in maintaining dynamic equilibrium of free radicals and peroxide agents in embryonic liver, as well as demonstrate the specific mechanism using oxidative stress-challenged hepatocytes. Compared to 36-week-old breeding hens, decreased hatchability and increased embryonic mortality were observed in 65-week-old breeding hens. Meanwhile, the older group showed the increased MDA levels and decreased SOD and GSH-Px activities in embryonic liver, muscle and serum. Embryonic mortality was significantly positively correlated with MDA level and negatively correlated with GSH-Px activity in embryonic liver. In addition, 363 differentially expressed genes (DEGs) were identified in embryonic liver, 13 differentially expressed miRNAs (DE-miRNAs) were identified in egg exosomes. These DEGs and DE-miRNAs were involved in oxidoreductase activity, glutathione metabolic process, MAPK signaling pathway, apoptosis and autophagy. miRNA-mRNA network analysis further found that DEGs targeted by DE-miRNAs were mainly enriched in programmed cell death, such as apoptosis and autophagy. Wherein, MAPK10 with highest MCC and AUC values was significantly related to GSH-Px activity and MDA level, and served as the target gene of miR-145-5p based on dual luciferase reporter experiment and correlation analysis. Bioinformatics analysis found that miR-145-5p/MAPK10 axis might alleviate peroxide generation and apoptosis. In primary hepatocytes of chick embryos, miR-145-5p transfection significantly reversed H2O2-induced mitochondrial ROS increase, MAPK10, BAX and CASP3 overexpression and excessive apoptosis. Exosome miR-145-5p in eggs could target MAPK10 and decrease mitochondrial ROS, attenuating oxidative damage and apoptosis in hepatocytes of chick embryos. These findings may provide new theoretical basis for the improvement of maternal physiological status to maintain embryonic redox homeostasis by nutritional or genetic modifications.
{"title":"Egg exosome miR-145-5p decreases mitochondrial ROS to protect chicken embryo hepatocytes against apoptosis through targeting MAPK10","authors":"Fengdong Zhang, Yongchang Han, Fan Li, Boya Guo, Jian Chen, Wenchuan Zhou, Pan Xiao, Hui Ma, Yongyan Jin, Jia Feng, Yuna Min","doi":"10.1186/s40104-025-01203-y","DOIUrl":"https://doi.org/10.1186/s40104-025-01203-y","url":null,"abstract":"Higher embryonic mortality, especially in aged breeding hens, is associated with insufficient hepatic functionality in maintaining redox homeostasis. Our previous study demonstrated that egg exosome-derived miRNAs may play a key role in modulating embryonic oxidation-reduction process, whereas the exact function and mechanism were still poorly understood. The present study aimed to investigate the roles of egg exosome miRNAs in maintaining dynamic equilibrium of free radicals and peroxide agents in embryonic liver, as well as demonstrate the specific mechanism using oxidative stress-challenged hepatocytes. Compared to 36-week-old breeding hens, decreased hatchability and increased embryonic mortality were observed in 65-week-old breeding hens. Meanwhile, the older group showed the increased MDA levels and decreased SOD and GSH-Px activities in embryonic liver, muscle and serum. Embryonic mortality was significantly positively correlated with MDA level and negatively correlated with GSH-Px activity in embryonic liver. In addition, 363 differentially expressed genes (DEGs) were identified in embryonic liver, 13 differentially expressed miRNAs (DE-miRNAs) were identified in egg exosomes. These DEGs and DE-miRNAs were involved in oxidoreductase activity, glutathione metabolic process, MAPK signaling pathway, apoptosis and autophagy. miRNA-mRNA network analysis further found that DEGs targeted by DE-miRNAs were mainly enriched in programmed cell death, such as apoptosis and autophagy. Wherein, MAPK10 with highest MCC and AUC values was significantly related to GSH-Px activity and MDA level, and served as the target gene of miR-145-5p based on dual luciferase reporter experiment and correlation analysis. Bioinformatics analysis found that miR-145-5p/MAPK10 axis might alleviate peroxide generation and apoptosis. In primary hepatocytes of chick embryos, miR-145-5p transfection significantly reversed H2O2-induced mitochondrial ROS increase, MAPK10, BAX and CASP3 overexpression and excessive apoptosis. Exosome miR-145-5p in eggs could target MAPK10 and decrease mitochondrial ROS, attenuating oxidative damage and apoptosis in hepatocytes of chick embryos. These findings may provide new theoretical basis for the improvement of maternal physiological status to maintain embryonic redox homeostasis by nutritional or genetic modifications. ","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"22 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-22DOI: 10.1186/s40104-025-01191-z
Yanli Chen, Yan Wang, Weike Shaoyong, Yanmin He, Yalin Liu, Siyu Wei, Yujie Gan, Lu Sun, Youming Wang, Xin Zong, Yun Xiang, Yizhen Wang, Mingliang Jin
Compelling evidence has established a strong link between the gut microbiota and host reproductive health. However, the specific regulatory roles of individual bacterial species on reproductive performance are not well-understood. In the present study, Jinhua sows with varying reproductive performances under the same diet and management conditions were selected to explore potential mechanisms on the intricate relationship between the gut microbiome and host reproductive performance using 16S rRNA sequencing, metagenomics and serum metabolomics. Our findings revealed that the KEGG pathways for base excision repair and DNA replication were enriched, along with gene-level enhancements in spore formation, in sows with higher reproductive performance, indicating that the gut microbiome experiences stress. Further analysis showed a positive correlation between these changes and litter size, indicating that the host acts as a stressor, reshaping the microbiome. This adaptation allows the intestinal microbes in sows with high reproductive performance to enrich specific serotonin-related bacteria, such as Oxalobacter formigenes, Ruminococcus sp. CAG 382, Clostridium leptum, and Clostridium botulinum. Subsequently, the enriched microbiota may promote host serotonin production, which is positively correlated with reproductive performance in our study, known to regulate follicle survival and oocyte maturation. Our study provides a theoretical basis for understanding the interactions between gut microbes and the host. It highlights new insights into reassembling gut microbiota in sows with higher litter sizes and the role of serotonin-related microbiota and serotonin in fertility.
{"title":"High-fertility sows reshape gut microbiota: the rise of serotonin-related bacteria and its impact on sustaining reproductive performance","authors":"Yanli Chen, Yan Wang, Weike Shaoyong, Yanmin He, Yalin Liu, Siyu Wei, Yujie Gan, Lu Sun, Youming Wang, Xin Zong, Yun Xiang, Yizhen Wang, Mingliang Jin","doi":"10.1186/s40104-025-01191-z","DOIUrl":"https://doi.org/10.1186/s40104-025-01191-z","url":null,"abstract":"Compelling evidence has established a strong link between the gut microbiota and host reproductive health. However, the specific regulatory roles of individual bacterial species on reproductive performance are not well-understood. In the present study, Jinhua sows with varying reproductive performances under the same diet and management conditions were selected to explore potential mechanisms on the intricate relationship between the gut microbiome and host reproductive performance using 16S rRNA sequencing, metagenomics and serum metabolomics. Our findings revealed that the KEGG pathways for base excision repair and DNA replication were enriched, along with gene-level enhancements in spore formation, in sows with higher reproductive performance, indicating that the gut microbiome experiences stress. Further analysis showed a positive correlation between these changes and litter size, indicating that the host acts as a stressor, reshaping the microbiome. This adaptation allows the intestinal microbes in sows with high reproductive performance to enrich specific serotonin-related bacteria, such as Oxalobacter formigenes, Ruminococcus sp. CAG 382, Clostridium leptum, and Clostridium botulinum. Subsequently, the enriched microbiota may promote host serotonin production, which is positively correlated with reproductive performance in our study, known to regulate follicle survival and oocyte maturation. Our study provides a theoretical basis for understanding the interactions between gut microbes and the host. It highlights new insights into reassembling gut microbiota in sows with higher litter sizes and the role of serotonin-related microbiota and serotonin in fertility. ","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"153 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-22DOI: 10.1186/s40104-025-01210-z
Xueqing Ye, Yuying Yang, Qinghua Yao, Mengyi Huang, Balamuralikrishnan Balasubramanian, Rajesh Jha, Wenchao Liu
Aflatoxin B1 (AFB1) risks animal and human health, and the liver is considered the most crucial detoxification organ. Phlorotannin (PT) is a polyhydroxy phenol that has a wide range of biological activities, including anti-oxidation and hepatoprotection, which can promote the ability of liver detoxification. This study aimed to elucidate the protective effect of PT on AFB1-induced liver damage in broilers. In vivo experiment showed that the PT reduced AFB1 content and AFB1-exo-8,9-epoxide DNA (AFBO-DNA) concentration in serum and liver (P < 0.05), improved the histomorphology of liver and hepatic mitochondria, and activated nuclear factor erythroid 2-related factor 2 (Nrf2)-related antioxidant and detoxification pathway by upregulating the activities of antioxidant enzymes (catalase [CAT], glutathione S-transferase [GST]) and total antioxidant capacity (T-AOC) level (P < 0.05), and inhibited the mRNA expression of CYP1A1 (cytochrome P450 family 1 subfamily A member 1) and phase II detoxification enzyme related genes (GPX1, GSTT1, and NQO1) of broilers exposed to AFB1 (P < 0.05). Meanwhile, PT upregulated the Nrf1 pathway-related mitochondrial biosynthetic genes (Nrf1, mitochondrial transcription factor A [TFAM], mitofusin 1 [MFN1]) in broilers fed AFB1 contaminated diet (P < 0.05). In vitro verification study suggested that the use of Nrf2/Nrf1 inhibitors suppressed the ameliorative role of PT on AFB1-induced liver injury of broilers, which was manifested in the mRNA expression of Nrf2, NQO1, GSTT3, Nrf1, TFAM, and other genes decreasing (P < 0.05), and down-regulation of the protein expression of Nrf2, total and nucleus p-Nrf2, and total and nucleus p-Nrf1 (P < 0.05). The PT ameliorates oxidative stress and hepatotoxicity by activating the Nrf2-mediated phase II detoxification enzymes pathway and maintains mitochondrial homeostasis by activating the Nrf1 signaling pathway in broilers exposed to AFB1.
{"title":"The ameliorative role of phlorotannin on aflatoxin B1-induced liver oxidative stress and mitochondrial injury is related to the activation of Nrf2 and Nrf1 signaling pathways in broilers","authors":"Xueqing Ye, Yuying Yang, Qinghua Yao, Mengyi Huang, Balamuralikrishnan Balasubramanian, Rajesh Jha, Wenchao Liu","doi":"10.1186/s40104-025-01210-z","DOIUrl":"https://doi.org/10.1186/s40104-025-01210-z","url":null,"abstract":"Aflatoxin B1 (AFB1) risks animal and human health, and the liver is considered the most crucial detoxification organ. Phlorotannin (PT) is a polyhydroxy phenol that has a wide range of biological activities, including anti-oxidation and hepatoprotection, which can promote the ability of liver detoxification. This study aimed to elucidate the protective effect of PT on AFB1-induced liver damage in broilers. In vivo experiment showed that the PT reduced AFB1 content and AFB1-exo-8,9-epoxide DNA (AFBO-DNA) concentration in serum and liver (P < 0.05), improved the histomorphology of liver and hepatic mitochondria, and activated nuclear factor erythroid 2-related factor 2 (Nrf2)-related antioxidant and detoxification pathway by upregulating the activities of antioxidant enzymes (catalase [CAT], glutathione S-transferase [GST]) and total antioxidant capacity (T-AOC) level (P < 0.05), and inhibited the mRNA expression of CYP1A1 (cytochrome P450 family 1 subfamily A member 1) and phase II detoxification enzyme related genes (GPX1, GSTT1, and NQO1) of broilers exposed to AFB1 (P < 0.05). Meanwhile, PT upregulated the Nrf1 pathway-related mitochondrial biosynthetic genes (Nrf1, mitochondrial transcription factor A [TFAM], mitofusin 1 [MFN1]) in broilers fed AFB1 contaminated diet (P < 0.05). In vitro verification study suggested that the use of Nrf2/Nrf1 inhibitors suppressed the ameliorative role of PT on AFB1-induced liver injury of broilers, which was manifested in the mRNA expression of Nrf2, NQO1, GSTT3, Nrf1, TFAM, and other genes decreasing (P < 0.05), and down-regulation of the protein expression of Nrf2, total and nucleus p-Nrf2, and total and nucleus p-Nrf1 (P < 0.05). The PT ameliorates oxidative stress and hepatotoxicity by activating the Nrf2-mediated phase II detoxification enzymes pathway and maintains mitochondrial homeostasis by activating the Nrf1 signaling pathway in broilers exposed to AFB1. ","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"19 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-22DOI: 10.1186/s40104-025-01198-6
Mingyi Huang, Lei Xue, Yifan Wu, Qinzheng Sun, Yanwei Xu, Jia Li, Xiaoyi Yu, Yu Cao, Jingyi Huang, Zeyu Zhang, Jinbiao Zhao, Dandan Han, Defa Li, Junjun Wang
Pigs fed diets with different ingredients but identical nutritional levels show significant differences in growth performance, indicating that growth may also be influenced by the synchronicity of dietary carbon and nitrogen supply. Therefore, this study aimed to determine glucose release kinetics of various feed ingredients, to investigate a glucose release pattern that is conducive to synchronized carbon–nitrogen supply, and to elucidate the underlying mechanisms by which this synchronization optimizes growth of pigs. We analyzed the glucose release kinetics of 23 feed ingredients in vitro and found that their glucose release rates and amounts varied greatly. Based on this, a nitrogen-free diet and 5 purified diets, which represented the observed variations in glucose release rates and quantities among feed ingredients, were designed for 18 ileal-cannulated pigs. The results demonstrated that slower glucose release pattern could disrupt the synchrony of dietary carbon and nitrogen supply, reducing the growth of pigs and increasing nitrogen losses. Specifically, the diet with slower and moderate amounts of glucose release showed a relatively slower release of amino acids. Pigs fed this diet had the lower amino acid digestibility and the enrichment of harmful bacteria, such as Streptococcus, in the terminal ileum. Conversely, the diets with slower and lower glucose release exhibited a relatively rapid release of amino acids but also resulted in poor growth. They increased glucogenic amino acid digestibility and potentially enriched bacteria involved in nitrogen cycling and carbon metabolism. Notably, only the diet with rapid glucose release achieved synchronized and rapid release of nutrients. Pigs fed this diet exhibited higher amino acid digestibility, decreased harmful bacteria enrichment, improved nutrient utilization, and enhanced short-term growth performance. Our research analyzed significant differences in glucose release kinetics among swine feed ingredients and revealed that slow glucose release disrupted dietary carbon–nitrogen supply synchrony, shifting amino acid utilization and enriching pathogens, negatively impacting growth and nutrient utilization. Consequently, choosing feed ingredients releasing glucose at a rapid rate to balance dietary carbon and nitrogen supply helps promote pig growth, and ensures efficient feed utilization.
{"title":"Glucose release kinetics of different feed ingredients and their impact on short-term growth of pigs by influencing carbon-nitrogen supply synchronization","authors":"Mingyi Huang, Lei Xue, Yifan Wu, Qinzheng Sun, Yanwei Xu, Jia Li, Xiaoyi Yu, Yu Cao, Jingyi Huang, Zeyu Zhang, Jinbiao Zhao, Dandan Han, Defa Li, Junjun Wang","doi":"10.1186/s40104-025-01198-6","DOIUrl":"https://doi.org/10.1186/s40104-025-01198-6","url":null,"abstract":"Pigs fed diets with different ingredients but identical nutritional levels show significant differences in growth performance, indicating that growth may also be influenced by the synchronicity of dietary carbon and nitrogen supply. Therefore, this study aimed to determine glucose release kinetics of various feed ingredients, to investigate a glucose release pattern that is conducive to synchronized carbon–nitrogen supply, and to elucidate the underlying mechanisms by which this synchronization optimizes growth of pigs. We analyzed the glucose release kinetics of 23 feed ingredients in vitro and found that their glucose release rates and amounts varied greatly. Based on this, a nitrogen-free diet and 5 purified diets, which represented the observed variations in glucose release rates and quantities among feed ingredients, were designed for 18 ileal-cannulated pigs. The results demonstrated that slower glucose release pattern could disrupt the synchrony of dietary carbon and nitrogen supply, reducing the growth of pigs and increasing nitrogen losses. Specifically, the diet with slower and moderate amounts of glucose release showed a relatively slower release of amino acids. Pigs fed this diet had the lower amino acid digestibility and the enrichment of harmful bacteria, such as Streptococcus, in the terminal ileum. Conversely, the diets with slower and lower glucose release exhibited a relatively rapid release of amino acids but also resulted in poor growth. They increased glucogenic amino acid digestibility and potentially enriched bacteria involved in nitrogen cycling and carbon metabolism. Notably, only the diet with rapid glucose release achieved synchronized and rapid release of nutrients. Pigs fed this diet exhibited higher amino acid digestibility, decreased harmful bacteria enrichment, improved nutrient utilization, and enhanced short-term growth performance. Our research analyzed significant differences in glucose release kinetics among swine feed ingredients and revealed that slow glucose release disrupted dietary carbon–nitrogen supply synchrony, shifting amino acid utilization and enriching pathogens, negatively impacting growth and nutrient utilization. Consequently, choosing feed ingredients releasing glucose at a rapid rate to balance dietary carbon and nitrogen supply helps promote pig growth, and ensures efficient feed utilization.","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"57 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mitophagy is an essential cellular autophagic process which maintains mitochondrial homeostasis, but its role in high fat diet (HFD)-induced lipid accumulation is unclear in the yellow catfish. Thus, this study aimed to elucidate mechanism of mitochondria mediating HFD-induced hepatic fat accumulation. In the present study, yellow catfish were fed three diets with dietary fat at 6.31% (low fat; LFD, control), 12.03% (middle fat; MFD) and 15.32% (high fat; HFD), respectively, for 8 weeks. High dietary fat addition raised hepatic lipid accumulation, and declined mRNA and protein levels of Parkin-dependent mitophagy, down-regulated the Parkin protein expression and the estrogen-related receptor alpha (Errα) ubiquitination, and induced Errα protein levels; fatty acid (FA) incubation reduced Parkin-dependent mitophagy, inhibited Errα ubiquitination and increased Errα protein expression, and raised TG accumulation. Furthermore, yellow catfish hepatocytes were isolated and cultured. Nicotinamide mononucleotide, N-acetyl-L-cysteine, Parkin and errα siRNA knockdown were used under FA incubation, respectively. Parkin downregulation mediated FA incubation-induced TG accumulation and mitoautophagic inhibition; Parkin ubiquitinated Errα, and K63 was an important ubiquitination site for deubiquitinating Parkin activity; Errα targets fas, acca and pparγ genes, whose activation contributed to FA-induced lipogenesis and lipid accumulation. Thus, high fat diet (HFD) and FA incubation inhibited Parkin activity, suppressed mitophagy and activated Errα pathway, and induced hepatic lipogenic metabolism and lipotoxicity. Overall, our study provided new targets against HFD-induced hepatic lipid accumulation and non-alcoholic fatty liver disease in the vertebrates.
{"title":"High fat diet (HFD) induced hepatic lipogenic metabolism and lipotoxicity via Parkin-dependent mitophagy and Errα signal of Pelteobagrus fulvidraco","authors":"Angen Yu, Zhiwei Hao, Xiaolei Wei, Xiaoying Tan, Ester Zito, Hua Zheng, Zhi Luo","doi":"10.1186/s40104-025-01200-1","DOIUrl":"https://doi.org/10.1186/s40104-025-01200-1","url":null,"abstract":"Mitophagy is an essential cellular autophagic process which maintains mitochondrial homeostasis, but its role in high fat diet (HFD)-induced lipid accumulation is unclear in the yellow catfish. Thus, this study aimed to elucidate mechanism of mitochondria mediating HFD-induced hepatic fat accumulation. In the present study, yellow catfish were fed three diets with dietary fat at 6.31% (low fat; LFD, control), 12.03% (middle fat; MFD) and 15.32% (high fat; HFD), respectively, for 8 weeks. High dietary fat addition raised hepatic lipid accumulation, and declined mRNA and protein levels of Parkin-dependent mitophagy, down-regulated the Parkin protein expression and the estrogen-related receptor alpha (Errα) ubiquitination, and induced Errα protein levels; fatty acid (FA) incubation reduced Parkin-dependent mitophagy, inhibited Errα ubiquitination and increased Errα protein expression, and raised TG accumulation. Furthermore, yellow catfish hepatocytes were isolated and cultured. Nicotinamide mononucleotide, N-acetyl-L-cysteine, Parkin and errα siRNA knockdown were used under FA incubation, respectively. Parkin downregulation mediated FA incubation-induced TG accumulation and mitoautophagic inhibition; Parkin ubiquitinated Errα, and K63 was an important ubiquitination site for deubiquitinating Parkin activity; Errα targets fas, acca and pparγ genes, whose activation contributed to FA-induced lipogenesis and lipid accumulation. Thus, high fat diet (HFD) and FA incubation inhibited Parkin activity, suppressed mitophagy and activated Errα pathway, and induced hepatic lipogenic metabolism and lipotoxicity. Overall, our study provided new targets against HFD-induced hepatic lipid accumulation and non-alcoholic fatty liver disease in the vertebrates.","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"2 1","pages":"71"},"PeriodicalIF":7.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144104528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-20DOI: 10.1186/s40104-025-01211-y
Qian Zhang, Shuaijie Wang, Mengjun Wu, Zihan Tan, Tao Wu, Dan Yi, Lei Wang, Di Zhao, Yongqing Hou
Porcine epidemic diarrhea virus (PEDV) infection poses a significant challenge to the swine industry, with limited effective control measures available. Poria cocos polysaccharides (PCP) is the primary active ingredient of Poria cocos, and has been demonstrated to show beneficial effects on intestinal damage in previous studies. However, its mechanism has not been fully understood. In the present study, 18 seven-day-old piglets were divided into 3 groups: Control group, PEDV group, and PCP + PEDV group. After three days of adaptation, piglets in the PCP + PEDV group were orally administered 10 mg/kg body weight/d PCP from d 4 to 10. On d 8, piglets were orally administered with PEDV at the dose of 104.5 TCID50/piglet. This study aimed to investigate the potential effects of PCP on PEDV-induced intestinal injury and explored the underlying mechanisms. The results showed that PCP administration effectively alleviated diarrhea, reduced PEDV replication in the small intestine and colon of piglets, and significantly improved intestinal mucosal morphology. Specifically, PCP increased the villus height in both the jejunum and ileum and increased the villus height to crypt depth ratio in the ileum (P < 0.05). Improved intestinal function was further evidenced by elevated plasma D-xylose levels and decreased diamine oxidase activity (P < 0.05). Transcriptomic and proteomic analyses revealed that lipid metabolism is a key pathway regulated by PCP during PEDV infection. Notably, PCP significantly upregulated sphingolipid metabolism-related genes, including ectonucleotide pyrophosphatase/phosphodiesterase family member 7 and N-acylsphingosine amidohydrolase 2. Metabolomic analysis revealed that PCP primarily modulated the levels of plasmanylphosphoethanolamine, lysophosphatidylcholine, and carnitine. Additionally, PCP reversed the expression of key genes involved in fatty acid uptake, intracellular lipid transport, and fatty acid synthesis, such as fatty acid binding protein 2, fatty acid transport protein 4, apolipoprotein B, apolipoprotein C3, fatty acid synthase, long-chain fatty acyl CoA synthetase 3, lipoprotein lipase and acyl-CoA thioesterases 12 (P < 0.05). These findings demonstrate that PCP mitigates PEDV-induced intestinal injury by modulating lipid metabolism and highlight its potential as a dietary supplement for enhancing anti-PEDV defenses and promoting intestinal health in piglets.
{"title":"Multi-omics profiling reveals Poria cocos polysaccharides mitigate PEDV-induced intestinal injury by modulating lipid metabolism in piglets","authors":"Qian Zhang, Shuaijie Wang, Mengjun Wu, Zihan Tan, Tao Wu, Dan Yi, Lei Wang, Di Zhao, Yongqing Hou","doi":"10.1186/s40104-025-01211-y","DOIUrl":"https://doi.org/10.1186/s40104-025-01211-y","url":null,"abstract":"Porcine epidemic diarrhea virus (PEDV) infection poses a significant challenge to the swine industry, with limited effective control measures available. Poria cocos polysaccharides (PCP) is the primary active ingredient of Poria cocos, and has been demonstrated to show beneficial effects on intestinal damage in previous studies. However, its mechanism has not been fully understood. In the present study, 18 seven-day-old piglets were divided into 3 groups: Control group, PEDV group, and PCP + PEDV group. After three days of adaptation, piglets in the PCP + PEDV group were orally administered 10 mg/kg body weight/d PCP from d 4 to 10. On d 8, piglets were orally administered with PEDV at the dose of 104.5 TCID50/piglet. This study aimed to investigate the potential effects of PCP on PEDV-induced intestinal injury and explored the underlying mechanisms. The results showed that PCP administration effectively alleviated diarrhea, reduced PEDV replication in the small intestine and colon of piglets, and significantly improved intestinal mucosal morphology. Specifically, PCP increased the villus height in both the jejunum and ileum and increased the villus height to crypt depth ratio in the ileum (P < 0.05). Improved intestinal function was further evidenced by elevated plasma D-xylose levels and decreased diamine oxidase activity (P < 0.05). Transcriptomic and proteomic analyses revealed that lipid metabolism is a key pathway regulated by PCP during PEDV infection. Notably, PCP significantly upregulated sphingolipid metabolism-related genes, including ectonucleotide pyrophosphatase/phosphodiesterase family member 7 and N-acylsphingosine amidohydrolase 2. Metabolomic analysis revealed that PCP primarily modulated the levels of plasmanylphosphoethanolamine, lysophosphatidylcholine, and carnitine. Additionally, PCP reversed the expression of key genes involved in fatty acid uptake, intracellular lipid transport, and fatty acid synthesis, such as fatty acid binding protein 2, fatty acid transport protein 4, apolipoprotein B, apolipoprotein C3, fatty acid synthase, long-chain fatty acyl CoA synthetase 3, lipoprotein lipase and acyl-CoA thioesterases 12 (P < 0.05). These findings demonstrate that PCP mitigates PEDV-induced intestinal injury by modulating lipid metabolism and highlight its potential as a dietary supplement for enhancing anti-PEDV defenses and promoting intestinal health in piglets.","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"158 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144097536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Viral diseases have profoundly influenced the sustainable development of the swine farming industry. With the development of genomics technology, the combination of transcriptome, genetic variation, immune response, and QTL mapping data to illustrate the interactions between pathogen and host immune system, will be an effective tool for identification of disease resistance genes in pigs. The immune system of an organism is the source of disease resistance in livestock, consisting of various immune tissues, as well as the immune cells and cytokines they produced. However, comprehensive systematic studies on transcriptome of porcine immune tissues are still rare. Poly(I:C), as a viral mimic, is commonly used to study immune responses of the body during viral infections, and serves as a valuable tool for investigating immune mechanisms in swine. WGCNA analysis identified core immune genes across six immune tissues (bone marrow, jejunum, lymph node, PBMC, spleen, thymus) in Landrace pigs, which are also crucial for the development of PBMCs. The examination of the changes in the proportion of immune cells during three developmental stages (1-month-old, 4-month-old, 7-month-old) shows a shift from innate immunity to humoral immunity. By integrating different epigenetic genomics datasets, we identified several core immune genes and their causal variants, including IFI44, IFIT5, EIF2AK2 and others, which are closely related to immune development and response. Functional validation studies reveal that the IFI44 gene acts as a negative regulator of the antiviral response; its inhibition effect significantly reduced Poly(I:C)-induced cell necrosis, while enhancing apoptosis to combat viral infections. Our study elucidated the fundamental transcriptional program in porcine immune tissues and the immunodynamics underlying development of PBMCs, identifying many core immune genes, including IFI44, which plays a critical negative regulator role in the antiviral response, providing valuable insights for breeding programs aimed at enhancing pig disease resistance.
{"title":"The comprehensive transcriptomic atlas of porcine immune tissues and the peripheral blood mononuclear cell (PBMC) immune dynamics reveal core immune genes","authors":"Qingyao Zhao, Jiahao Wang, Fuping Ma, Quanzhen Chen, Huatao Liu, Jinyan Yang, Siqian Chen, Yongjie Tang, Siyuan Mi, Lulu Wang, Xini Wang, Guohong Liu, Kai Xing, Ying Yu, Chuduan Wang","doi":"10.1186/s40104-025-01184-y","DOIUrl":"https://doi.org/10.1186/s40104-025-01184-y","url":null,"abstract":"Viral diseases have profoundly influenced the sustainable development of the swine farming industry. With the development of genomics technology, the combination of transcriptome, genetic variation, immune response, and QTL mapping data to illustrate the interactions between pathogen and host immune system, will be an effective tool for identification of disease resistance genes in pigs. The immune system of an organism is the source of disease resistance in livestock, consisting of various immune tissues, as well as the immune cells and cytokines they produced. However, comprehensive systematic studies on transcriptome of porcine immune tissues are still rare. Poly(I:C), as a viral mimic, is commonly used to study immune responses of the body during viral infections, and serves as a valuable tool for investigating immune mechanisms in swine. WGCNA analysis identified core immune genes across six immune tissues (bone marrow, jejunum, lymph node, PBMC, spleen, thymus) in Landrace pigs, which are also crucial for the development of PBMCs. The examination of the changes in the proportion of immune cells during three developmental stages (1-month-old, 4-month-old, 7-month-old) shows a shift from innate immunity to humoral immunity. By integrating different epigenetic genomics datasets, we identified several core immune genes and their causal variants, including IFI44, IFIT5, EIF2AK2 and others, which are closely related to immune development and response. Functional validation studies reveal that the IFI44 gene acts as a negative regulator of the antiviral response; its inhibition effect significantly reduced Poly(I:C)-induced cell necrosis, while enhancing apoptosis to combat viral infections. Our study elucidated the fundamental transcriptional program in porcine immune tissues and the immunodynamics underlying development of PBMCs, identifying many core immune genes, including IFI44, which plays a critical negative regulator role in the antiviral response, providing valuable insights for breeding programs aimed at enhancing pig disease resistance.","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"128 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144088318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-15DOI: 10.1186/s40104-025-01205-w
Jessica P. Acosta, Charmaine D. Espinosa, Gemma González-Ortiz, Hans H. Stein
Exogenous xylanase can increase utilization of fiber and energy when included in diets for pigs, and xylo-oligosaccharides (XOS) may improve growth performance of pigs by modulating intestinal fermentation. However, it is unclear if a stimbiotic (i.e., a combination of xylanase and XOS) has superior effects compared with a xylanase alone, and there is a lack of data demonstrating if xylanase fed to lactating sows influences growth performance of weanling pigs. Therefore, two hypotheses were tested: 1) xylanase and stimbiotic improve growth performance, apparent total tract digestibility (ATTD) of gross energy (GE) and total dietary fiber (TDF), digestible energy (DE), and intestinal health of weanling pigs and 2) offspring of sows fed xylanase in lactation have greater growth performance after weaning than offspring of sows fed no xylanase during lactation. One hundred and twenty pigs were weaned from sows fed a diet without xylanase, and 120 pigs were weaned from sows fed a lactation diet containing 16,000 beechwood xylanase units per kg (initial weight: 5.81 ± 0.50 kg). Pigs were allotted to a 2 × 3 factorial with two sow groups (lactation diet without or with xylanase) and three dietary treatments (i.e., control, control plus xylanase, or control plus stimbiotic). There were no interactions between sow treatment and post-weaning pig treatment, and sow treatment did not impact post-weaning growth or ATTD of GE and TDF in weaned pigs. From d 15 to 28 post-weaning, the ADG, G:F, ATTD of GE and TDF, and concentration of DE were greater (P < 0.05) for pigs fed the diet with stimbiotic than if fed the xylanase diet or the control diet, and pigs fed the xylanase diet had greater (P < 0.05) ADG, G:F, ATTD of GE and TDF, and concentration of DE than pigs fed the control diet. From d 29 to 42 post-weaning, pigs fed the diets with xylanase or stimbiotic had greater (P < 0.05) ADG, ATTD of GE and TDF, and DE than pigs fed the control diet. Pigs fed xylanase or stimbiotic had greater ATTD of GE and TDF, greater DE, and greater overall ADG, G:F, and final body weight on d 42 post-weaning than pigs fed the control diet, but feeding sows xylanase in lactation did not influence post-weaning growth performance.
{"title":"Growth performance and total tract digestibility of nutrients for weanling pigs are improved by an exogenous xylanase and a stimbiotic regardless of maternal xylanase consumption","authors":"Jessica P. Acosta, Charmaine D. Espinosa, Gemma González-Ortiz, Hans H. Stein","doi":"10.1186/s40104-025-01205-w","DOIUrl":"https://doi.org/10.1186/s40104-025-01205-w","url":null,"abstract":"Exogenous xylanase can increase utilization of fiber and energy when included in diets for pigs, and xylo-oligosaccharides (XOS) may improve growth performance of pigs by modulating intestinal fermentation. However, it is unclear if a stimbiotic (i.e., a combination of xylanase and XOS) has superior effects compared with a xylanase alone, and there is a lack of data demonstrating if xylanase fed to lactating sows influences growth performance of weanling pigs. Therefore, two hypotheses were tested: 1) xylanase and stimbiotic improve growth performance, apparent total tract digestibility (ATTD) of gross energy (GE) and total dietary fiber (TDF), digestible energy (DE), and intestinal health of weanling pigs and 2) offspring of sows fed xylanase in lactation have greater growth performance after weaning than offspring of sows fed no xylanase during lactation. One hundred and twenty pigs were weaned from sows fed a diet without xylanase, and 120 pigs were weaned from sows fed a lactation diet containing 16,000 beechwood xylanase units per kg (initial weight: 5.81 ± 0.50 kg). Pigs were allotted to a 2 × 3 factorial with two sow groups (lactation diet without or with xylanase) and three dietary treatments (i.e., control, control plus xylanase, or control plus stimbiotic). There were no interactions between sow treatment and post-weaning pig treatment, and sow treatment did not impact post-weaning growth or ATTD of GE and TDF in weaned pigs. From d 15 to 28 post-weaning, the ADG, G:F, ATTD of GE and TDF, and concentration of DE were greater (P < 0.05) for pigs fed the diet with stimbiotic than if fed the xylanase diet or the control diet, and pigs fed the xylanase diet had greater (P < 0.05) ADG, G:F, ATTD of GE and TDF, and concentration of DE than pigs fed the control diet. From d 29 to 42 post-weaning, pigs fed the diets with xylanase or stimbiotic had greater (P < 0.05) ADG, ATTD of GE and TDF, and DE than pigs fed the control diet. Pigs fed xylanase or stimbiotic had greater ATTD of GE and TDF, greater DE, and greater overall ADG, G:F, and final body weight on d 42 post-weaning than pigs fed the control diet, but feeding sows xylanase in lactation did not influence post-weaning growth performance.","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"4 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143979583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Necrotic enteritis (NE) in broiler chickens leads to significant economic losses in poultry production. This study examined the inhibitory effects of usnic acid and tannic acid on coccidia, sporozoite, and Clostridium perfringens and assessed their influence on growth performance and intestinal health in NE-challenged broilers through in vitro and in vivo experiments. The in vitro experiment included 5 treatment groups: the negative control (NC), 2 μmol/L diclazuril (DZ), 30 μmol/L usnic acid (UA), 90 μmol/L tannic acid (TA), and 15 μmol/L usnic acid + 45 μmol/L tannic acid (UTA) groups. The in vivo experiment involved 320 broilers divided into four groups: PC (NE-challenged), SA (500 mg/kg salinomycin premix + NE-challenged), UA (300 mg/kg usnic acid + NE-challenged), and UTA (300 mg/kg usnic acid + 500 mg/kg tannic acid + NE-challenged) groups. In the in vitro study, the UA, TA, and UTA treatments significantly increased apoptosis in coccidian oocysts and sporozoites, lowered the mitochondrial membrane potential (P < 0.05), and disrupted the oocyst structure compared with those in the NC group. UA and TA had inhibitory effects on C. perfringens, with the strongest inhibition observed in the UTA group. The in vivo results demonstrated that the SA group presented significantly improved growth performance on d 13, 21, and 28 (P < 0.05), whereas the UA and UTA groups presented improvements on d 13 and 21 (P < 0.05). The SA, UA, and UTA treatments reduced the intestinal lesion scores by d 28 and the fecal coccidian oocyst counts from d 19 to 21 (P < 0.05). Compared with the PC group, the UA and UTA groups presented lower intestinal sIgA levels and CD8+ cell percentages (P < 0.05), with a trend toward a reduced CD3+ cell percentage (P = 0.069). The SA, UA, and UTA treatments significantly reduced the serum diamine oxidase activity, crypt depth, and platelet-derived growth factor levels in the intestinal mucosa while increasing the villus height to crypt depth ratio and number of goblet cells (P < 0.05). The UTA treatment also significantly increased the acetate and butyrate concentrations in the cecum (P < 0.05). With respect to the gut microbiota, significant changes in β diversity in the ileum and cecum were observed in the SA, UA, and UTA groups, indicating that the microbial community compositions differed among the groups. Romboutsia dominated the SA group, Bacillales dominated the UA group, and Lactobacillales and Lachnospirales dominated the UTA group in the ileal microbiota. In the cecal microbiota, Lactobacillus, Butyricicoccus, and Blautia abundances were significantly elevated in the UTA group (P < 0.05). Usnic acid and tannic acid induce apoptosis in coccidia and sporozoites by lowering the mitochondrial membrane potential. Both usnic acid alone and in combination with tannic acid alleviate NE-induced adverse effects in broilers by modulating intestinal immunity, altering the microbial composition, and improving intestinal barrier functio
{"title":"Usnic acid and tannic acid as inhibitors of coccidia and Clostridium perfringens: alleviating necrotic enteritis and improving intestinal health in broiler chickens","authors":"Huiping Xu, Minghao Yang, Jianyang Fu, Huiyuan Lv, Jiang Guo, Changji Lu, Zengpeng Lv, Yuming Guo","doi":"10.1186/s40104-025-01201-0","DOIUrl":"https://doi.org/10.1186/s40104-025-01201-0","url":null,"abstract":"Necrotic enteritis (NE) in broiler chickens leads to significant economic losses in poultry production. This study examined the inhibitory effects of usnic acid and tannic acid on coccidia, sporozoite, and Clostridium perfringens and assessed their influence on growth performance and intestinal health in NE-challenged broilers through in vitro and in vivo experiments. The in vitro experiment included 5 treatment groups: the negative control (NC), 2 μmol/L diclazuril (DZ), 30 μmol/L usnic acid (UA), 90 μmol/L tannic acid (TA), and 15 μmol/L usnic acid + 45 μmol/L tannic acid (UTA) groups. The in vivo experiment involved 320 broilers divided into four groups: PC (NE-challenged), SA (500 mg/kg salinomycin premix + NE-challenged), UA (300 mg/kg usnic acid + NE-challenged), and UTA (300 mg/kg usnic acid + 500 mg/kg tannic acid + NE-challenged) groups. In the in vitro study, the UA, TA, and UTA treatments significantly increased apoptosis in coccidian oocysts and sporozoites, lowered the mitochondrial membrane potential (P < 0.05), and disrupted the oocyst structure compared with those in the NC group. UA and TA had inhibitory effects on C. perfringens, with the strongest inhibition observed in the UTA group. The in vivo results demonstrated that the SA group presented significantly improved growth performance on d 13, 21, and 28 (P < 0.05), whereas the UA and UTA groups presented improvements on d 13 and 21 (P < 0.05). The SA, UA, and UTA treatments reduced the intestinal lesion scores by d 28 and the fecal coccidian oocyst counts from d 19 to 21 (P < 0.05). Compared with the PC group, the UA and UTA groups presented lower intestinal sIgA levels and CD8+ cell percentages (P < 0.05), with a trend toward a reduced CD3+ cell percentage (P = 0.069). The SA, UA, and UTA treatments significantly reduced the serum diamine oxidase activity, crypt depth, and platelet-derived growth factor levels in the intestinal mucosa while increasing the villus height to crypt depth ratio and number of goblet cells (P < 0.05). The UTA treatment also significantly increased the acetate and butyrate concentrations in the cecum (P < 0.05). With respect to the gut microbiota, significant changes in β diversity in the ileum and cecum were observed in the SA, UA, and UTA groups, indicating that the microbial community compositions differed among the groups. Romboutsia dominated the SA group, Bacillales dominated the UA group, and Lactobacillales and Lachnospirales dominated the UTA group in the ileal microbiota. In the cecal microbiota, Lactobacillus, Butyricicoccus, and Blautia abundances were significantly elevated in the UTA group (P < 0.05). Usnic acid and tannic acid induce apoptosis in coccidia and sporozoites by lowering the mitochondrial membrane potential. Both usnic acid alone and in combination with tannic acid alleviate NE-induced adverse effects in broilers by modulating intestinal immunity, altering the microbial composition, and improving intestinal barrier functio","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"26 1","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143933589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study was carried out to investigate the individual and combined contamination of aflatoxin B1 (AFB1), deoxynivalenol (DON), and zearalenone (ZEN) in feeds in China between 2021 and 2024. A total of 23,003 feed samples, including 17,489 feedstuff samples and 5,514 complete feed samples, were collected from different provinces of China for mycotoxin analysis. The analyzed mycotoxins displayed considerably high contamination in the feed samples, with the individual contamination of AFB1, DON, and ZEN were 20.0%–100%, 33.3%–100%, and 85.0%–100%, respectively. The average concentrations of AFB1, DON, and ZEN were 1.2–728.7 μg/kg, 106–8,634.8 μg/kg, and 18.1–3,341.6 μg/kg, respectively. Notably, the rates over China’s safety standards for AFB1, DON, and ZEN in raw ingredients were 9.7%, 2.7%, and 15.7%, respectively. Meanwhile, 3.5%, 1.1%, and 8.7% of analyzed complete feeds exceeded China’s safety standards for AFB1, DON, and ZEN, respectively. Moreover, the co-contamination rates of AFB1, DON, and ZEN in more than 70% of raw ingredients and 87.5% of complete feed products were 60.0%–100% and 61.5%–100%, respectively. This study reveals that the feeds in China have commonly been contaminated with AFB1, DON, and ZEN alone and their combination during the past four years. These findings highlight the significance of monitoring mycotoxin contaminant levels in domestic animal feed and the importance of carrying out feed administration and remediation strategies for mycotoxin control.
{"title":"Contamination of aflatoxin B1, deoxynivalenol and zearalenone in feeds in China from 2021 to 2024","authors":"Meng Liu, Zhiyuan Xia, Yu Zhang, Rengui Yang, Weicai Luo, Lijia Guo, Ying Liu, Dessalegn Lamesgen, Hua Sun, Jiangfeng He, Lvhui Sun","doi":"10.1186/s40104-025-01213-w","DOIUrl":"https://doi.org/10.1186/s40104-025-01213-w","url":null,"abstract":"This study was carried out to investigate the individual and combined contamination of aflatoxin B1 (AFB1), deoxynivalenol (DON), and zearalenone (ZEN) in feeds in China between 2021 and 2024. A total of 23,003 feed samples, including 17,489 feedstuff samples and 5,514 complete feed samples, were collected from different provinces of China for mycotoxin analysis. The analyzed mycotoxins displayed considerably high contamination in the feed samples, with the individual contamination of AFB1, DON, and ZEN were 20.0%–100%, 33.3%–100%, and 85.0%–100%, respectively. The average concentrations of AFB1, DON, and ZEN were 1.2–728.7 μg/kg, 106–8,634.8 μg/kg, and 18.1–3,341.6 μg/kg, respectively. Notably, the rates over China’s safety standards for AFB1, DON, and ZEN in raw ingredients were 9.7%, 2.7%, and 15.7%, respectively. Meanwhile, 3.5%, 1.1%, and 8.7% of analyzed complete feeds exceeded China’s safety standards for AFB1, DON, and ZEN, respectively. Moreover, the co-contamination rates of AFB1, DON, and ZEN in more than 70% of raw ingredients and 87.5% of complete feed products were 60.0%–100% and 61.5%–100%, respectively. This study reveals that the feeds in China have commonly been contaminated with AFB1, DON, and ZEN alone and their combination during the past four years. These findings highlight the significance of monitoring mycotoxin contaminant levels in domestic animal feed and the importance of carrying out feed administration and remediation strategies for mycotoxin control.","PeriodicalId":14928,"journal":{"name":"Journal of Animal Science and Biotechnology","volume":"35 1","pages":"66"},"PeriodicalIF":7.0,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143927012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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