Both genetic and environmental factors contribute to the development of Type 2 diabetes (T2D). Hyperinsulinemia is frequently observed in pregnant women with prediabetes, obesity, or gestational diabetes, and their offspring are at increased risk of developing T2D. However, there is a lack of longitudinal studies examining the long-term metabolic outcomes in offspring of hyperinsulinemic mothers. Moreover, the mechanistic link between maternal hyperinsulinemia and the programming of metabolic disease in offspring remains poorly understood. The prevailing view is that insulin does not cross the placenta to regulate fetal growth directly. Nonetheless, maternal insulin can function as a growth factor and anabolic hormone by binding to insulin receptors (IR) and insulin-like growth factor 1 receptors (IGF1R) on the placenta. This interaction can drive key placental functions, including nutrient transport to the fetus. As a result, maternal insulin may indirectly alter fetal development by modifying placental nutrient delivery to fetal metabolic tissues, potentially causing permanent changes that predispose offspring to T2D in adulthood. This seminar will examine the metabolic phenotypes of offspring born to hyperinsulinemic murine dams. It will also highlight findings on metabolic outcomes in offspring from otherwise normal pregnancies where insulin or IGF1 receptors were selectively deleted in the placenta during gestation. Finally, evidence from genetic mouse models demonstrating that both loss- and gain-of-function alterations in placental mTOR signaling can significantly influence susceptibility to type 2 diabetes will be presented. These effects appear to be mediated through changes in placental nutrient transport and subsequent altered nutrient sensing by fetal pancreatic beta cells in the offspring. Collectively, these observations support the concept that insulin/mTOR signaling in the placenta integrates maternal metabolic signals with fetal nutrient exposure, ultimately programming the metabolic health of the offspring.
{"title":"1 Unlocking metabolic fate: How placental insulin/IGF-1 and mTOR signaling shape offspring health","authors":"Emilyn U Alejandro*","doi":"10.1093/jas/skaf398.001","DOIUrl":"https://doi.org/10.1093/jas/skaf398.001","url":null,"abstract":"Both genetic and environmental factors contribute to the development of Type 2 diabetes (T2D). Hyperinsulinemia is frequently observed in pregnant women with prediabetes, obesity, or gestational diabetes, and their offspring are at increased risk of developing T2D. However, there is a lack of longitudinal studies examining the long-term metabolic outcomes in offspring of hyperinsulinemic mothers. Moreover, the mechanistic link between maternal hyperinsulinemia and the programming of metabolic disease in offspring remains poorly understood. The prevailing view is that insulin does not cross the placenta to regulate fetal growth directly. Nonetheless, maternal insulin can function as a growth factor and anabolic hormone by binding to insulin receptors (IR) and insulin-like growth factor 1 receptors (IGF1R) on the placenta. This interaction can drive key placental functions, including nutrient transport to the fetus. As a result, maternal insulin may indirectly alter fetal development by modifying placental nutrient delivery to fetal metabolic tissues, potentially causing permanent changes that predispose offspring to T2D in adulthood. This seminar will examine the metabolic phenotypes of offspring born to hyperinsulinemic murine dams. It will also highlight findings on metabolic outcomes in offspring from otherwise normal pregnancies where insulin or IGF1 receptors were selectively deleted in the placenta during gestation. Finally, evidence from genetic mouse models demonstrating that both loss- and gain-of-function alterations in placental mTOR signaling can significantly influence susceptibility to type 2 diabetes will be presented. These effects appear to be mediated through changes in placental nutrient transport and subsequent altered nutrient sensing by fetal pancreatic beta cells in the offspring. Collectively, these observations support the concept that insulin/mTOR signaling in the placenta integrates maternal metabolic signals with fetal nutrient exposure, ultimately programming the metabolic health of the offspring.","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"14 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wonders O Ogundare*, Linda M Beckett, Vishal Suresh, Theresa M Casey
: Introduction Greater colostrum intake increases milk production during lactation in mature sows and cows. Although, we know that the number of mammary epithelial cells drives milk production during lactation, the mechanism however, is not clearly understood. Thus, we aimed to evaluate how neonate colostrum and formula intake administered at varying levels, affect epithelial and stromal cell proliferation in the neonatal mammary gland. Methods We randomly assigned piglets to one of six treatment groups: bottle-fed pooled colostrum at 20% (COL 20, n = 10) or 10% (COL 10, n = 10) of body weight, milk replacer at 20% (MR 20, n = 10) or 10% (MR 10, n = 10) of body weight, suckled ad libitum on the sow (SOS, n = 9), or not fed (zero hour, ZH, n = 8). All groups were euthanized 24 hours postnatally except ZH which were euthanized immediately after birth. Mammary tissues were obtained, fixed, and stained with Ki67 to identify proliferating cells using ImageJ and analyzed statistically with SAS software. Results Colostrum significantly increased epithelial cell proliferation (P = 0.05) compared to formula. Higher feeding dose also significantly increased epithelial cells (P = 0.0003) and stroma cells (P = 0.0005) than lower dose. Notably, stroma proliferation was significantly higher (P < 0.05) in COL 20 compared to other groups including COL 10, MR 20, MR 10, SOS and ZH. Conclusion These findings indicate that sufficient colostrum intake promotes proliferation of epithelial and stromal cells in the neonatal mammary gland, suggesting a potential role in enhancing the gland’s future lactation capacity. (Funded by USDA 2110002200)
当前位置介绍大初乳摄入量可提高成熟母猪和奶牛的泌乳产奶量。虽然我们知道哺乳期间乳腺上皮细胞的数量驱动泌乳，但其机制尚不清楚。因此，我们旨在评估不同水平的新生儿初乳和配方奶摄入对新生儿乳腺上皮细胞和基质细胞增殖的影响。方法将仔猪随机分为6个处理组，分别为体重的20% （COL 20, n = 10）或10% （COL 10, n = 10）混合初乳瓶饲组、体重的20% （MR 20, n = 10）或10% （MR 10, n = 10）代奶组、母猪自由喂奶组（SOS, n = 9）和不喂奶组（零时，ZH, n = 8）。除ZH组在出生后立即实施安乐死外，其余各组均在出生后24 h实施安乐死。取乳腺组织固定，用Ki67染色，用ImageJ识别增殖细胞，用SAS软件进行统计学分析。结果与配方奶相比，初乳显著提高了上皮细胞的增殖能力（P = 0.05）。饲喂剂量高也显著增加了上皮细胞（P = 0.0003）和基质细胞（P = 0.0005）。与COL 10、MR 20、MR 10、SOS和ZH组相比，COL 20组间质增殖显著增加（P < 0.05）。结论充足的初乳摄入可促进新生儿乳腺上皮细胞和基质细胞的增殖，可能对提高乳腺泌乳能力有潜在作用。（美国农业部资助2110002200）
{"title":"39 Colostrum intake promotes mammary cell proliferation in neonatal piglets","authors":"Wonders O Ogundare*, Linda M Beckett, Vishal Suresh, Theresa M Casey","doi":"10.1093/jas/skaf398.032","DOIUrl":"https://doi.org/10.1093/jas/skaf398.032","url":null,"abstract":": Introduction Greater colostrum intake increases milk production during lactation in mature sows and cows. Although, we know that the number of mammary epithelial cells drives milk production during lactation, the mechanism however, is not clearly understood. Thus, we aimed to evaluate how neonate colostrum and formula intake administered at varying levels, affect epithelial and stromal cell proliferation in the neonatal mammary gland. Methods We randomly assigned piglets to one of six treatment groups: bottle-fed pooled colostrum at 20% (COL 20, n = 10) or 10% (COL 10, n = 10) of body weight, milk replacer at 20% (MR 20, n = 10) or 10% (MR 10, n = 10) of body weight, suckled ad libitum on the sow (SOS, n = 9), or not fed (zero hour, ZH, n = 8). All groups were euthanized 24 hours postnatally except ZH which were euthanized immediately after birth. Mammary tissues were obtained, fixed, and stained with Ki67 to identify proliferating cells using ImageJ and analyzed statistically with SAS software. Results Colostrum significantly increased epithelial cell proliferation (P = 0.05) compared to formula. Higher feeding dose also significantly increased epithelial cells (P = 0.0003) and stroma cells (P = 0.0005) than lower dose. Notably, stroma proliferation was significantly higher (P &lt; 0.05) in COL 20 compared to other groups including COL 10, MR 20, MR 10, SOS and ZH. Conclusion These findings indicate that sufficient colostrum intake promotes proliferation of epithelial and stromal cells in the neonatal mammary gland, suggesting a potential role in enhancing the gland’s future lactation capacity. (Funded by USDA 2110002200)","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"26 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Upasna Sharma, Simeiyun Liu, Andrew D Holmes, Sol Katzman
: Introduction Transmission of parental traits to offspring is the most fundamental process for the perpetuation of life and is vital for the process of evolution. Although there is mounting evidence from worms to humans that parental environment can influence phenotypes in offspring, the mechanism of such intergenerational inheritance remains deeply mysterious. Our previous studies implicated sperm small RNAs in intergenerational epigenetic inheritance of paternal environmental effects. We found that cleavage products of tRNAs, known as tRNA-derived small RNAs or tRNA fragments (tRF), are highly abundant in mature sperm and environmental conditions alter their levels. A 5’ fragment of tRNA-Valine-CAC-2 (tRFValCAC) as one of the most abundant tRNA fragments in mature mouse sperm. tRFValCAC is enriched in sperm during epididymal maturation, and extracellular vesicles (EVs) secreted by epididymal epithelial cells can deliver tRFValCAC to sperm. Objective Here, we investigated how tRFValCAC is delivered to sperm and what functions it carries out upon deposition in the embryo at fertilization to elucidate the mechanism of sperm tRF-mediated intergenerational inheritance. Methods We used a combination of RNA-sequencing, assisted reproduction, and embryo microinjections to study the dynamics and functions of tRFValCAC. Results Our studies demonstrate that heterogeneous nuclear ribonucleoprotein A/B (hnRNPAB) binds tRFValCAC in the epididymis and regulates its abundance in EVs, thereby modulating its levels in sperm. Inhibition of tRFValCAC in preimplantation embryos alters transcript abundance of genes involved in RNA splicing and mRNA processing, dysregulates alternative splicing, and delays preimplantation development. Conclusions Our work revealed that a sperm-enriched tRF regulates early embryonic gene expression and the pace of preimplantation development, providing a potential mechanism of sperm small RNAs-mediated intergenerational inheritance. (Supported by NIH 1DP2AG066622-01, Searle Scholars Program 20-SSP-109)
{"title":"51 Intergenerational transmission of paternal environmental effects via sperm small RNAs in mice","authors":"Upasna Sharma, Simeiyun Liu, Andrew D Holmes, Sol Katzman","doi":"10.1093/jas/skaf398.044","DOIUrl":"https://doi.org/10.1093/jas/skaf398.044","url":null,"abstract":": Introduction Transmission of parental traits to offspring is the most fundamental process for the perpetuation of life and is vital for the process of evolution. Although there is mounting evidence from worms to humans that parental environment can influence phenotypes in offspring, the mechanism of such intergenerational inheritance remains deeply mysterious. Our previous studies implicated sperm small RNAs in intergenerational epigenetic inheritance of paternal environmental effects. We found that cleavage products of tRNAs, known as tRNA-derived small RNAs or tRNA fragments (tRF), are highly abundant in mature sperm and environmental conditions alter their levels. A 5’ fragment of tRNA-Valine-CAC-2 (tRFValCAC) as one of the most abundant tRNA fragments in mature mouse sperm. tRFValCAC is enriched in sperm during epididymal maturation, and extracellular vesicles (EVs) secreted by epididymal epithelial cells can deliver tRFValCAC to sperm. Objective Here, we investigated how tRFValCAC is delivered to sperm and what functions it carries out upon deposition in the embryo at fertilization to elucidate the mechanism of sperm tRF-mediated intergenerational inheritance. Methods We used a combination of RNA-sequencing, assisted reproduction, and embryo microinjections to study the dynamics and functions of tRFValCAC. Results Our studies demonstrate that heterogeneous nuclear ribonucleoprotein A/B (hnRNPAB) binds tRFValCAC in the epididymis and regulates its abundance in EVs, thereby modulating its levels in sperm. Inhibition of tRFValCAC in preimplantation embryos alters transcript abundance of genes involved in RNA splicing and mRNA processing, dysregulates alternative splicing, and delays preimplantation development. Conclusions Our work revealed that a sperm-enriched tRF regulates early embryonic gene expression and the pace of preimplantation development, providing a potential mechanism of sperm small RNAs-mediated intergenerational inheritance. (Supported by NIH 1DP2AG066622-01, Searle Scholars Program 20-SSP-109)","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"5 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rebecca L Wilson, Baylea N Davenport, Alyssa Williams, Helen N Jones
: Introduction Chronic maternal stress during pregnancy can have lasting impacts on both maternal health and fetal development, yet the underlying maternal physiological adaptations remain poorly understood. Objective Investigate increased chronic maternal stress, through food insecurity, on maternal physiological parameters at two gestational (GD) timepoints. Methods Female Hartley guinea pigs were fed either an ad libitum (Control) or a restricted diet (MNR) from 4 weeks prior to pregnancy until sacrifice. MNR dams were provided food at 1000h daily which was generally consumed within 4-6h leaving a period of ∼18-20h without food. Dams were euthanized at GD35-38 (mid-pregnancy: Control n = 7, MNR n = 6) or GD57-63 (near-term: Control n = 6, MNR n = 6) and weights recorded. Maternal plasma was analyzed for various metabolic markers. Statistical significance was determined using generalized linear modelling. Results While maternal weight (minus fetal and maternal-fetal interface weight) and maternal-fetal interface weight increased between timepoints (P < 0.001, both respectively), they remained similar between MNR and Control. MNR maintained litter size but had reduced fetal weight at both mid-pregnancy and near-term (13-19%; P = 0.014). Between mid-pregnancy and near-term, maternal cortisol (P = 0.041), glucose (P = 0.001), and calcium (P = 0.004) increased, while progesterone (P < 0.001), lactate (P < 0.001), and sodium (P = 0.021) decreased. MNR dams showed elevated cortisol (53-85%, P = 0.016), progesterone (13-35%, P = 0.036), and BUN (8-38%, P = 0.012) and reduced cholesterol (24-32%, P = 0.019) compared to Controls at both gestational timepoints. Conclusion Chronic maternal stress from before pregnancy leads to a metabolic state characterized by elevated cortisol and altered energy utilization (increased BUN, decreased cholesterol), suggesting metabolic adaptations to prioritize maternal survival but with compromised fetal growth. (Supported by NIH K99HD109458 & R01HD090657)
{"title":"62 Investigating maternal physiological responses to pregnancy in a guinea pig model of increased maternal stress","authors":"Rebecca L Wilson, Baylea N Davenport, Alyssa Williams, Helen N Jones","doi":"10.1093/jas/skaf398.053","DOIUrl":"https://doi.org/10.1093/jas/skaf398.053","url":null,"abstract":": Introduction Chronic maternal stress during pregnancy can have lasting impacts on both maternal health and fetal development, yet the underlying maternal physiological adaptations remain poorly understood. Objective Investigate increased chronic maternal stress, through food insecurity, on maternal physiological parameters at two gestational (GD) timepoints. Methods Female Hartley guinea pigs were fed either an ad libitum (Control) or a restricted diet (MNR) from 4 weeks prior to pregnancy until sacrifice. MNR dams were provided food at 1000h daily which was generally consumed within 4-6h leaving a period of ∼18-20h without food. Dams were euthanized at GD35-38 (mid-pregnancy: Control n = 7, MNR n = 6) or GD57-63 (near-term: Control n = 6, MNR n = 6) and weights recorded. Maternal plasma was analyzed for various metabolic markers. Statistical significance was determined using generalized linear modelling. Results While maternal weight (minus fetal and maternal-fetal interface weight) and maternal-fetal interface weight increased between timepoints (P &lt; 0.001, both respectively), they remained similar between MNR and Control. MNR maintained litter size but had reduced fetal weight at both mid-pregnancy and near-term (13-19%; P = 0.014). Between mid-pregnancy and near-term, maternal cortisol (P = 0.041), glucose (P = 0.001), and calcium (P = 0.004) increased, while progesterone (P &lt; 0.001), lactate (P &lt; 0.001), and sodium (P = 0.021) decreased. MNR dams showed elevated cortisol (53-85%, P = 0.016), progesterone (13-35%, P = 0.036), and BUN (8-38%, P = 0.012) and reduced cholesterol (24-32%, P = 0.019) compared to Controls at both gestational timepoints. Conclusion Chronic maternal stress from before pregnancy leads to a metabolic state characterized by elevated cortisol and altered energy utilization (increased BUN, decreased cholesterol), suggesting metabolic adaptations to prioritize maternal survival but with compromised fetal growth. (Supported by NIH K99HD109458 & R01HD090657)","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"38 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lyle G Best, C Azure, H Davis, L Jeanotte, S LaRocque, S Poitra, J Poitra, S Standish, T J Parisien, K Morin
: Introduction Maternal variants including C-Reactive Protein, CRP rs1205 have previously been associated with risk of pre-eclampsia (PE). These findings were replicated in two non-American Indian populations. The rs1205 T allele is associated with reduced serum levels of CRP. Our objective was to determine if the fetal rs1205 genotype contributed to maternal risk of PE independent of maternal rs1205 genotype. Methods Only offspring of both case and control mothers heterozygous for rs1205 were enrolled, thus controlling for maternal genetic influence at this locus. Offspring were then genotyped for rs1205 by TaqMan assay. Association was assessed by chi-square and multivariate logistic regression. Results Offspring of 10 of 45 normal pregnancies and 11 of 24 PE pregnancies exhibited the rs1205 C allele recessive genotype (Pearson chi square p = 0.042). Multivariate logistic regression analysis adjusted for maternal age, nulliparity and BMI demonstrates an odds ratio of 3.603, p = 0.043, 95% CI 1.042-12.457 for the fetal, C recessive genotype. Discussion Among 69 women, heterozygous for the rs1205 allele, both chi-square and multivariate adjusted logistic analysis shows significant association of PE among pregnancies with fetal rs1205 C recessive genotypes. This is consistent with previous findings of reduced risk associated with this maternal genotype, and with a pathophysiologic model wherein increased placental CRP expression increases risk of PE. (Supported by NIGMS P20GM103442)
{"title":"4 Fetal c-reactive protein rs1205 genotype is associated with maternal pre-eclampsia","authors":"Lyle G Best, C Azure, H Davis, L Jeanotte, S LaRocque, S Poitra, J Poitra, S Standish, T J Parisien, K Morin","doi":"10.1093/jas/skaf398.004","DOIUrl":"https://doi.org/10.1093/jas/skaf398.004","url":null,"abstract":": Introduction Maternal variants including C-Reactive Protein, CRP rs1205 have previously been associated with risk of pre-eclampsia (PE). These findings were replicated in two non-American Indian populations. The rs1205 T allele is associated with reduced serum levels of CRP. Our objective was to determine if the fetal rs1205 genotype contributed to maternal risk of PE independent of maternal rs1205 genotype. Methods Only offspring of both case and control mothers heterozygous for rs1205 were enrolled, thus controlling for maternal genetic influence at this locus. Offspring were then genotyped for rs1205 by TaqMan assay. Association was assessed by chi-square and multivariate logistic regression. Results Offspring of 10 of 45 normal pregnancies and 11 of 24 PE pregnancies exhibited the rs1205 C allele recessive genotype (Pearson chi square p = 0.042). Multivariate logistic regression analysis adjusted for maternal age, nulliparity and BMI demonstrates an odds ratio of 3.603, p = 0.043, 95% CI 1.042-12.457 for the fetal, C recessive genotype. Discussion Among 69 women, heterozygous for the rs1205 allele, both chi-square and multivariate adjusted logistic analysis shows significant association of PE among pregnancies with fetal rs1205 C recessive genotypes. This is consistent with previous findings of reduced risk associated with this maternal genotype, and with a pathophysiologic model wherein increased placental CRP expression increases risk of PE. (Supported by NIGMS P20GM103442)","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"23 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Camila Arroyo-Salvo, Luis Aguila-Paredes, Silvina Perez-Martinez, Rafael Fissore, Pablo Visconti, Maria G Gervasi
: Introduction Despite advances in Assisted Reproductive Technologies (ART), obtaining developmentally competent embryos remains a major challenge. We previously demonstrated that modulating sperm metabolism through Sperm Energy Restriction and Recovery (SER) enhances sperm function and improves fertilization and embryo development rates following in vitro fertilization in mice. Objective To optimize SER in bovine and equine species. Methods Cryopreserved sperm were incubated in either complete medium (control) or nutrient-deficient medium (ST), followed by recovery with metabolic substrates (SER). Sperm function was assessed by evaluating motility and capacitation-associated markers, including phosphorylation of PKA substrates (pPKAs), tyrosine phosphorylation (pY), and intracellular Ca2+ levels. Control and SER bovine sperm were then used for intracytoplasmic sperm injection (ICSI). Results SER improved sperm motility in both species, while no differences were observed in pPKAs or pY levels in either species. ST equine sperm showed higher intracellular Ca2+ levels and a greater percentage of live, acrosome-reacted cells compared to controls (14.4% vs. 6.6%, p < 0.05). In bovines, ICSI using SER sperm yielded higher 2-cell embryo rates than controls (50% vs. 16%, p < 0.05), and 17% of these embryos developed to the blastocyst stage, whereas none did in the control. SER also enhanced egg activation post-ICSI, with more oocytes displaying greater than 3 Ca2+ peaks (40% vs. 10%, p < 0.05). Conclusion SER improves sperm function in both bovine and equine species and enhances egg activation after bovine ICSI. These findings suggest that targeting sperm metabolism may increase the efficiency of in vitro embryo production across species. (Supported by USDA 2022-67016-41939)
尽管辅助生殖技术（ART）取得了进步，但获得发育正常的胚胎仍然是一个重大挑战。我们之前已经证明，通过精子能量限制和恢复（SER）调节精子代谢可以增强精子功能，提高小鼠体外受精后的受精和胚胎发育率。目的优化牛和马的SER。方法冷冻精子在完全培养基（对照组）和营养缺乏培养基（ST）中孵育，然后用代谢底物（SER）恢复。精子功能通过评估运动和容量相关标记来评估，包括PKA底物磷酸化（pPKAs）、酪氨酸磷酸化（pY）和细胞内Ca2+水平。对照和SER牛精子用于胞浆内单精子注射（ICSI）。结果SER改善了两种物种的精子活力，而pPKAs和pY水平在两种物种中均无差异。与对照组相比，ST马精子显示出更高的细胞内Ca2+水平和更高的活细胞百分比，顶体反应细胞（14.4%比6.6%,p < 0.05）。在牛中，使用SER精子的ICSI产生了比对照组更高的2细胞胚胎率（50%对16%，p < 0.05），这些胚胎中有17%发育到囊胚期，而对照组没有。SER还增强了icsi后卵子的活化，更多的卵母细胞显示大于3个Ca2+峰（40% vs. 10%, p < 0.05）。结论SER改善了牛和马的精子功能，并增强了牛ICSI后卵子的活化。这些发现表明，靶向精子代谢可能会提高跨物种体外胚胎产生的效率。（美国农业部资助：2022-67016-41939）
{"title":"18 Metabolic manipulation of spermatozoa improves sperm function with implications for Assisted Reproductive Technologies","authors":"Camila Arroyo-Salvo, Luis Aguila-Paredes, Silvina Perez-Martinez, Rafael Fissore, Pablo Visconti, Maria G Gervasi","doi":"10.1093/jas/skaf398.014","DOIUrl":"https://doi.org/10.1093/jas/skaf398.014","url":null,"abstract":": Introduction Despite advances in Assisted Reproductive Technologies (ART), obtaining developmentally competent embryos remains a major challenge. We previously demonstrated that modulating sperm metabolism through Sperm Energy Restriction and Recovery (SER) enhances sperm function and improves fertilization and embryo development rates following in vitro fertilization in mice. Objective To optimize SER in bovine and equine species. Methods Cryopreserved sperm were incubated in either complete medium (control) or nutrient-deficient medium (ST), followed by recovery with metabolic substrates (SER). Sperm function was assessed by evaluating motility and capacitation-associated markers, including phosphorylation of PKA substrates (pPKAs), tyrosine phosphorylation (pY), and intracellular Ca2+ levels. Control and SER bovine sperm were then used for intracytoplasmic sperm injection (ICSI). Results SER improved sperm motility in both species, while no differences were observed in pPKAs or pY levels in either species. ST equine sperm showed higher intracellular Ca2+ levels and a greater percentage of live, acrosome-reacted cells compared to controls (14.4% vs. 6.6%, p &lt; 0.05). In bovines, ICSI using SER sperm yielded higher 2-cell embryo rates than controls (50% vs. 16%, p &lt; 0.05), and 17% of these embryos developed to the blastocyst stage, whereas none did in the control. SER also enhanced egg activation post-ICSI, with more oocytes displaying greater than 3 Ca2+ peaks (40% vs. 10%, p &lt; 0.05). Conclusion SER improves sperm function in both bovine and equine species and enhances egg activation after bovine ICSI. These findings suggest that targeting sperm metabolism may increase the efficiency of in vitro embryo production across species. (Supported by USDA 2022-67016-41939)","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"29 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emerging research reveals that epigenetic mechanisms of paternal inheritance are a significant driver of adverse developmental outcomes, including those associated with fetal alcohol spectrum disorders (FASD). In recognition of the urgent need to understand the combined effects of maternal and paternal alcohol consumption, our laboratory established a preclinical multiplex mouse model to compare alcohol-induced developmental defects in offspring resulting from maternal, paternal, and dual parental exposures. Our findings reveal that both maternal and paternal alcohol consumption independently impair placental development and alter craniofacial patterning in a dose-dependent manner. Strikingly, in the male offspring, we observed an interaction between maternal and paternal alcohol use, with adverse developmental outcomes in the dual-parental offspring exceeding those induced by either maternal or paternal alcohol use alone. Our ongoing experiments reveal that parental alcohol exposure heritably disrupts offspring mitochondrial complex I activity in the placenta and fetal brain. These deficits persist into adulthood, resulting in elevated oxidative stress, chronic inflammation, and premature cellular aging in the brain and liver. Our results underscore that chronic toxicant-induced mitochondrial stress, particularly in males, programs enduring bioenergetic dysfunction that elevates the risk of birth defects and long-term disease. These findings emphasize the critical importance of considering both maternal and paternal health in preconception planning.
{"title":"19 Paternal drinking and the epigenetic influences on mitochondrial function, placental dysfunction, and structural birth defects","authors":"Michael C Golding*","doi":"10.1093/jas/skaf398.015","DOIUrl":"https://doi.org/10.1093/jas/skaf398.015","url":null,"abstract":"Emerging research reveals that epigenetic mechanisms of paternal inheritance are a significant driver of adverse developmental outcomes, including those associated with fetal alcohol spectrum disorders (FASD). In recognition of the urgent need to understand the combined effects of maternal and paternal alcohol consumption, our laboratory established a preclinical multiplex mouse model to compare alcohol-induced developmental defects in offspring resulting from maternal, paternal, and dual parental exposures. Our findings reveal that both maternal and paternal alcohol consumption independently impair placental development and alter craniofacial patterning in a dose-dependent manner. Strikingly, in the male offspring, we observed an interaction between maternal and paternal alcohol use, with adverse developmental outcomes in the dual-parental offspring exceeding those induced by either maternal or paternal alcohol use alone. Our ongoing experiments reveal that parental alcohol exposure heritably disrupts offspring mitochondrial complex I activity in the placenta and fetal brain. These deficits persist into adulthood, resulting in elevated oxidative stress, chronic inflammation, and premature cellular aging in the brain and liver. Our results underscore that chronic toxicant-induced mitochondrial stress, particularly in males, programs enduring bioenergetic dysfunction that elevates the risk of birth defects and long-term disease. These findings emphasize the critical importance of considering both maternal and paternal health in preconception planning.","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"23 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nicole Moran, Rebecka Sadler, Umesh K Shandilya, Niel A Karrow
: Introduction Global pre-weaning lamb mortalities have remained above 10%, a detriment to farm profits. Selenium (Se) is a trace mineral vital to several functions in sheep. Se supplementation during late pregnancy and lactation, particularly organic Se supplementation, may produce more robust lambs. Objective To determine how differences in maternal Se supplementation impact lamb health within 10 days postpartum (ppd 10). Methods Ewes (n = 110) were enrolled in a feeding trial from gestation day (gd) 110 to ppd 10, and supplemented with either no Se, 0.3 mg/day inorganic Se, or 0.3 or 0.6 mg/day organic Se. Lambs only received Se via maternal nursing. Lamb serum was collected on ppd 0, 2, and 10 to assess maternal transfer of Se, and muscle samples were collected on ppd 10 to assess lamb Se stores. Serum glutathione peroxidase (GPx) levels, thyroid hormone triiodothyronine (T3) levels, and a complete ovine 23-parameter biochemistry panel were assessed on ppds 0 and 10. Results Maternal organic Se supplementation significantly increased Se levels in lamb serum (P < 0.0001) and muscle (P < 0.0001) as compared to other treatments. Organic Se supplementation significantly increased GPx activity at birth (P > 0.001), but T3 levels were not affected. From the biochemical panel, serum levels of non-esterified fatty acid, potassium, chloride, albumin, total bilirubin, creatine kinase, aspartate aminotransferase, and glutamate dehydrogenase showed significant treatment differences. Conclusions Organic Se supplementation to ewes during late gestation and lactation improved lamb Se status and antioxidant capacity at birth. Other serum biochemistry parameters were only marginally affected by Se treatment. (Supported by NSERC 401814)
{"title":"36 Impact of feeding different selenium (Se) sources to pregnant and lactating ewes on lamb Se enrichment and serum biochemistry profiles","authors":"Nicole Moran, Rebecka Sadler, Umesh K Shandilya, Niel A Karrow","doi":"10.1093/jas/skaf398.030","DOIUrl":"https://doi.org/10.1093/jas/skaf398.030","url":null,"abstract":": Introduction Global pre-weaning lamb mortalities have remained above 10%, a detriment to farm profits. Selenium (Se) is a trace mineral vital to several functions in sheep. Se supplementation during late pregnancy and lactation, particularly organic Se supplementation, may produce more robust lambs. Objective To determine how differences in maternal Se supplementation impact lamb health within 10 days postpartum (ppd 10). Methods Ewes (n = 110) were enrolled in a feeding trial from gestation day (gd) 110 to ppd 10, and supplemented with either no Se, 0.3 mg/day inorganic Se, or 0.3 or 0.6 mg/day organic Se. Lambs only received Se via maternal nursing. Lamb serum was collected on ppd 0, 2, and 10 to assess maternal transfer of Se, and muscle samples were collected on ppd 10 to assess lamb Se stores. Serum glutathione peroxidase (GPx) levels, thyroid hormone triiodothyronine (T3) levels, and a complete ovine 23-parameter biochemistry panel were assessed on ppds 0 and 10. Results Maternal organic Se supplementation significantly increased Se levels in lamb serum (P &lt; 0.0001) and muscle (P &lt; 0.0001) as compared to other treatments. Organic Se supplementation significantly increased GPx activity at birth (P &gt; 0.001), but T3 levels were not affected. From the biochemical panel, serum levels of non-esterified fatty acid, potassium, chloride, albumin, total bilirubin, creatine kinase, aspartate aminotransferase, and glutamate dehydrogenase showed significant treatment differences. Conclusions Organic Se supplementation to ewes during late gestation and lactation improved lamb Se status and antioxidant capacity at birth. Other serum biochemistry parameters were only marginally affected by Se treatment. (Supported by NSERC 401814)","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"9 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jennifer L Hurlbert, Francisco B Scremini, Roberta B Dahlen, Ana Clara B Menezes, Kendall C Swanson, Kevin K Sedivec, Carl R Dahlen
: Introduction Vitamins and minerals support nutrient metabolism, immunity, reproduction, and fetal development in beef cattle, with prenatal supplementation potentially impacting offspring growth, health, and tissue development. Objective Objectives were to assess intestinal vascularization and proliferation in neonatal calves in response to prenatal vitamin and mineral supplementation. Angus heifers (n = 14) were bred using female-sexed semen, stratified by body weight, and randomly assigned to receive either a basal diet (CON; n = 7) or the basal diet plus a vitamin and mineral supplement (VTM; n = 7) from day 60 before breeding to calving. Calves were hand reared and euthanized at 30 h of age for duodenum, jejunum, and ileum collection. Tissues were stained with CD31/CD34 and Ki-67 to assess intestinal vascularity and proliferation. Images were analyzed for capillary area density (CAD), capillary number density (CND), Ki-67 positivity ratio (KPR), and spatial cell density (SCD) within villi, crypts, and total capillary area. Results Maternal supplementation increased (P ≤ 0.05) CAD in duodenal crypts and in villi and total capillary area of the jejunum and duodenum, and tended (P ≤ 0.06) to increase CAD in jejunal crypts and villi of VTM calves. However, SCD was greater (P ≤ 0.03) in duodenal villi and total duodenal capillary area, and KPR tended (P = 0.08) to be greater in jejunal crypts of CON calves. Conclusion Maternal supplementation during pregnancy enhanced intestinal vascularity in neonates, while greater SCD and KPR in CON calves may reflect compensatory adaptations to nutrient restriction.
维生素和矿物质支持肉牛的营养代谢、免疫、繁殖和胎儿发育，产前补充维生素和矿物质可能会影响后代的生长、健康和组织发育。目的研究产前维生素和矿物质补充对新生牛犊肠道血管形成和增殖的影响。选用雌性安格斯小母牛（n = 14），按体重分层，从繁殖前第60天至产犊，随机分配饲喂基础饲粮（CON, n = 7）或基础饲粮加维生素和矿物质补充剂（VTM, n = 7）。犊牛人工饲养，30 h时安乐死，收集十二指肠、空肠和回肠。组织用CD31/CD34和Ki-67染色评估肠血管和增殖。分析绒毛、隐窝和总毛细面积的毛细面积密度（CAD）、毛细数密度（CND）、Ki-67阳性比（KPR）和空间细胞密度（SCD）。结果母体添加使VTM犊牛十二指肠隐窝、空肠和十二指肠绒毛及总毛细血管面积的CAD增加（P≤0.05），并有增加VTM犊牛空肠隐窝和绒毛CAD的趋势（P≤0.06）。CON犊牛十二指肠绒毛和十二指肠总毛细血管面积的SCD较大（P≤0.03），空肠隐窝的KPR较大（P = 0.08）。结论孕期母体补充营养可增强新生儿肠道血管，而CON犊牛较高的SCD和KPR可能反映了对营养限制的代偿性适应。
{"title":"23 Trainee Award: Vitamin and mineral supplementation in beef heifers and the impacts on intestinal vascularity and proliferation in neonatal calves at 30 hours of age","authors":"Jennifer L Hurlbert, Francisco B Scremini, Roberta B Dahlen, Ana Clara B Menezes, Kendall C Swanson, Kevin K Sedivec, Carl R Dahlen","doi":"10.1093/jas/skaf398.019","DOIUrl":"https://doi.org/10.1093/jas/skaf398.019","url":null,"abstract":": Introduction Vitamins and minerals support nutrient metabolism, immunity, reproduction, and fetal development in beef cattle, with prenatal supplementation potentially impacting offspring growth, health, and tissue development. Objective Objectives were to assess intestinal vascularization and proliferation in neonatal calves in response to prenatal vitamin and mineral supplementation. Angus heifers (n = 14) were bred using female-sexed semen, stratified by body weight, and randomly assigned to receive either a basal diet (CON; n = 7) or the basal diet plus a vitamin and mineral supplement (VTM; n = 7) from day 60 before breeding to calving. Calves were hand reared and euthanized at 30 h of age for duodenum, jejunum, and ileum collection. Tissues were stained with CD31/CD34 and Ki-67 to assess intestinal vascularity and proliferation. Images were analyzed for capillary area density (CAD), capillary number density (CND), Ki-67 positivity ratio (KPR), and spatial cell density (SCD) within villi, crypts, and total capillary area. Results Maternal supplementation increased (P ≤ 0.05) CAD in duodenal crypts and in villi and total capillary area of the jejunum and duodenum, and tended (P ≤ 0.06) to increase CAD in jejunal crypts and villi of VTM calves. However, SCD was greater (P ≤ 0.03) in duodenal villi and total duodenal capillary area, and KPR tended (P = 0.08) to be greater in jejunal crypts of CON calves. Conclusion Maternal supplementation during pregnancy enhanced intestinal vascularity in neonates, while greater SCD and KPR in CON calves may reflect compensatory adaptations to nutrient restriction.","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"70 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hannah C Cunningham-Hollinger, Kelly L Woodruff, Gwendolynn L Hummel, Ryan M Knuth
: Introduction Despite ruminant livestock being born with a non-functional rumen, the early rumen microbiome can have lasting impacts on animal performance. Identifying key sources of colonization of this early rumen microbiome are imperative to harnessing the programming potential of this microbial niche to improve long term health and performance. Objectives The objective of this collective work is to identify maternal influences on colonization of the neonatal gut microbiome. We hypothesize that environmental, genetic, and pathogenic disruptions during gestation and early lactation will have lasting impacts on the offspring, partially via impacts on the gut microbiome. Methods Research projects involving beef cattle and range sheep have been employed to characterize maternal influence on the neonatal gut microbiome. In all studies, microbial characterizations have been completed utilizing amplicon sequencing of the 16S rRNA and analysis via QIIME2. Alpha- and beta-diversity metrics in additional to differences in relative abundance of taxa have been evaluated. Results It is apparent across all studies that the neonate does in fact have a unique microbiome immediately after birth. Data also indicates that maternal factors impact offspring rumen microbiome including nutritional status of the dam during gestation and early lactation and mammary health. Furthermore, these studies have revealed several potential sources of colonization of the neonatal gut. Conclusion These data from several projects highlight opportunities for programming of the rumen microbiome to enhance long term health and performance.
{"title":"22 The pre-ruminant microbiome: why do we care and where does it come from?","authors":"Hannah C Cunningham-Hollinger, Kelly L Woodruff, Gwendolynn L Hummel, Ryan M Knuth","doi":"10.1093/jas/skaf398.018","DOIUrl":"https://doi.org/10.1093/jas/skaf398.018","url":null,"abstract":": Introduction Despite ruminant livestock being born with a non-functional rumen, the early rumen microbiome can have lasting impacts on animal performance. Identifying key sources of colonization of this early rumen microbiome are imperative to harnessing the programming potential of this microbial niche to improve long term health and performance. Objectives The objective of this collective work is to identify maternal influences on colonization of the neonatal gut microbiome. We hypothesize that environmental, genetic, and pathogenic disruptions during gestation and early lactation will have lasting impacts on the offspring, partially via impacts on the gut microbiome. Methods Research projects involving beef cattle and range sheep have been employed to characterize maternal influence on the neonatal gut microbiome. In all studies, microbial characterizations have been completed utilizing amplicon sequencing of the 16S rRNA and analysis via QIIME2. Alpha- and beta-diversity metrics in additional to differences in relative abundance of taxa have been evaluated. Results It is apparent across all studies that the neonate does in fact have a unique microbiome immediately after birth. Data also indicates that maternal factors impact offspring rumen microbiome including nutritional status of the dam during gestation and early lactation and mammary health. Furthermore, these studies have revealed several potential sources of colonization of the neonatal gut. Conclusion These data from several projects highlight opportunities for programming of the rumen microbiome to enhance long term health and performance.","PeriodicalId":14895,"journal":{"name":"Journal of animal science","volume":"14 1","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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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