With the extensive use of plastics and brominated flame retardants, polystyrene microplastics (Ps-MPs) and polybrominated diphenyl ethers (PBDEs) frequently co-occur in the environment, raising growing concerns about their combined reproductive hazards. However, the synergistic toxicity of Ps-MPs and PBDEs on female fertility and oocyte quality remains insufficiently characterized. In this study, we established a 28-day oral exposure model in female ICR mice to evaluate the effects of Ps-MPs, PBDE-47, and their co-exposure on ovarian function, oocyte meiotic competence, and reproductive outcomes. Both Ps-MPs and PBDE-47 alone reduced ovarian weight, decreased antral follicles, increased follicular atresia, and markedly lowered ovulation and litter size, whereas co-exposure produced the most severe impairments. At the oocyte level, exposure significantly reduced germinal vesicle breakdown and first polar body extrusion, increased abnormal spindle formation and erroneous kinetochore-microtubule attachments, and suppressed TPX2 expression and α-tubulin acetylation. Cortical F-actin polarization, spindle migration, and membrane localization of JUNO and ovastacin were also disrupted, indicating widespread defects in meiotic and membrane maturation. Mechanistically, Ps-MPs and PBDE-47 induced a decline in mitochondrial membrane potential, aberrant mitochondrial distribution, excessive lipid accumulation, and Ca²⁺ imbalance, accompanied by autophagosome accumulation, lysosomal dysfunction, elevated ROS, increased γ-H2AX signals, and enhanced Annexin V labeling, ultimately triggering DNA damage and apoptosis. All alterations were most pronounced under co-exposure. Collectively, Ps-MPs and PBDE-47 synergistically impair female fertility by converging on mitochondrial dysfunction, autophagy-lysosome imbalance, and oxidative stress-mediated DNA damage, leading to substantial reductions in oocyte quality. These findings provide key mechanistic evidence for evaluating reproductive risks associated with real-world mixtures of microplastics and persistent organic pollutants.

Studies on the effects of nutrition on the placenta mainly focus on early to middle pregnancy due to rapid fetal development during this period. In late gestation, although nutrient restriction has been linked to adverse fetal outcomes and altered uteroplacental physiology, the placental transcriptional programs that coordinate substrate transport, metabolic adaptation, and immune-related pathways under maternal undernutrition remain incompletely characterized, particularly in large-animal models. Therefore, this study aims to characterize transcriptional alterations associated with placental metabolism, nutrient transport, and immune regulation in response to nutritional restriction during late pregnancy. In this study, late-gestation ewes were restricted to 30

This study evaluated the effects of replacing corn with defective jujube (DJ) on growth, digestibility, blood biochemical indices, meat performance, and the presence of Alternaria toxin residues in Karakul lambs. Thirty-six lambs were split into groups given 0%, 15%, or 30% DJ, replacing 0%, 45.45%, and 90.91% of corn. The trial lasted 75 days, with 15 days for adaptation and 60 days for measurement. Digestibility for crude protein and ether extract of male lambs increased in the DJ30 group over CON (p < 0.05). High-density lipoprotein decreased in DJ30 (p < 0.01), while triglycerides and total cholesterol in DJ30 dropped (p < 0.05). Blood urea nitrogen and aspartate aminotransferase decreased in DJ15 and DJ30 (p < 0.01). Superoxide dismutase and catalase rose in DJ30 (p < 0.01), while malondialdehyde declined (p < 0.05). Growth hormone and insulin-like growth factor-1 increased in DJ30 (p < 0.01). Feeding DJ did not affect meat production or quality. No Alternaria toxins were detected in rumen, liver, or meat. Feeding 15-30% DJ improved nitrogen utilization, lipid metabolism, and blood antioxidant levels in lambs and reduced the risk of liver damage, while no Alternaria toxin remained in organs. A 30% DJ substitution for corn is a safe strategy for lamb feeding.

BACKGROUND:Undernutrition disrupts pregnant ewe's metabolic homeostasis and severely inhibits fetal growth and development. In this study, undernourished and nutrition-recovery pregnant sheep models and rumen epithelial cells were utilized to investigate the mechanisms behind undernutrition-induced disruptions in male fetal rumen metabolism and development. RESULTS:Maternal undernutrition significantly reduced male fetal rumen weight and papilla length, width and surface area. Maternal undernutrition extremely suppressed nutrient metabolism and energy production in male fetal rumen via JAK3/STAT3 signaling to inhibit cell cycle progression and male fetal rumen development, while maternal nutritional recovery partially restored metabolic inhibition but failed to alleviate male fetal rumen development. Meanwhile, 64 differentially expressed miRNAs (DEMs) were identified in male fetal rumen between undernourished ewes and controls. Novel miR-736 was overexpressed both in male fetal rumen of undernourished and nutrition-recovery models. E2F transcription factor 2 (E2F2) and MYB proto-oncogene like 2 (MYBL2) were the intersection of male fetal rumen differentially expressed genes (DEGs) and DEMs target genes integrated analysis and were predicted as novel miR-736 target genes. Further, we confirmed that novel miR-736 targeted and downregulated E2F2 and MYBL2 expression levels. Silencing E2F2 and MYBL2 promoted apoptosis and inhibited S-phase entry in rumen epithelial cells. CONCLUSIONS:In summary, maternal undernutrition disrupted male fetal rumen metabolism and elevated novel miR-736, which targeted and downregulated E2F2 and MYBL2 to inhibit cell cycle progression and promote apoptosis, finally inhibited male fetal rumen development. This study provides new insights into the epigenetic mechanisms underlying maternal undernutrition-induced male fetal rumen developmental deficits.

High-fertility sheep experience undernutrition during late gestation, which induces body metabolic disruption and intestinal inflammation. Crucially, the gut microbiota-bile acid axis is a promising intestinal inflammation target, but how choline modulates this axis in livestock enteritis is unknown. This study investigated choline’s protective mechanisms against undernutrition-induced intestinal inflammation in sheep, focusing on gut microbiota and bile acid regulation. Choline consistently alleviates colitis severity, restores epithelial barrier integrity, and suppresses intestinal inflammation. These protective effects are accompanied by pronounced remodeling of the colonic microbial ecosystem, characterized by the enrichment of Clostridiales bacterium to elevate bile salt hydrolase activity and regulate bile acid homeostasis. Concomitantly, choline reshapes colonic bile acid profiles, normalizing total bile acid levels and selectively restoring DCA abundances. Mechanistically, the anti-inflammatory effects of DCA depend on Nur77 activation and subsequent suppression of NF-κB signaling across in vivo and in vitro systems. These findings provide preliminary evidence for a putative choline-microbiota-bile acid-immune signaling axis that confers protection against undernutrition-associated colitis and support choline intervention as a pregnancy-compatible nutritional strategy for intestinal inflammatory disorders in animal.

Heat stress (HS) is a major environmental factor that impairs female fertility by disrupting oocyte quality and developmental competence. Pyrroloquinoline quinone (PQQ), a redox cofactor with strong antioxidant and mitochondrial-protective properties, has recently attracted attention for its cytoprotective roles in mammalian cells. Here, we investigated whether PQQ supplementation could alleviate HS-induced porcine oocyte damage and improve subsequent embryonic development. Our results showed that PQQ treatment significantly restored the rates of germinal vesicle breakdown (GVBD) and first polar body extrusion (PBE) in heat-stressed oocytes. PQQ markedly reduced intracellular reactive oxygen species (ROS) accumulation, enhanced mitochondrial membrane potential (ΔΨm), and maintained ATP levels, indicating improved mitochondrial function. Furthermore, PQQ attenuated DNA damage (γH2A.X foci) and apoptosis (Caspase-3 activation), preserved spindle morphology and actin distribution, and normalized cortical granule and ovastacin localization, suggesting improved cytoplasmic maturation. Importantly, embryos derived from PQQ-treated oocytes exhibited higher cleavage and blastocyst formation rates compared with the HS group. Collectively, these findings demonstrate that PQQ effectively mitigates HS-induced oocyte dysfunction by maintaining mitochondrial integrity, redox balance, and cytoskeletal organization, thereby improving oocyte competence and early embryonic development under heat stress.

Improving meat tenderness and flavor potential without relying on excessive fat deposition is a major challenge. This study investigated the effects of dietary rumen-protected betaine (RPB) on lamb meat quality in Hu-sheep. Twenty lambs were fed basal diets with or without RPB (8 g/day) during the 56-day formal trial. RPB improved several meat quality traits, including tenderness, water-holding capacity, and redness, despite reducing intramuscular fat. Notably, RPB enriched total and umami-related amino acids (Glu, Asp), suggesting enhanced amino acid-derived taste potential. RPB supplementation was accompanied by enhanced antioxidant capacity and upregulated oxidative phosphorylation and ribosome biogenesis pathways. This coordinated molecular reprogramming was associated with remodeling toward a more oxidative muscle fiber phenotype, characterized by reduced fiber cross-sectional area. In vitro assays showed that betaine promoted myogenic differentiation toward an oxidative lineage. Collectively, by coupling metabolic and structural remodeling, RPB provides a promising nutritional strategy for high-quality mutton production.

Pingliang Red cattle is renowned for its tender meat and symmetrical intramuscular fat (IMF) deposition. Rumen microbiota are crucial for energy metabolism and nutrient acquisition in cattle, significantly influencing IMF deposition. Therefore, this study aimed to explore how rumen microbiota impact IMF deposition in Pingliang Red cattle. 34 castrated Pingliang Red cattle were subjected to the same management for 2 months, followed by centralized and unified slaughtering. Based on the measured IMF content in the longissimus dorsi, 18 cattle were selected and divided into a high-intramuscular-fat group (HIMF, n = 9) and a low-intramuscular-fat group (LIMF, n = 9). Rumen fluid was subsequently collected for metagenomic sequencing. Results showed significant differences in taxonomic abundance at both the genus and species levels, the relative abundance of carbohydrate-active enzyme (CAZy) families, and functional profiles (p < 0.05). Specific rumen microbes, such as Limosilactobacillus panis (AUC = 0.765) and Fibrobacter succinogenes (AUC = 0.753), served as potential biomarkers for HIMF deposition in Pingliang Red cattle. With the exception of Bacillus, Fibrobacter succinogenes, Limosilactobacillus panis, Prevotella intermedia, and Streptomyces exhibited positive correlations with IMF content. Functional analysis based on KEGG orthology (KO) indicated that specific enzymes promote IMF deposition by regulating the metabolism of short-chain fatty acids (SCFAs), long-chain fatty acids (LCFAs), and lipopolysaccharides, as well as insulin signaling. These findings provide a theoretical reference for regulating rumen microbial communities to improve IMF deposition.

Both yaks and Simmental are dual-purpose highland varieties, but the mechanisms behind the differences in their milk production are not yet fully understood. This study compared milk composition, rumen microbial communities, and metabolomes across a range of lactation stages for both breeds. Yak milk yields were lower and it had higher levels of fat, protein, long-chain and polyunsaturated fatty acids, key amino acids, and essential minerals than Simmental milk. The microbial community of yak rumen exhibited unique characteristics, with the Family_XIII_AD3011_group persistently enriched and positively correlated with rumen fermentation parameters and milk quality, and the content of glutamate and glutamine in yak rumen was higher than in Simmental and positively correlated with milk quality. Therefore, key microorganisms and metabolites in yak rumen are crucial factors for high-yield dairy production, providing new insights to enhance milk production in ruminant dairy cattle.

Pregnant ewes mobilize body fat to increase energy supply for fetal growth and development upon undernutrition, which disrupts the metabolic homeostasis of the body. However, the comprehensive metabolic changes in subcutaneous adipose tissue upon undernutrition are poorly understood. In this study, an undernutrition sheep model was established to investigate the effects of undernutrition on metabolic changes, immune response, and inflammation in subcutaneous fat through transcriptome, RT-qPCR, and metabolome analysis. Results showed that undernutrition changed the total transcriptional and metabolic profiles of adipose tissue. Compared to the controls, differentially expressed genes (DEGs) involved in fatty acid synthesis, triglyceride genesis, and lipid transport were downregulated in undernourished ewes, while DEGs related to fatty acid and triglyceride degradation were upregulated. Almost all lipid-related differential metabolites (DMs) were downregulated. DEGs and DMs involved in glucose metabolism and glycogen degradation were downregulated, while glycogen synthesis and carbohydrate transport were upregulated. DEGs linked to amino acid degradation were upregulated and some amino acids and derivatives were downregulated. KEGG pathway analysis showed complement and coagulation cascades were enriched significantly by DEGs, and DEGs related to coagulation, macrophage, and inflammation were upregulated while DEGs associated with the complement system were downregulated. Undernutrition during late gestation disrupted the metabolism of lipids, carbohydrates, and amino acids in adipose tissue, which weakened the complement system and immune response and may have ultimately led to inflammation.

Malnutrition is common during gestation, which threats maternal health, survival, and fetal development. The mechanisms of malnutrition-induced metabolic disorders and fetal maldevelopment are however poorly understood. In recent years, numerous studies in human and animal models have filled the gaps in the field of mother-child metabolism regarding malnutrition during gestation. This review summarizes and analyzes the lipid metabolic disorders in maternal and fetal livers, as well as fetal maldevelopment in response to malnutrition during gestation, and the regulatory mechanisms involved. Malnutrition elevates fatty acid oxidation, esterification, and lipolysis while suppressing fatty acid, cholesterol, steroid synthesis, and phospholipid metabolism both in maternal and fetal livers. Intriguingly, ketogenesis is inhibited in maternal liver but enhanced in fetal liver. Maternal malnutrition induces fetal hepatic lipid metabolic dysregulation, which suppresses DNA replication machinery and disrupts cell cycle progression, thereby creating an imbalance between cellular proliferation and apoptosis, ultimately culminating in fetal maldevelopment. Under conditions of malnutrition, non-esterified fatty acids stimulate peroxisome proliferator-activated receptor alpha (PPARA) signaling to upregulate fatty acid β-oxidation and ketogenesis, whereas β-hydroxybutyrate inhibits these metabolic processes through suppression of retinoid X receptor alpha (RXRA) signaling. Activation of PPARA/RXRA signaling pathway improves liver lipid metabolic homeostasis and alleviates oxidative stress. This review contributes to the research on mother-child nutritional metabolism and the development of novel strategies during gestation to advance the health of mother and offspring.

OBJECTIVE:This study aimed to elucidate the mechanisms underlying milk composition divergence between naks (female yaks) and Simmental cows (S-cows) by integrating longitudinal multi-omics analyses of gut microbiota and metabolomes. METHODS:We determined the gut microbiota and metabolites of both species over a 54-day period (day 26 to 80 of lactation) of ten naks and ten S-cows. Gut microbiota dynamics were assessed via 16S rRNA sequencing, while serum and fecal metabolomes were profiled using ultra-high performance liquid chromatography-tandem mass spectrometry. Statistical analyses included Wilcoxon rank-sum tests, linear discriminant analysis effect size (linear discriminant analysis>2, p<0.05), and Spearman correlations (r>0.70). RESULTS:Milk yield was lesser (0.53-0.91 vs. 2.07-3.88 kg/d) but concentrations of fat (5.63%-6.30% vs. 3.30%-3.74%), protein (5.66%-6.30% vs. 3.39%-3.74%), and conjugated linoleic acid (CLA) (1.74%-2.35% vs. 1.40%-1.75%) were greater (p<0.001) in nak than Scow milk. Species-specific microbial signatures emerged. In naks, the g-Family-XIIIAD3011-group and g-norank-Ruminococcaceae were correlated with bile acid metabolism and CLA synthesis via 13-hydroxyoctadecadienoic acid transport. Additionally, the naks gut had a greater concentration of 13-hydroxyoctadecadienoic acid, a precursor of CLA, which may be transported to mammary cells via phosphatidylcholine and converted to CLA under the catalysis of fatty acid desaturase2. S-cows harbored g-Succinivibrio and g-Eubacterium-ruminantium-group, which are linked to galactose utilization and mTORmediated amino acid allocation. Metabolomics revealed naks-enriched steroid biosynthesis and taurine pathways (false discovery rate<0.05), while S-cows exhibited a lactating network associated with greater milk yield. CONCLUSION:Host-specific gut microbiota mediated nutrient allocation trade-offs. Naks optimized lipid-rich milk through bile acid and CLA metabolic networks, whereas S-cows enhanced yield via microbial-galactose synergies. This research underscores the pivotal role of the gut microbiome in mediating milk composition and suggests that microbiome manipulation could be a promising strategy to enhance milk quality in ruminants.

This experiment aimed to explore the effects of nutritional intervention on the composition and content of routine nutrients, amino acids, and fatty acids in the colostrum of lactating yaks. Twenty yaks in the late pregnancy stage with the same parity and similar body conditions were selected as and randomly divided into two groups (n = 10). The control group were allowed to graze freely from 8:00 to 18:00, and treatment (TR) group, yaks were supplemented with 3.0 kg of oat hay and 1.0 kg of concentrate feed per day. The experimental period lasted for 28 days, including 21 days before parturition and 7 days after parturition. From 1u20137 days after parturition, colostrum was collected daily to determine the routine nutrients, amino acids, and fatty acids profile of colostrum. The results showed that the colostrum protein, non-fat colostrum solids, and lactose contents were extremely significantly higher (P u0026lt; 0.01) in the TR group. The lysine content in the TR group increased significantly (P u0026lt; 0.05), additionally the prolongation of lactation time, the ratio of essential to non-essential amino acids increased significantly (P u0026lt; 0.05) higher in colostrum of lactating yaks. The C18:1 n-9t, C18:3 n-3, and polyunsaturated fatty acids (PUFA) contents extremely significantly increased (P u0026lt; 0.01) with supplementation in the TR group. Compared to day 1, the contents of C6:0 and C10:0 increased extremely significantly on day 7 (P u0026lt; 0.01). In contrast, the contents of C14:1, C18:2 n-6c, and PUFA decreased significantly (P u0026lt; 0.05), and the content of C16:1 decreased extremely significantly (P u0026lt; 0.01). Colostrum protein content was significantly positively correlated with methionine content (P u0026lt; 0.05), and lactose content was significantly negatively correlated (P u0026lt; 0.05) with C4:0 and C18:0 contents. The non-fat colostrum solids content was extremely significantly negatively correlated with C4:0 and C18:0 contents (P u0026lt; 0.01), while colostrum fat content was significantly positively correlated (P u0026lt; 0.05) with C18:0 content, additionally the colostrum fat content was extremely significantly positively correlated (P u0026lt; 0.01) with histidine content. Perinatal supplementation with oat hay and concentrate significantly improved yak colostrum quality by increasing protein, non-fat colostrum solids, lactose, lysine, and beneficial fatty acids (C18:1 n-9t, C18:3 n-3, PUFA) contents. Key correlations (protein-methionine, fat-C18:0/histidine) suggest nutrient interventions regulate fatty acid and amino acid metabolism to enhance colostrum synthesis. This study demonstrates the importance of targeted perinatal nutrition for optimizing neonatal yak health and livestock productivity in high-altitude pastoral systems, and offering a sustainable strategy to address nutritional challenges in grazing-based management.

Nutrition consistently affects microbe-host interactions in the gastrointestinal tract. This study aimed to unravel how undernutrition reshapes the microbial composition and the homeostasis of epithelium in the jejunum and ileum. Sixteen late-gestation Hu-sheep were randomly assigned to the control group (n = 8, 100% ad libitum feeding levels) or the undernutrition group (n = 8, which received 30% ad libitum feeding levels). After 15-d treatment, all ewes were slaughtered, and jejunal and ileal digesta and epithelium samples were collected for 16S rRNA gene sequencing and transcriptome sequencing, respectively. Results indicated that undernutrition decreased the jejunal and ileal tissue weights (P = 0.005 and P = 0.022) and the levels of volatile fatty acids (P = 0.019 and P = 0.007) and microbial protein levels (P = 0.019 and P = 0.031) in jejunal and ileal digesta. The relative abundance of acetate producing microbiota, including Clostridia UCG-014 norank, Ruminococcus, [Ruminococcus] gauvreauii, and Lachnospiraceae _Blautia, were significantly reduced (P < 0.05) in the jejunum and ileum. Undernutrition up-regulated (P < 0.05) the expression of genes involved in amino acid synthesis and fatty acid oxidation, but down-regulated (P < 0.05) the expression of genes associated with amino acid degradation, fatty acid synthesis, and extracellular structures in jejunal and ileal epithelium. In the jejunal epithelium, genes associated with extracellular matrix-receptor interactions, cell growth, and immune response were down-regulated (P < 0.05) upon undernutrition. Taken together, undernutrition changed the microbial community in the jejunum and ileum, which altered the fermentation mode and the production of volatile fatty acids and microbial protein. These affected the energy and protein system in the epithelium and reprogrammed substance metabolism and extracellular structures, which probably further influenced cell growth and immune response. These insights provide a foundation for completely clarifying the crosstalk between small intestinal microbiota and the host.

This study investigated the effect of replacing part of the dietary soybean meal with either polymer-coated urea or gelatinized starch urea on the production performance, blood indexes, and ruminal fermentation of Angus heifers. A total of 210 purebred Angus cattle (BW = 314.26 kg) were divided into three groups: the no urea group (CON), the polymer-coated urea group (PCU), and the gelatinized starch urea group (GSU); 20 g/kg polymer-coated urea or 25 g/kg gelatinized starch urea was used to replace part of soybean meal in the concentrate feed, according to the principle of isometabolic energy and isonitrogenous. The result showed that the PCU group had higher ADG and ADF apparent digestibility, while it had a lower feed–weight ratio. On the 86th day, the serum albumin (ALB) content in the PCU group was significantly higher than that in the CON group. In rumen, compared with the CON group, the contents of acetic acid and total volatile fatty acid were significantly higher in the PCU group, whereas butyric acid and propionic acid were significantly higher in the PCU group and GSU group. Ruminal bacterial diversity analysis found that the abundance of Firmicutes was higher in the PCU group at the phylum level, and an inverse result was observed in Bacteroidetes. The abundance of Paraprevotella was higher in the PCU group, whereas higher abundance of Prevotella was found in the GSU group at the genus level. These results indicate that slow-release urea can replace part of soybean meal in the diet, and the amount of substitution in this trial had no diverse effect on the performance of Angus heifers.

This study investigated the impact of diallyl disulfide (DADS) on oxidative stress induced by hydrogen peroxide (H2O2) in ovine rumen epithelial cells (RECs). Initially, the effects of DADS were evaluated on cellular reactive oxygen species (ROS) levels, antioxidant capacity in RECs were estimated. Then, RNA-seq analysis was conducted in DADS-treated and untreated cells to analyze the differential gene expression, as well as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Finally, the effects of DADS on Kelch-like ECH associated protein 1/the nuclear factor erythroid 2-related factor 2 (Keap1/Nrf2) signaling pathway in RECs were evaluated. Results showed that DADS remarkably enhanced superoxide dismutase (SOD) activity and total antioxidant capacity (T-AOC) (P < 0.05) while reducing ROS and malonaldehyde production (P < 0.05) in H2O2-treated RECs. Transcriptomic analysis revealed that DADS might influence glutathione synthesis through cysteine and methionine metabolism, thereby affecting the transcription of genes involved in immunity and oxidative stress. The DADS treatment resulted in increased nuclear translocation of Nrf2 and upregulation of mRNA and protein levels of quinone oxidoreductase 1, heme oxygenase 1, and Nrf2. The Nrf2-specific inhibitor nullified the protective effects of DADS on malonaldehyde formation induced by H2O2 and decreased T-AOC and SOD activities. In conclusion, DADS demonstrated the ability to alleviate oxidative stress in RECs by promoting antioxidative capacity through the Keap1/Nrf2 signaling pathway.

The yak (Poephagus grunniens) has evolved unique adaptations to survive the harsh environment of the Qinghai–Tibetan Plateau, while their gut microorganisms play a crucial role in maintaining the health of the animal. Gut microbes spread through the animal population not only by horizontal transmission but also vertically, which enhances microbial stability and inheritance between generations of the population. Homogenization of gut microbes in different animal species occurs in the same habitat, promoting interspecies coexistence. Using the yak as a model animal, this paper discusses the adaptive strategies under extreme environments, and how the gut microbes of the yak circulate throughout the Tibetan Plateau system, which not only affects other plateau animals such as plateau pikas, but can also have a profound impact on the health of people. By examining the relationships between yaks and their gut microbiota, this review offers new insights into the adaptation of yaks and their ecological niche on the Qinghai–Tibetan plateau.

Copper oxides nanoparticles (CuO NPs) are widely used for a variety of industrial and life science applications. In addition to cause neurotoxicity, hepatotoxicity, immunotoxicity, CuO NPs have also been reported to adversely affect the reproductive system in animals; However, little is known about the effects and potential mechanism of CuO NPs exposure on oocyte quality, especially oocyte maturation. In the present study, we reported that CuO NPs exposure impairs the oocyte maturation by disrupting meiotic spindle assembly and chromosome alignment, as well as kinetochore-microtubule attachment. In addition, CuO NPs exposure also affects the acetylation level of α-tubulin in mice oocyte, which hence impairs microtubule dynamics and organization. Besides, CuO NPs exposure would result in the mis-localization of Juno and Ovastacin, which might be one of the critical factors leading to the failure of oocyte maturation. Finally, CuO NPs exposure impairs the mitochondrial distribution and induced high levels of ROS, which led to the accumulation of DNA damage and occurrence of apoptosis. In summary, our results indicated that CuO NPs exposure had potential toxic effects on female fertility and led to the poor oocyte quality in female mice.

Maternal nutrition during pregnancy regulates the offspring's metabolic homeostasis, including insulin sensitivity and the metabolism of glucose and lipids. The fetus undergoes a crucial period of plasticity in the uterus; metabolic changes in the fetus during pregnancy caused by maternal nutrition not only influence fetal growth and development but also have a long-term or even life-long impact for the offspring. Epigenetic modifications, such as DNA methylation, histone modification, and non-coding RNAs, play important roles in intergenerational and transgenerational effects. In this context, this narrative review comprehensively summarizes and analyzes the molecular mechanisms underlying how maternal nutrition, including a high-fat diet, polyunsaturated fatty acid diet, methyl donor nutrient supplementation, feed restriction, and protein restriction during pregnancy, impacts the genes involved in glucolipid metabolism in the liver, adipose tissue, hypothalamus, muscle, and oocytes of the offspring in terms of the epigenetic modifications. This will provide a foundation for the further exploration of nutrigenetic and epigenetic mechanisms for integrative mother-child nutrition and promotion of the offspring's health through the regulation of maternal nutrition during pregnancy. Note: This paper is part of the Nutrition Reviews Special Collection on Precision Nutrition.