Circular RNAs (circRNAs) have been identified from various tissues and species, but their regulatory functions during developmental processes are not well understood. We examined circRNA expression profiles of two developmental stages of bovine skeletal muscle (embryonic and adult musculus longissimus) to provide first insights into their potential involvement in bovine myogenesis. We identified 12 981 circRNAs and annotated them to the Bos taurus reference genome, including 530 circular intronic RNAs (ciRNAs). One parental gene could generate multiple circRNA isoforms, with only one or two isoforms being expressed at higher expression levels. Also, several host genes produced different isoforms when comparing development stages. Most circRNA candidates contained two to seven exons, and genomic distances to back-splicing sites were usually less than 50 kb. The length of upstream or downstream flanking introns was usually less than 105 nt (mean≈11 000 nt). Several circRNAs differed in abundance between developmental stages, and real-time quantitative PCR (qPCR) analysis largely confirmed differential expression of the 17 circRNAs included in this analysis. The second part of our study characterized the role of circLMO7—one of the most down-regulated circRNAs when comparing adult to embryonic muscle tissue—in bovine muscle development. Overexpression of circLMO7 inhibited the differentiation of primary bovine myoblasts, and it appears to function as a competing endogenous RNA for miR-378a-3p, whose involvement in bovine muscle development has been characterized beforehand. Congruent with our interpretation, circLMO7 increased the number of myoblasts in the S-phase of the cell cycle and decreased the proportion of cells in the G0/G1 phase. Moreover, it promoted the proliferation of myoblasts and protected them from apoptosis. Our study provides novel insights into the regulatory mechanisms underlying skeletal muscle development and identifies a number of circRNAs whose regulatory potential will need to be explored in the future.

Abnormal placental angiogenesis contributes significantly to fetal growth restriction (FGR) and related complications. Methionine adenosyl-transferase 2A (MAT2A) can regulate the process of embryonic development; however, the role of MAT2A in placental angiogenesis during fetal development remains poorly understood. In this study, placentas from paired normal birth weight (NBW) and FGR piglets were used to quantify placental vascular density and biochemical indexes, while porcine trophoblast cells (pTrs) and porcine vascular endothelial cells (PVECs) were used to investigate the regulatory mechanism of MAT2A on placental angiogenesis. Here, we found that FGR placentas exhibited reduced vascular density and increased glycogen levels. Moreover, FGR placentas showed reduced S-adenosylmethionine (SAM) levels and downregulated protein expression of MAT2A and CD31. Placental SAM levels were positively correlated with vascular density, while MAT2A expression was positively correlated with CD31 expression. Further study showed that MAT2A knockdown disrupted the metabolism of methionine, glycolysis, the tricarboxylic acid cycle and oxidative phosphorylation, and hindered protein synthesis, thereby impairing cell proliferation and migration in pTrs and/or PVECs, and inhibited angiogenesis in a co-culture system. In contrast, SAM supplementation promoted phosphorylation of ribosomal protein S6 kinase 1 (S6K1), downstream of the mammalian target of rapamycin complex 1 signalling pathway, and upregulated vascular endothelial growth factor-A protein expression, thereby increasing endothelial cell tube formation. In conclusion, our study demonstrates the potential of MAT2A in interventional therapy for placental development of FGR. KEY POINTS: Placental vascular density is correlated with decreased S-adenosylmethionine (SAM) levels caused by downregulated adenosyl-transferase 2A (MAT2A) expression. MAT2A regulates the placental mTORC1 signalling pathway and protein synthesis. MAT2A knockdown disrupts methionine metabolism, glycolysis, the tricarboxylic acid cycle and oxidative phosphorylation. MAT2A regulates the proliferation and migration capacity of placental trophoblast and endothelial cells. MAT2A regulates placental angiogenesis via the SAM-mTORC1-S6K1-VEGF-A signalling pathway.

As a prevalent and highly toxic environmental contaminant, 1‑nitropyrene (1‑NP) poses a significant threat to reproductive health, embryonic development, and genomic integrity. However, the specific mechanisms by which it impairs oocyte quality remain incompletely understood. Melatonin, a potent free‑radical scavenger, has been shown to protect the reproductive system from oxidative damage. In this study, we investigated the deleterious effects of 1‑NP on mouse oocytes and evaluated the potential of melatonin to counteract such toxicity. Our results demonstrate that 1‑NP exposure severely compromises oocyte maturation, fertilization, and subsequent preimplantation development. Transcriptomic sequencing revealed that 1‑NP dramatically alters the oocyte gene expression profile, leading to defective clearance of maternally inherited mitochondrial transcripts. This disruption subsequently induces mitochondrial dysfunction and oxidative stress. In parallel, 1‑NP treatment also perturbed key epigenetic modifications. In contrast, melatonin co‑treatment effectively ameliorated 1‑NP‑induced meiotic spindle anomalies, chromosomal aneuploidy, mitochondrial dysfunction, oxidative stress, and epigenetic aberrations, thereby restoring oocyte quality and post‑fertilization developmental competence. Notably, melatonin reversed the majority of the aberrant gene expression patterns elicited by 1‑NP. Strikingly, treatment with the mitochondria‑targeted antioxidant Mito‑TEMPO alone in the 1‑NP exposure system significantly improved oocyte maturation rates, restored mitochondrial membrane potential, and reduced ROS levels. Together, these findings indicate that melatonin protects mouse oocytes from 1‑NP‑induced damage primarily by targeting mitochondria and clearing mitochondrial ROS, thereby alleviating oxidative stress and revealing a promising therapeutic strategy against environmental reproductive toxicants.

Background Identifying recurrent genetic mutations is crucial for advancing the understanding and treatment of hepatocellular carcinoma (HCC). The chromatin regulator ARID1A is frequently mutated in cancers, but its integrated impact on prognosis and the tumor immune microenvironment (TIME) in HCC is unclear. Methods Somatic mutation and transcriptome data from TCGA and ICGC databases were analyzed. Associations with tumor mutation burden (TMB) and prognosis were evaluated. Immune infiltration was estimated using CIBERSORT/ssGSEA. Pathway and immunomodulator analyses were performed. ARID1A expression was validated via tissue microarray and an independent cohort (GSE76427). Results Among 19 commonly mutated genes, ARID1A mutation was an independent prognostic factor for poorer overall survival and was associated with higher TMB. A nomogram integrating ARID1A status, TMB, and stage showed good predictive accuracy. ARID1A mRNA/protein was upregulated in HCC tissues, correlating with advanced stage. ARID1A-mutant tumors exhibited distinct pathway enrichments (e.g., p53 signaling, drug metabolism). The ARID1A-mutant TIME was characterized by an increased proportion of naive CD4+ T cells and significantly elevated expression of specific immunomodulators, including the immunosuppressive molecules IDO1 and BTLA. Correlation analysis further linked this molecular signature to the specific immune cell landscape, suggesting an “inflamed but suppressed” TME. Conclusions ARID1A mutation defines an aggressive HCC subtype characterized by high TMB coupled with a distinct immunosuppressive TIME. These findings suggest ARID1A status has prognostic value and may inform combination immunotherapy strategies, such as targeting IDO1 or BTLA, warranting further clinical and mechanistic validation.

[This retracts the article DOI: 10.1016/j.omtn.2018.02.012.].

[This retracts the article DOI: 10.1016/j.omtn.2020.09.011.].

Background:Wilson's disease (WD), caused by mutations in the ATP7B gene, leads to copper accumulation and multi-organ damage. Exosomal microRNAs (miRNAs) play a crucial role in cell-to-cell communication and the pathogenesis of diseases, yet their study in WD remains unreported. This study aims to characterize the serum exosomal miRNA signature in WD patients and investigate its potential as a source of biomarkers and therapeutic targets. Methods:Serum exosomes from WD patients and healthy controls were isolated for RNA sequencing to identify differentially expressed miRNAs (DE-miRNAs). An integrated bioinformatics approach was employed, encompassing Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Reactome, and Disease Ontology (DO) analyses to systematically decipher the functional roles, pathway involvements, and disease associations of the DE-miRNAs. Selected DE-miRNAs were validated by RT-qPCR. Results:We identified 59 DE-miRNAs (23 upregulated, 34 downregulated) in WD patient serum exosomes. GO analysis revealed their significant involvement in signal transduction, metal ion binding, and metabolic pathways. KEGG analysis highlighted alterations in key signaling cascades, including Ras, PI3K-Akt, and Hippo pathways. Reactome analysis further uncovered disruptions in specific biological modules, notably ubiquitin-mediated proteolysis, GPCR signaling, and spliceosome assembly. DO enrichment demonstrated significant associations with hepatocellular carcinoma, neuropsychiatric disorders, and metabolic diseases. RT-qPCR validation confirmed the reliability of DE-miRNA expression patterns (p  < 0.05). Conclusions:This study establishes the first comprehensive landscape of serum exosomal miRNAs in WD, revealing their involvement in an interconnected network of pathological processes. Our findings provide a novel conceptual framework for understanding WD pathophysiology and pinpoint promising candidates for biomarker development.

Many factors affect bovine skeletal muscle development, among which noncoding RNAs are very important. While circular RNAs (circRNAs) play a central role in various physiological and pathological processes, their potential role in muscle development is poorly understood. Here, we identified several differentially expressed circRNAs in fetal and adult skeletal muscle tissue sequencing data. They included a circRNA originating from exon 24 circularization of the myosin heavy chain protein 8 gene (MYH8), circMYH8, which was significantly downregulated in the adult muscle tissue. We examined circMYH8’s role in skeletal muscle cell proliferation, apoptosis, and differentiation through its overexpression or inhibition. Specifically, we used luciferase reporter gene assays, western blots, real-time reverse transcription quantitative PCR, cell counting kit 8, and 5-ethynyl-2-deoxyuridine to explore circMYH8’s molecular sponge effect on bovine myoblast proliferation, apoptosis, and differentiation via competitively binding microRNA 221 to activate cyclin-dependent kinase inhibitor 1B. Then, we investigated circMYH8’s role in promoting muscle regeneration by injecting a circMYH8 overexpression plasmid into muscle-injured mice. The results suggest that circMYH8 inhibits bovine myoblast proliferation and facilitates cell apoptosis and differentiation acts through the miR-221/P27 axis. This study shows that circMYH8 is a potential myogenesis-related factor and provides new evidence for elucidating complex molecular mechanisms and a better understanding of the function of mammalian circular RNAs in muscle development.

BACKGROUND:The clinical manifestations, progression and therapeutic outcomes associated with ACAN variants exhibit considerable heterogeneity, rendering identification difficult. This characterizes the phenotypic profiles, genotypic spectrum and treatment strategies of Chinese patients with ACAN-related short stature. METHODS:We identified 20 short stature patients from a large single-center cohort who carried heterozygous ACAN variants. Among them, 15 patients received recombinant human growth hormone (rhGH) and/or gonadotropin-releasing hormone analog (GnRHa) therapy. RESULTS:All 20 patients had proportionally short stature, with or without mild facial dysmorphism and skeletal abnormalities. Furthermore, a less common characteristic was identified, that is 27.3% (3/11) of the female patients presented with central precocious puberty (CPP). Notably, intellectual disability/global developmental delay (ID/GDD) was observed in four males, a feature hardly documented in ACAN-related disorders. We identified 16 variants, of which 14 were novel. In addition, height improved in all 15 patients after treated with rhGH alone or combined with GnRHa. The clinical spectrum of ACAN variants exhibits extensive heterogeneity. CONCLUSIONS:This study underscores the significant clinical heterogeneity of ACAN-related disorders. Cognitive impairment and signs of early pubertal development were identified in a subset of patients in our cohort, suggesting that the clinical manifestations of ACAN variants may be broader than previously recognized. These observations warrant further evaluation in larger cohorts. IMPACT:We explored the characteristics and genetic profile of ACAN variants. ACAN-related disorders had a diversity of clinical manifestations. ACAN variants should be considered in children with short stature, including those showing subnormal GH responses on stimulation testing, particularly with a family history.

Circular RNAs (circRNAs) have emerged as critical regulators of skeletal muscle development, yet the functions of many muscle-derived circRNAs remain uncharacterized. In this study, we identified a novel circRNA, circAIDA, formed by exons 2 to 6 of the AIDA gene, based on bovine muscle sequencing data. Mechanistically, we demonstrate that circAIDA acts as a molecular sponge for miR-29a, thereby relieving the repression of its downstream targets, AKT3 and CLCN2. Functionally, circAIDA promotes bovine myoblast proliferation while inhibiting apoptosis and differentiation in vitro. Furthermore, experiments in vivo suggested circAIDA could attenuate regeneration of skeletal muscle in mice. In brief, we discovered a novel circAIDA/miR-29a interaction that regulates bovine myogenesis, providing new insights into the molecular networks controlling skeletal muscle development.

Conventional water retention heavily depends on phosphate additives, which are unfavorable for health and clean-label requirements. This study therefore employed the new green alternatives as lactic acid bacteria fermentation broth (LAB broth) and L-arginine (L-Arg). Sodium bicarbonate (SB) was served as a positive control. Cooking loss rates and textural properties were measured to reflect water retention and chicken feet structure. Further, infrared spectroscopy and laser confocal microscopy were observed to reveal protein secondary structures and collagen fibers. The results demonstrated that both treatments significantly enhanced protein hydration. The LAB broth group reduced cooking loss to 4.27%, lower than the control (9.74%), SB (5.06%) and L-Arg (5.25%) groups, with a weight gain rate of 15.47%, significantly higher than the control but lower than the L-Arg group (26.41%). L-Arg increased the product yield to 119.74%, markedly higher than the control (90.26%), SB (113.42%) and LAB broth (110.60%) groups, and decreased centrifugal loss to 4.54%, significantly lower than the control (8.31%) yet higher than LAB broth (3.95%). Further analysis revealed that LAB broth induced mild collagen unfolding and elevated α-helix proportion with slight collagen fiber swelling, enhancing bound water stability and thus achieving excellent WHC. In contrast, L-Arg caused intense swelling and absorbed large amounts of water, yet bound water was easily converted to free water with high water loss, while it increased β-turn content and formed a gel network to partially retain moisture.

Gefitinib resistance remains a major obstacle to the effective treatment of non-small cell lung cancer (NSCLC), and the underlying molecular mechanisms have not yet been fully elucidated. Lysosomal-associated transmembrane protein 4B (LAPTM4B) has been shown to be involved in cancer progression, but its specific role in gefitinib resistance and the prognosis of NSCLC patients remains unclear. In this study, we conducted functional experiments including CCK-8, Transwell, and tumor sphere formation assays in LAPTM4B-overexpressing or knockdown HCC827 cells and gefitinib-resistant HCC827-R cells. In vivo validation was performed using a NSCLC xenograft model in nude mice. The results showed that LAPTM4B was upregulated in NSCLC, with a further increase in gefitinib-resistant NSCLC samples. Functional experiments demonstrated that knockdown or overexpression of LAPTM4B regulated gefitinib resistance, cell migration, and stemness in HCC827 cells. Furthermore, RPS3 was identified as a key interacting target of LAPTM4B, and LAPTM4B could enhance the stability of RPS3 protein by inhibiting its ubiquitination. In vivo xenograft experiments showed that knockdown of LAPTM4B significantly suppressed tumor growth and tumor stemness, and this inhibitory effect could be reversed by overexpression of RPS3. Collectively, our findings indicate that LAPTM4B promotes gefitinib resistance and NSCLC progression by stabilizing RPS3 protein through inhibiting its ubiquitination, and the LAPTM4B-RPS3 axis may serve as a potential therapeutic target for overcoming gefitinib resistance in NSCLC.

Osteoporosis poses a significant threat to human health. Long non-coding RNAs (LncRNAs) have been deemed as crucial regulators in the pathogenesis of osteoporosis. However, the accuracy and efficiency of LncRNA-mediated regulation of bone formation require further improvement. Our previous study identified a repeat sequence in the human-derived LncRNA CTD-2555A7.2, suggesting its potential role in osteoporosis regulation. To investigate this hypothesis, we conducted systematic functional analyses of CTD-2555A7.2 in osteogenesis and explored its mechanisms and potential therapeutic applications. Through over-expression, siRNA silencing and repeat sequence over-expression in vitro and in vivo, our research demonstrate that CTD-2555A7.2 enhances bone formation by sequestering multiple miR-381-3p molecules through its repeat sequence. Through Western blot, siRNA silencing and luciferase reporter assay, we illuminated miR-381-3p suppresses osteogenic differentiation by concurrently targeting four essential genes of the Wnt signaling pathway: Apc, Lef1, wnt5a, and Lrp6. Notably, the mRNA of CTD-2555A7.2 repeat sequence exhibited pronounced therapeutic efficacy in ovariectomy osteoporosis models. Taken together, we identified a dual-amplification osteogenic axis (CTD-2555A7.2-miR-381-Wnt) that demonstrates significant regulatory effects on osteoporosis. This study has established an important theoretical framework for understanding osteogenic LncRNA mechanisms and provides novel insights for developing targeted therapeutics against osteoporosis.

Gayal (Bos frontalis) an endangered bovine species inhabitingChina, India, Bangladesh, Myanmar and Bhutan, has a mysterious evolutionary origin. Shaped by natural selection, its unique traits make it a valuable genetic resource; however, its populations are rapidly declining. In this study, comprehensive whole-genome resequencing of fifty-eight samples of Gayal from China, India, Myanmar and Bangladesh was performed. We identified over 44 million SNPs across four Gayal populations. Nucleotide diversity analysis revealed variations in genetic diversity, with the lowest occurring in India and the highest occurring in China. Phylogenetic tree analysis revealed three distinct clades representing China, India and Bangladesh-Myanmar, which were further confirmed by principal component and admixture analyses. The genetic exchanges between Gayal and other bovine species indicate limited influence from domestic cattle in both the Chinese and Bangladeshi Gayal populations. Mitochondrial DNA sequences and a phylogenetic tree highlighted the unique mitochondrial genome of Gayal. Genome-wide selection signals pinpointed candidate genes linked to mitochondrial function, immunity, musculoskeletal development, reproduction and growth performance. Distinct haplotype patterns emerged for the CCDC157, KIAA0753 and MTFP1 genes in the Chinese and Bangladesh-Myanmar Gayal populations, indicating artificial selection in the Chinese population. KEGG pathway and gene ontology enrichment analyses provided insights into processes related to neurodevelopment, cardiac function, tissue growth, immunity and metabolism. In summary, our study enhances our understanding of Gayal genetics, population structure and selection signals across four countries. This knowledge is crucial for conserving this endangered species amid its rapid decline.

OBJECTIVES:To evaluate the application value of genetic newborn screening (gNBS) in the Yunnan region. METHODS:A prospective study was conducted with a random selection of 3 001 newborns born in the Yunnan region from February to December 2021. Traditional newborn screening (tNBS) was used to test biochemical indicators, and targeted next-generation sequencing was employed to screen 159 genes related to 156 diseases. Positive-screened newborns underwent validation and confirmation tests, and confirmed cases received standardized treatment and long-term follow-up. RESULTS:Among the 3 001 newborns, 166 (5.53%) were initially positive for genetic screening, and 1 435 (47.82%) were genetic carriers. The top ten genes with the highest variation frequency were GJB2 (21.29%), DUOX2 (7.27%), HBA (6.14%), GALC (3.63%), SLC12A3 (3.33%), HBB (3.03%), G6PD (2.94%), SLC25A13 (2.90%), PAH (2.73%), and UNC13D (2.68%). Among the initially positive newborns from tNBS and gNBS, 33 (1.10%) and 47 (1.57%) cases were confirmed, respectively. A total of 48 (1.60%) cases were confirmed using gNBS+tNBS. The receiver operating characteristic curve analysis demonstrated that the areas under the curve for tNBS, gNBS, and gNBS+tNBS in diagnosing diseases were 0.866, 0.982, and 0.968, respectively (P<0.05). DeLong's test showed that the area under the curve for gNBS and gNBS+tNBS was higher than that for tNBS (P<0.05). CONCLUSIONS:gNBS can expand the range of disease detection, and its combined use with tNBS can significantly shorten diagnosis time, enabling early intervention and treatment.

BackgroundSeptic shock in children is an infectious disease caused by low immunity, and its mortality is very high. Early prediction of the risk of death in children with septic shock is helpful for clinicians to judge the severity of the disease, take active treatment measures, and improve the adverse outcomes of patients. However, the mechanism of death from sepsis in children remains unclear. This study aims to use bioinformatics and machine learning algorithms to identify key genes and pathways associated with fatal sepsis in children, and provide theoretical basis for rational drug use in follow-up TCM treatment.MethodsGene expression profiles were obtained from the GEO database (GSE4607) for 15 blank patients and 14 children with sepsis death. Differentially expressed genes (DEGs) were enriched by GO and KEGG pathways. Construct and visualize protein-protein interaction (PPI) networks to identify candidate genes responsible for fatal sepsis in children. Three kinds of machine learning models were established, and the candidate genes were screened by intersection to obtain the core genes with diagnostic value. ROC curve was drawn for core genes to clarify the diagnostic value of genetic markers.ResultsAnalysis of differences in the preprocessed dataset identified 83 genes, including 78 up-regulated genes and 5 down-regulated genes. 17 candidate genes were screened by protein interaction network analysis. Three machine learning algorithms LASSO, random forest (RF), and support vector machine recursive feature elimination (SVM-RFE) were used to finally screen out three core genes: CD163, MCEMP1 and RETN. CD163, MCEMP1 and RETN may jointly regulate complement and coagulation cascades, toll like receptor signaling pathway, graft versus host disease, type I diabetes mellitus.ConclusionIn this study, three core genes (CD163, MCEMP1 and RETN) that lead to sepsis death in children were screened out, providing a new understanding of the lethal mechanism of sepsis in children and a promising new therapeutic approach.

The neuroactive β-N-oxalyl-L-α,β-diaminopropionic acid (β-ODAP) was first identified in Lathyrus sativus and present also in several Chinese traditional herbs including Panax notoginseng. It exhibit toxicological effects as the causative agent of neurolathyrism when L. sativus was over-consumed under drought-triggered famines or pharmacological effects including neuroprotection and wound healing. Determinating of β-ODAP synthetase (BOS) will accelerate plant improvement and utilisation of those species containing β-ODAP. In this report, trace level of β-ODAP was confirmed in several cultivars of Pisum sativum, a close relative of L. sativus. Functions of LsBAHD3 and LsAAE3 were investigated via its transient expression in Nicotiana benthamiana, in vitro enzymatic activity assay and overexpression in hairy roots of L. sativus and P. sativum, etc. The results suggested that LsBAHD3 act as BOS, while LsAAE3 function as oxalyl-CoA synthetase to catalyse/promote β-ODAP biosynthesis. Further comparison and verification of LsBAHD3-specific and LsAAE3-specific protein interactome suggested that the LsBAHD3-LsAAE3 module catalyses β-ODAP biosynthesis, and the ubiquitin/26S proteasome system is highly involved in the regulation of BOS and β-ODAP content and may be responsible for the different level of β-ODAP in L. sativus and P. sativum. These results provide valuable insight into the biochemical and genetic mechanisms of β-ODAP biosynthesis.

Diquat (DQ) is a commonly used herbicide, and its improper use can lead to multi-organ damage. The characteristics of multi-organ damage induced by DQ are not yet well understood. In this study, we conducted single-cell/single-nucleus RNA sequencing (scRNA-seq/snRNA-seq) on the lungs, liver, and kidneys of mice at consecutive time points (10 hours, 20 hours, and 36 hours) after DQ poisoning, as well as in a control group. In a multi-organ single-cell atlas comprising over 270,000 cells from mice, we found that DQ induces an oxidative stress microenvironment in endothelial and parenchymal cells, primarily characterized by activation of the oxidative phosphorylation pathway and an enhanced inflammatory response. This oxidative stress microenvironment prompted regulatory cell death in parenchymal and immune cells, releasing inflammatory factors and further exacerbating the oxidative environment. Additionally, metabolic reprogramming occurred in both parenchymal and immune cells under oxidative stress, leading to alterations in energy metabolism, reduced hepatic detoxification capabilities, and changes in the activation modes of immune cells, thereby intensifying tissue damage. Notably, no significant fibrosis was observed in the tissue damage caused by DQ, underscoring the importance of early intervention. Overall, using a mouse model, this study revealed the central role of the DQ-induced oxidative stress microenvironment in multi-organ damage and enhanced our understanding of the pathophysiology and complex molecular mechanisms underlying DQ-induced multi-organ injury.

Yajiangxue cattle (XF) is three-way crossbred cattle developed specifically for producing high-quality beef in the Tibetan Plateau by introducing the bloods of Tibetan yellow cattle (HF) and Angus cattle into Tibetan yak (MF). In the present study, we mainly focused on fat deposition and metabolism changes and used RNA-seq and LC-MS/MS-based metabolomics to partially explain the meat quality improvement in Yajiangxue cattle. Differential expression analysis revealed 1762, 2949, and 2931 different expression genes in XF vs. HF, XF vs. MF, and XF vs. cattle–yak (PF), respectively, such as BMP2, WISP2, FGF1, IL1B, IL6, and WNT5B. Immune response, oxidation–reduction processes, and fatty acid metabolism were markedly enriched. Furthermore, an initial identification revealed 319 metabolites using positive ion mode and 289 metabolites using negative ion mode in bovine adipose tissue across four breeds/populations. Of these, 143 were differential metabolites in positive ion mode, while 166 were in negative ion mode. The main pathways of metabolism affected by breed/population were unsaturated fatty acid biosynthesis, tryptophan and tyrosine biosynthesis, primary bile acid biosynthesis, cholesterol metabolism, beta-alanine metabolism, etc. Similarly, both the transcriptome and the metabolome results highlighted fatty acid metabolism. These results could help elucidate the biological mechanisms involved in fat deposition and identify valuable biomarkers for specific metabolite accumulation.