Lactobacillus spp., as probiotics, have shown efficacy in alleviating nonalcoholic fatty liver disease (NAFLD). Here, we screened a new probiotic strain, Lactobacillus salivarius SNK-6 (L. salivarius SNK-6), which was isolated from the ileum of healthy Xinyang black-feather laying hens in China. We investigated the beneficial activity of L. salivarius SNK-6 in a NAFLD model in laying hens and found that L. salivarius SNK-6 inhibited liver fat deposition and decreased serum triglyceride levels and activity of aspartate transaminase and alanine transaminase. MBOAT2 (membrane-bound O-acyltransferase domain containing 2) was directly targeted by miR-130a-5p, which was downregulated in the liver of NAFLD laying hens but reversed after L. salivarius SNK-6 treatment. Downregulation of MBOAT2, L. salivarius SNK-6 supplementation in vivo, and L. salivarius SNK-6 cell culture treatment in vitro suppressed the mRNA expression of genes involved in the PPAR/SREBP pathway. In addition, 250 metabolites were identified in the supernatants of L. salivarius SNK-6 culture media, and most of them participated in metabolic pathways, including amino acid, carbohydrate, and lipid metabolism. Targeted metabolomic analysis revealed that acetate, butyrate, and propionate were the most abundant short-chain fatty acids, while cholic acid, ursodeoxycholic acid, chenodeoxycholic acid, and tauroursodeoxycholic acid were the four most-enriched bile acids among L. salivarius SNK-6 metabolites. This may have contributed to the reparative effect of L. salivarius SNK-6 in the NAFLD chicken model. Our study suggested that L. salivarius SNK-6 alleviated liver damage partly via the miR-130a-5p/MBOAT2 signaling pathway.

Although geese possess an adaptive physiological capacity for lipid storage, few candidate genes contributing to this ability are characterised. By comparing the genomes of individuals with extremely high and low fatty liver weights (FLW), candidate genes were identified, includingARAP2,GABRE, andIL6. Single-nucleotide polymorphisms in or near these genes were significantly (p < 0.05) associated with carcass traits (FLW) and biochemical indexes (very-low-density lipoprotein and N-terminal procollagen III), suggesting contribution to trait variation. A common variant at the 5′-end ofLCORLexplained ~ 18% and ~ 26% of the phenotypic variance in body weight with/without overfeeding and had significant effects on FLW (p < 0.01).ZFF36L1,ARHGEF1andIQCJ,involved in bile acid metabolism, blood pressure, and lipid concentration modulation, were also identified. The presence of highly divergent haplotypes within these genes suggested involvement in protection against negative effects from excessive lipids in the liver or circulatory system. Based on this and transcriptomic data, we concluded that geese hepatosteatosis results from severe imbalance between lipid accumulation and secretion, comparable to human non-alcohol fatty liver disease but involving other genes. Our results provided valuable insights into the genesis of geese fatty liver and detected potential target genes for treatment of lipid-related diseases.

Skeletal muscle satellite cells (SMSCs) are quiescent stem cells located in skeletal muscle tissue and function as the primary reservoir of myogenic progenitors for muscle growth and regeneration. However, the molecular and metabolic mechanisms governing their differentiation in geese remain largely unexplored. This study comprehensively examined the morphological, transcriptional, and metabolic dynamics of goose SMSCs across three critical differentiation stages: the quiescent stage (DD0), the differentiation stage (DD4), and the late differentiation stage (DD6). By integrating transcriptomic and metabolomic analyses, stage-specific molecular signatures and regulatory networks involved in SMSC differentiation were identified. Principal component analysis revealed distinct clustering patterns in gene expression and metabolite profiles across these stages, highlighting dynamic shifts in lipid metabolism and myogenesis. The PPAR signaling pathway emerged as a key regulator, with crucial genes such as PPARG, IGF1, ACSL5, FABP5, and PLIN1 exhibiting differentiation-dependent expression patterns. Notably, PPARG and IGF1 displayed negative correlations with adenosine and L-carnitine levels, suggesting their role in metabolic reprogramming during myotube formation. Additionally, MYOM2 and MYBPC1 exhibited stage-specific regulation and positively correlated with 2,3-dimethoxyphenylamine. This study provides a foundational framework for understanding muscle development and regeneration, offering valuable insights for both agricultural and biomedical research.

Muscle growth is a critical determinant of meat yield and quality in livestock. Although follistatin (FST) is recognized as a key regulator of skeletal muscle development and fat metabolism, its specific function in geese remains largely unexplored. In this study, we identified two transcript variants of goose FST (gFST) in Zhedong White geese: gFST-X1 (1125 bp), encoding a 343-amino acid protein with a 28-amino acid signal peptide and four conserved domains, and gFST-X2, which contains a 243 bp insertion within the gFST-X1 transcript. RT-qPCR analysis revealed that gFST mRNA expression varied across tissues from female embryos (25 days), adults (70 days), and laying geese (270 days), as well as in skeletal muscle satellite cells (SMSCs) at embryonic day 16 (E16d). Overexpression of gFST in SMSCs resulted in 3596 differentially expressed genes (DEGs), including 2247 upregulated and 1349 downregulated genes (padj < 0.01). Key stemness markers (PAX7, PAX3) and myogenic regulators (MYOG, MYOD, MYF5) were significantly downregulated, whereas genes associated with lipid metabolism (PPARG, FABP5, ACSL5) and myosin-related processes (MYO1D, MYO1F, MYO1E) were markedly upregulated (padj < 0.01). Functional enrichment analysis linked these DEGs to the TGF-β, PPAR signaling, fatty acid metabolism, and Notch signaling pathways. These transcriptomic findings were further validated by qRT-PCR. Collectively, our results demonstrate the dual regulatory role of gFST in skeletal muscle development and provide new mechanistic insights into muscle development in geese.

Bi-directional selection for increased and decreased 56-day body weights (BW56) has been applied to two lines of White Plymouth Rock chickens—the Virginia high (HWS) and low (LWS) body weight lines. Correlated responses have been observed, including negative effects on traits related to fitness. Here, we use high and low body weight as proxies for fitness. On a genome-wide level, relaxed lines (HWR, LWR) bred from HWS and LWS purged some genetic variants in the selected lines. Whole-genome re-sequencing was here used to identify individual loci where alleles that accumulated during directional selection were purged when selection was relaxed. In total, 11 loci with significant purging signals were identified, five in the low (LW) and six in the high (HW) body weight lineages. Associations between purged haplotypes in these loci and BW56 were tested in an advanced intercross line (AIL). Two loci with purging signals and haplotype associations to BW56 are particularly interesting for further functional characterization, one locus on chromosome 6 in the LW covering the sour-taste receptor gene PKD2L1, a functional candidate gene for the decreased appetite observed in the LWS and a locus on chromosome 20 in the HW containing a skeletal muscle hypertrophy gene, DNTTIP1.

Insulin-like growth factor 2 (IGF2) plays a pivotal role in regulating growth and development; however, its functional involvement in skeletal muscle satellite cells (SMSCs) remains incompletely understood. To elucidate the regulatory role of IGF2, goose SMSCs were engineered to overexpress IGF2 via lentiviral transduction, followed by comprehensive transcriptomic profiling. Comparative analysis revealed 2802 differentially expressed genes (DEGs) in IGF2-overexpressing cells relative to controls, comprising 1202 upregulated and 1600 downregulated genes. IGF2 overexpression markedly activated fibrogenic programs, as evidenced by the upregulation of AP-1 complex components (FOS, JUN), extracellular matrix-related genes (COL1A1, COL5A3), and Wnt signaling receptors (FZD1, FZD7). In contrast, genes involved in myogenic differentiation and contractile function were broadly suppressed, including key myogenic transcription factors (MEF2C, MEF2D), sarcomeric structural proteins (MYBPC1, ACTN2, MYOM3), and metabolic enzymes. Through the construction of protein–protein interaction networks coupled with functional enrichment analysis, we observed a concerted suppression of myogenic regulatory networks critical for myofiber formation. Quantitative real-time PCR validation further confirmed the reliability of the transcriptomic data. Collectively, these findings suggest that overexpression of IGF2 induces a phenotypic shift from myoblasts toward a fibroblast-like state, uncoupling proliferation from differentiation while enhancing fibrogenic identity. This study provides novel insights into IGF2-mediated regulatory mechanisms underlying skeletal muscle development and fibrotic processes.