Immune stress is a major challenge in the poultry industry, impairing growth, liver metabolism, and intestinal health. This study investigated whether dietary sodium butyrate (NaBu) could alleviate lipopolysaccharide (LPS)-induced immune stress in yellow-feathered broilers through modulation of the gut-liver axis. A total of 96 male broilers were assigned to a 2 × 2 factorial design with NaBu supplementation and LPS challenge as the main factors. Results showed that NaBu significantly improved growth performance, as reflected by increased average daily gain and average daily feed intake (P < 0.05). NaBu also markedly optimized serum lipid metabolism by decreasing total cholesterol (P < 0.05), and LDL-C (P < 0.05), while increasing HDL-C (P < 0.05). Moreover, NaBu significantly alleviated hepatic inflammation and oxidative injury, evidenced by reduced AST/ALT (P < 0.05) and MDA (P < 0.05) levels and enhanced T-AOC (P < 0.05) and SOD activities (P < 0.05). Intestinal barrier function was also restored, with significant upregulation of Claudin-1, Occludin, ZO-1, and MUC2 in the jejunum (P < 0.05). NaBu also modulated the PPARα/SIRT-1-AMPK signaling pathway, reduced pro-inflammatory cytokine expression, and reshaped the cecal microbiota by increasing beneficial bacteria (e.g., Blautia and Alistipes) and suppressing potential pathogens (e.g., Ruminococcus_torques_group and Escherichia-Shigella). These findings demonstrate that NaBu effectively mitigates LPS-induced immune stress by improving liver function, maintain intestinal homeostasis, supporting its potential as a green feed additive in poultry production.

In the efforts towards germplasm innovation of livestock and poultry, strategies to improve meat quality have faced some increasingly challenging and dynamic concerns. Intramuscular fat (IMF) content and backfat thickness are two important traits contributing to meat quality. MicroRNAs (miRNAs)—a class of endogenous noncoding RNAs maintaining cell homeostasis by inhibiting target gene expression—have been proven as critical regulators of body fat deposition, thus affecting farm animal production. Our previous in vitro and in vivo models of pigs have clarified that miR-130b overexpression can obviously suppress adipogenesis of subcutaneous preadipocytes and lower backfat thickness. However, the way miR-130b regulates proliferation and adipogenesis of primary cultured porcine intramuscular preadipocytes (PIMPA) and the underlying mechanism are still unknown. PIMPA derived from longissimus dorsi muscle were employed to examine the role of miR-130b in proliferation and adipogenesis and to further elucidate its underlying mechanism. Lipid deposition in cytoplasm was evaluated by TG quantification and ORO-staining, and EDU-staining was employed to measure cell proliferation. Adipogenic and proliferation-related gene expression were conducted by qPCR and Western blot. MiR-130b overexpression markedly stimulated proliferation of PIMPA by increasing cell cycle-related gene expression. Furthermore, overexpression of miR-130b significantly inhibited adipogenic differentiation of PIMPA, mainly by inhibiting expression of adipogenic differentiation marker genes PPAR-γ and SREBP1. In addition, we proved that miR-130b significantly inhibited expression of PPAR-γ downstream target genes and ultimately repressed adipogenesis. Ssc-miR-130b accelerated proliferation but inhibited adipogenic differentiation of PIMPA, contributing to an enhanced knowledge of the function of ssc-miR-130b in lipid deposition, and providing potential implications for enhancing pork quality.

In intensive livestock and poultry farming, chronic stress poses a significant threat to animal health, primarily through its impact on butyric acid levels and intestinal microbiota balance. In our previous study, we found that the intestinal butyric acid level was significantly reduced in chronic stress models, suggesting that butyrate supplementation should be an effective anti-chronic stress strategy. Therefore, in this study, we aimed to investigate whether sodium butyrate (NaBu) prevents chronic stress-induced lipid metabolism disorders and intestinal injury by reducing intestinal damage and remodeling the microbiota. In vitro models, IEC-6 cells, a small intestinal epithelial cell line, were divided into three groups, including control (CON), corticosterone (CORT, 400 μM) and CORT + NaBu (400 μM CORT + 1 mM NaBu). In vivo models, sixty mice were divided into CON, CORT (intraperitoneal injection of 20 mg/kg CORT) and CORT + NaBu (intraperitoneal injection of 20 mg/kg CORT + intragastric gavage with 200 mg/kg NaBu). The results showed that NaBu effectively reversed CORT-induced IEC-6 migration inhibition, inhibited apoptosis, and restored barrier function, which was associated with downregulated IL-12 and upregulated LRP5 expression. In addition, NaBu administration prevented anorexia, promoted body weight gain, and improved lipid metabolism in a corticosterone-induced chronic stress model in mice, as evidenced by a significant reduction of serum alkaline phosphatase (AKP) and Low-density lipoprotein cholesterol (LDL-C). Histopathological staining and scanning electron microscopy analyses revealed that NaBu treatment restored the normal villi morphology of the small intestinal villi and mitigated epithelial cell damage caused by CORT. 16S rRNA sequencing demonstrated that NaBu facilitated intestinal microbiota remodeling, marked by significant increases in Desulfobacterota and Bacillus abundance and decreases in Proteobacteria and Enterorhabdus abundances. Furthermore, analysis suggests that CORT-induced chronic stress may disrupt the cecal microbiota-metabolite axis and lead to intestinal injury and metabolic abnormalitiesbased on previous metabolic evidence and current results of microbial imbalance and downstream metabolic/intestinal abnormalities. These findings indicate that NaBu exerts a protective role in the prevention of chronic stress-related disorders, providing a potential prophylactic strategy for animals at high risk of stress exposure.