The composition of skeletal muscle fiber types affects the quality of livestock meat and human athletic performance and health. L-arginine (Arg), a semi-essential amino acid, has been observed to promote the formation of slow-twitch muscle fibers in animal models. However, the precise molecular mechanisms are still unclear. This study investigates the role of Arg in skeletal muscle fiber composition and mitochondrial function through the mTOR signaling pathway. In vivo, 4-week C56BL/6J male mice were divided into three treatment groups and fed a basal diet supplemented with different concentrations of Arg in their drinking water. The trial lasted 7 weeks. The results show that Arg supplementation significantly improved endurance exercise performance, along with increased SDH enzyme activity and upregulated expression of the MyHC I, MyHC IIA, PGC-1α, and NRF1 genes in the gastrocnemius (GAS) and quadriceps (QUA) muscles compared to the control group. In addition, Arg activated the mTOR signaling pathway in the skeletal muscle of mice. In vitro experiments using cultured C2C12 myotubes demonstrated that Arg elevated the expression of slow-fiber genes (MyHC I and Tnnt1) as well as mitochondrial genes (PGC-1α, TFAM, MEF2C, and NRF1), whereas the effects of Arg were inhibited by the mTOR inhibitor rapamycin. In conclusion, these findings suggest that Arg modulates skeletal muscle fiber type towards slow-twitch fibers and enhances mitochondrial functions by upregulating gene expression through the mTOR signaling pathway.
Zearalenone (ZEA) is an estrogenic toxin produced by Fusarium species, which is widely distributed and posed a great health risk to both humans and farm animals. Reproductive disorders associated with ZEA such as premature puberty, infertility and abortion have plagued the animal husbandry, but the molecular mechanism is unclear. Because transforming growth factor-β1 (TGF-β1) signaling pathway is involved in the proliferation and apoptosis of cells, proliferating cell nuclear antigen (PCNA), B-cell lymphoma/leukemia-2 (BCL-2) and BCL-2 associated X protein (BAX) that all play indispensable roles in the normal development of the uterus, it is hypothesized that ZEA induces reproductive disorders is closely related to the expression of these genes. The objective of this study was to assess the effects of dietary ZEA at the concentrations of 0.5 to 1.5 mg/kg on the mRNA and protein expression of these genes in the uteri of post-weaning gilts and to explore the possible molecular mechanism. Forty healthy post-weaning female piglets (Duroc × Landrace × Large White) aged 38 d were randomly allocated to basal diet supplemented with 0 (Control), 0.5 (ZEA0.5), 1.0 (ZEA1.0), or 1.5 (ZEA1.5) mg/kg purified ZEA, and fed for 35 d. Piglets were euthanized at the end of the experiment and samples were taken and subjected to immunohistochemistry, qRT-PCR and Western blot analyses. The relative mRNA expressions of PCNA, BCL-2 and Smad3 in the uteri of post-weaning gilts increased linearly (p < 0.05) and quadratically (p < 0.05) as ZEA concentration increased in the diet. The relative protein expressions of PCNA, BAX, BCL-2, TGF-β1, Smad3, and phosphorylated Smad3 (p-Smad3) in the uteri of post-weaning gilts increased linearly (p < 0.05) and quadratically (p < 0.001) with an increasing level of ZEA. The results showed that uterine cells in the ZEA (0.5–1.5 mg/kg) treatments were in a high proliferation state, indicating that ZEA could accelerate the proliferation of uteri and promote the development of the uteri. At the same time, the results suggested that ZEA activates the TGF-β1/Smad3 signaling pathway, suggesting it plays an important role in accelerating the development of the uterus.
Zearalenone (ZEA) is a potent estrogenic mycotoxin known to disrupt reproductive functions, but its precise central neuroendocrine mechanisms remain unclear. This study investigated the effects of ZEA on the hypothalamic-pituitary Kiss1/GPR54 signaling pathway in weaned gilts. A total of 32 gilts were randomly assigned to four dietary treatments contained with 0, 0.15, 1.5, or 3.0 mg/kg ZEA for a 32-day feeding trial. Histopathology, immunohistochemistry, and mRNA/protein expression analyses of GPR30, Kiss1, GPR54, GnRH, and GnRHR in the hypothalamus and pituitary gland were conducted. ZEA exposure induced significant histological damage in both tissues. In the hypothalamus, Kiss1, GPR54, GnRH, and GnRHR exhibited a non-linear response, increasing at moderate doses and decreasing at 3.0 mg/kg ZEA, whereas GPR30 expression was continuously upregulated. In the pituitary gland, GnRHR showed a similar non-linear pattern. Furthermore, high-dose ZEA down-regulated pituitary Kiss1 and GPR54 while up-regulating GnRH and GPR30 expressions. In conclusion, ZEA induces reproductive neuroendocrine toxicity through a complex, dose-dependent modulation of the Kiss1/GPR54 signaling axis. The persistent upregulation of GPR30 suggests it acts as a crucial mediator in disrupting this endocrine feedback loop within the hypothalamus and pituitary gland.
Sustainable piglet farming faces challenges from weaning stress, which necessitates the exploration of effective, natural antimicrobial alternatives to enhance growth and gut health. So, this study evaluated the effects of algal oligosaccharide (OSA) supplementation (0, 200, 400, 600, 800 mg/kg) as a natural antimicrobial alternative. Results showed that OSA significantly (p < 0.05) improved slaughter performance and the apparent digestibility of nutrients (OM, CP, amino acids) and energy. OSA increasing serum glucose while decreasing urea nitrogen and cholesterol, suggesting a shift in energy substrate mobilization. Enhanced antioxidant capacity was evidenced by increased T-SOD and GSH-Px activities and reduced MDA content. Immunologically, OSA elevated serum IgA, IgM, and IL-10, while inhibiting pro-inflammatory cytokines (IL-1β, IL-6). In the jejunum, OSA obviously increased disaccharidase activities and sIgA levels. Microbial analysis revealed that OSA favorably modulated cecal microbiota by increasing the abundance of Firmicutes and beneficial genera while decreasing Proteobacteria and potential pathogens (e.g., Escherichia). In conclusion, dietary OSA improved antioxidant capacity, and immunity while optimizing nutrient utilization and gut microbiota. The optimal dosage was determined to be 600–800 mg/kg. These findings suggest that OSA serves as a promising antimicrobial alternative in piglet farming.
Whole sweet sorghum silage (WSS) is a locally available forage resource with potential application in sustainable swine production, yet its biological effects on the intestinal environment and production-related traits of heavy finishing pigs (defined here as pigs entering the trial at approximately 132 kg BW) remain unclear. This study evaluated the effects of replacing 20 percentage units of corn with WSS (on an as-fed basis) on growth performance, meat quality, jejunal morphology, and cecal bacterial composition. Seventy-two Duroc × Landrace × Yorkshire pigs were fed the corn-based control diet (CON) or the WSS diet for 30 d. Compared with CON, WSS reduced average daily gain and feed intake and increased the feed-to-gain ratio. It also decreased backfat thickness while increasing loin-eye area and marbling score. WSS reduced 48-h drip loss and increased inosine monophosphate concentrations in both the longissimus dorsi and psoas major muscles. Jejunal villus height and the villus-height-to-crypt-depth ratio were increased in WSS-fed pigs. No significant differences were detected in alpha-diversity indices or unweighted UniFrac community structure between diets, whereas an exploratory linear discriminant analysis effect size procedure identified Streptosporangium , Kribbella , Oxalobacter , and Planifilum as taxa associated with WSS and Bacteroides -related features as associated with CON. Because the diets were not nutrient-matched, these responses reflect the complete dietary contrast. Overall, WSS was associated with a pattern of reduced growth performance accompanied by selected changes in carcass and meat-quality traits, concurrent jejunal morphological adaptation, and exploratory cecal bacterial signals that warrant mechanistic validation.