The differences of pork quality characteristics among different pig breeds mainly came from the differences in myofiber type compositions. Growing evidence indicated the key role of miRNAs in myofiber specification. In the present study, we found that miR-152 is more abundant in the slow-twitch myofiber-enriched muscles. However, its role in myofiber type transformation and myogenesis is largely unknown. Overexpression of miR-152 in porcine myotubes promoted the formation of slow-twitch myofibers and myogenesis. While, inhibition of miR-152 expression showed the opposite effect to miR-152 mimics transfection. The luciferase reporter analysis confirmed that miR-152 straightly targets the 3′-untranslated region (3’-UTR) of uncoupling protein 3 (UCP3) to cause its post-transcriptional inhibition in the protein level. The knockdown of UCP3 by siRNA showed the similar effect of miR-152 on myofiber type transition. Furthermore, the rescue experiment in the porcine myotube transfected with miR-152 mimics or/and UCP3 overexpression plasmid with or without the 3’UTR revealed that UCP3 mediates the action of miR-152 in slow-twitch myofiber formation. Taken together, our findings proposed a novel molecular mechanism through which miR-152 epigenetically regulates meat quality via promoting slow-twitch myofiber formation and skeletal myogenesis.

This study was conducted to investigate the effects and mechanisms of all-trans lycopene on intestinal health by establishing lipopolysaccharide-induced (LPS-induced) jejunal inflammation model. Dietary lycopene supplementation enhanced serum and jejunum antioxidant capacity. Lycopene significantly reduced LPS-induced upregulation of toll-like receptor-4 (TLR-4) and nuclear factor kappa-B (NF-κB), suggesting that lycopene reduced the activation of TLR-4/NF-κB signaling pathway induced by LPS challenge, and further protected mice from LPS induced jejunal inflammation. Furthermore, lycopene increased jejunal zonula occludens-1 (ZO-1) protein expression that was reduced by LPS challenge, and increased abundance of Rikenella, Lachnospiraceae_NK4A136_group and Mucispirillum potentially associated with reducing gut inflammation. Overall, these results showed that pretreatment with lycopene can improve jejunal inflammation and ensure intestinal health in mice by improving antioxidant capacity, intestinal barrier function, microorganisms potentially associated with anti-inflammatory effects and reducing the activation of TLR-4/NF-κB signaling pathway by LPS. We provided a new insight into lycopene prevented LPS-induced jejunal inflammation by corresponding alterations in serum metabolites and gut microbiota, improving antioxidant capacity and regulating the TLR-4/NF-κB signaling pathway in mice.

This study investigated whether the supplementation of prebiotic inulin to gestating sows programmatically affects offspring growth performance and meat quality while exploring its epigenetic effects through histone acetylation modulation. After mating, sixty multiparous sows (Landrace × Yorkshire; parity 2–3) were assigned to a 2 × 2 factorial arrangement with inulin (0% vs. 1.5%) and fat (0% or 5%) supplementation until farrowing. Post-weaning, five litters (10 piglets per litter) per treatment were selected and maintained in their original litter for fattening under standardized feeding. The results demonstrated that maternal inulin supplementation during gestation accomplished the following: (1) Increased offspring liver index by 13.4% at weaning and 6.8% at finishing (p < 0.05) while reducing the finishing-phase backfat thickness by 11.6% (p < 0.01), with a significant inulin × fat interaction attenuating fat-induced abdominal lipid accumulation at weaning (p = 0.05). (2) Decreased longissimus dorsi muscle lightness (L*) by 4.5% in finishing pigs (p = 0.02) without altering the other meat quality parameters. (3) Suppressed offspring liver lipid deposition at birth and finishing (p < 0.05), concomitant with upregulated hepatic PGC-1α and CPT1A expression (p < 0.05). (4) Elevated neonatal serum butyrate by 15.6% (p = 0.06) while inhibiting hepatic histone deacetylase (HDAC) activity and enhancing histone H3/H4 acetylation (p < 0.01). These findings suggest that maternal inulin supplementation during gestation mitigates offspring hepatic lipid deposition through butyrate-mediated epigenetic regulation, where microbial-derived butyrate from inulin fermentation inhibits HDAC activity, enhances histone acetylation levels, and upregulates fatty acid β-oxidation gene expression. This study provides novel mechanistic insights into how maternal dietary fiber nutrition programs offspring development through epigenetic reprogramming.

This study investigated the effects of different dietary net energy (NE) concentrations on the growth performance, carcass traits, meat quality, and cecal microbiota of feed restricted pigs. In total, 32 Sichuan-Tibetan black pigs with similar initial body weights (25.98 ± 0.27 kg) were divided into four groups: a control group (ad libitum feeding, 2330 kcal NE kg⁻¹) and three treatment groups (twice-daily feeding with NE concentrations of 2330, 2370, and 2410 kcal kg⁻¹, respectively). This feeding trial lasted for 19 weeks. Decreasing feeding frequency reduced the final body weight, average daily gain (ADG), average daily feed intake (ADFI), and backfat thickness (p < 0.05). Elevation of NE concentration increased the final body weight, ADG, and fat deposition (p < 0.05), which eventually led to an improvement in feed efficiency (p < 0.05). The expression of lipid-metabolism-related genes was significantly downregulated as NE concentration increased under a restricted feeding regime (p < 0.05). Cecal microbiota analysis showed that a high NE concentration decreased microbial alpha-diversity (p < 0.05). These findings suggest that under the restricted feeding condition, 2370 kcal NE kg⁻¹ can improve feed efficiency and optimize carcass composition simultaneously, which are associated with the changes in gut microbiota structure and the lipid-metabolism-related gene expression.

The purpose of this study was to examine the effect of daidzein on the proliferation of porcine mammary epithelial cells (PMECs) and elucidate the underlying molecular mechanisms. PMECs were treated with varying daidzein or rapamycin levels, and then cell proliferation and mTOR pathway protein expression were detected. When the concentration of daidzein added was in the range of 0–80 μM, cell proliferation was significantly promoted (p < 0.05). These results were in agreement with those obtained using the 5-ethynyl-2′-deoxyuridine (EdU) assay. Daidzein administration at 20 and 40 μM concentrations triggered significant activation of the mTOR signaling cascade and enhanced expression of downstream cell-cycle-regulatory proteins (cyclin D1) (p < 0.05). Moreover, exposure to 40 μM daidzein attenuated apoptotic signaling, as evidenced by reduced levels of Bax protein and cleaved caspase-3 (p < 0.05). These effects were reversed when rapamycin was used to inhibit the mTOR pathway. In conclusion, our findings suggest that daidzein activates PMEC proliferation via the mTOR pathway. The present work not only characterizes new functional properties of daidzein but also establishes mechanistic evidence supporting its role in augmenting sow lactation efficiency.