Selenium is an indispensable essential micronutrient for humans and animals, and it can affect biological functions by combining into selenoproteins. The purpose of this study was to investigate the effects of 2-hydroxy-4-methylselenobutanoic acid (HMSeBA) on the antioxidant performance, immune function, and intestinal microbiota composition of gilts. From weaning to the 19th day after the second estrus, 36 gilts (Duroc × Landrace × Yorkshire) were assigned to three treatments: control group, sodium selenite group (0.3 mg Se/kg Na2SeO3), and HMSeBA group (0.3 mg Se/kg HMSeBA). Dietary supplementation with HMSeBA improved the gilts tissue selenium content (except in the thymus) and selenoprotein P (SelP1) concentration when compared to the Na2SeO3 or control group. Compared with the control group, the antioxidant enzyme activity in the tissues from gilts in the HMSeBA group was increased, and the concentration of malondialdehyde in the colon had a decreasing trend (p = 0.07). Gilts in the HMSeBA supplemented group had upregulated gene expression of GPX2, GPX4, and SelX in spleen tissue, TrxR1 in thymus; GPX1 and SelX in duodenum, GPX3 and SEPHS2 in jejunum, and GPX1 in the ileum tissues (p < 0.05). In addition, compared with the control group, the expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemotactic protein-1 (MCP-1) in the liver, spleen, thymus, duodenum, ileum, and jejunum of gilts in the HMSeBA group were downregulated (p < 0.05), while the expression of interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) in the liver, thymus, jejunum, and ileum were upregulated (p < 0.05). Compared with the control group and the Na2SeO3 group, HMSeBA had increased concentration of serum cytokines interleukin-2 (IL-2) and immunoglobulin G (IgG; p < 0.05), increased concentration of intestinal immunoglobulin A (sIgA; p < 0.05), and decreased concentration of serum IL-6 (p < 0.05). Dietary supplementation with HMSeBA also increased the abundance of intestinal bacteria (Ruminococcaceae and Phascolarctobacterium; p < 0.05) and selectively inhibited the abundance of some bacteria (Parabacteroides and Prevotellaceae; p < 0.05). In short, HMSeBA improves the antioxidant performance and immune function of gilts, and changed the structure of the intestinal microflora. And this study provided data support for the application of HMSeBA in gilt and even pig production.
Background We have previously found that the energy level in sows affects the activation of primordial follicles. Glucose is the primary metabolic substrate of dietary energy and its effect and mechanism of action with regards to the activation and development of primordial follicle remain unclear. Studies utilizing several different animal cells have shown that energy stress, induced by glucose starvation, activates AMPK and participates in a variety of cellular processes by regulating the Hippo and mTOR signaling pathways. However, whether glucose can affect primordial follicle activation through the above pathways has not been reported. Methods We developed an in vitro culture system for mouse ovaries to investigate the effects of glucose on the primordial follicle activation. Protein expression of AMPK‐Hippo‐YAP and AMPK‐mTOR pathway was investigated under glucose starvation and optimal glucose level treatment. Then, ovaries were treated with AICAR or Compound C in vitro to explore the effect of AMPK activation or inhibition on primordial follicle activation, and the changes of AMPK‐Hippo‐YAP and AMPK‐mTOR signaling pathways. Finally, investigated the signaling pathways affected by glucose potentially affecting the primordial follicle activation in vivo. Results The glucose was an essential nutrient for primordial follicle activation and we identified 25 mM glucose as the optimal level ( P < .05) for the primordial follicle activation in vitro. The glycolysis pathway was involved in primordial follicle activation ( P < .05) of ovaries cultured in vitro. The glucose affected the activation of primordial follicles in vitro through AMPK/mTOR signaling pathway by AMPK activation or inhibition treatment and follicle ratio count ( P < .05). Moreover, glucose affected the primordial follicle activation of ovary in vivo via mTOR signaling pathway. Conclusions This study demonstrates that glucose affects the primordial follicle activation through the AMPK/mTOR rather than the AMPK/Hippo signaling pathway.
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