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<p>As an essential trace element in aquatic organisms, Zn plays a crucial role in normal physiological functions of fish. However, both deficient and excessive dietary Zn levels exert adverse effects on the organism. Thus, the current study aimed to investigate the effects of deficiency and excess Zn on growth performance, glycolipid metabolism, and intestinal homeostasis of juvenile golden pompano (<i>Trachinotus ovatus</i>). The fish were fed three experimental diets with different Zn levels: 38 (Zn deficiency), 84.7 (adequate Zn), and 582 (Zn excess) mg/kg Zn for 8&#xa0;weeks, respectively. Compared with the adequate dietary Zn group, dietary Zn deficiency group showed no significant difference in growth performance (<i>p</i> &gt; 0.05), and dietary Zn excess group significantly decreased the weight gain and specific growth rate (<i>p</i> &lt; 0.05). In the dietary Zn deficiency group, glycogenesis-related expression was decreased and gluconeogenesis-related expression was altered, leading to reduced liver glycogen level and hepatic metabolic disorder. Dietary Zn excess induced higher expression of <i>gs</i>, <i>pepck</i> and <i>g6p</i> and increased liver glycogen accumulation. Dietary Zn deficiency led to excessive lipid deposition in the liver. By contrast, excess dietary Zn mitigated hepatic lipid metabolic dysfunction. This was evidenced by upregulated lipogenic genes (srebp-1, ppar-γ, and acc), downregulated lipolytic genes (lpl, ppar-α, and cd36), and oil red O staining. Intestinal pro-inflammatory cytokine gene expression was significantly upregulated in the Zn deficiency group (<i>p</i> &lt; 0.05). By analyzing the expression of physical barrier-related genes (occludin, claudin3, and claudin15), we found that both dietary Zn deficiency and excess induced intestinal physical barrier impairment. High-throughput sequencing of intestinal microbiota revealed that dietary Zn levels showed clear separation in the β-diversity of the intestinal microbial community, which was confirmed by non-metric multidimensional scaling (NMDS) analysis. Proteobacteria were identified as the core phylum across all communities. Network analysis indicated that the microbial network, whose structure was modulated by differential dietary Zn levels, conformed to the “small world” characteristic. In conclusion, dietary Zn deficiency resulted in liver lipid deposition and impaired glucose metabolism, whereas dietary Zn excess impaired the growth performance. Furthermore, both dietary Zn deficiency and dietary Zn excess disrupted intestinal homeostasis, while adequate Zn group mitigated these abnormalities.</p>

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Effects of dietary Zn deficiency and excess on growth performance, glycolipid metabolism, and intestinal homeostasis of juvenile golden pompano (Trachinotus ovatus)

  • 期刊论文

  • 发表日期：

    2026年6月30日

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  • Hongkai Ye,
  • Zhanzhan Wang,
  • Jun Wang,
  • Yun Wang,
  • Zhong Huang,
  • Wei Yu,
  • Heizhao Lin,
  • Zhenhua Ma,
  • Zhenyan Cheng,
  • Chuanpeng Zhou

摘要

As an essential trace element in aquatic organisms, Zn plays a crucial role in normal physiological functions of fish. However, both deficient and excessive dietary Zn levels exert adverse effects on the organism. Thus, the current study aimed to investigate the effects of deficiency and excess Zn on growth performance, glycolipid metabolism, and intestinal homeostasis of juvenile golden pompano (Trachinotus ovatus). The fish were fed three experimental diets with different Zn levels: 38 (Zn deficiency), 84.7 (adequate Zn), and 582 (Zn excess) mg/kg Zn for 8 weeks, respectively. Compared with the adequate dietary Zn group, dietary Zn deficiency group showed no significant difference in growth performance (p > 0.05), and dietary Zn excess group significantly decreased the weight gain and specific growth rate (p < 0.05). In the dietary Zn deficiency group, glycogenesis-related expression was decreased and gluconeogenesis-related expression was altered, leading to reduced liver glycogen level and hepatic metabolic disorder. Dietary Zn excess induced higher expression of gs, pepck and g6p and increased liver glycogen accumulation. Dietary Zn deficiency led to excessive lipid deposition in the liver. By contrast, excess dietary Zn mitigated hepatic lipid metabolic dysfunction. This was evidenced by upregulated lipogenic genes (srebp-1, ppar-γ, and acc), downregulated lipolytic genes (lpl, ppar-α, and cd36), and oil red O staining. Intestinal pro-inflammatory cytokine gene expression was significantly upregulated in the Zn deficiency group (p < 0.05). By analyzing the expression of physical barrier-related genes (occludin, claudin3, and claudin15), we found that both dietary Zn deficiency and excess induced intestinal physical barrier impairment. High-throughput sequencing of intestinal microbiota revealed that dietary Zn levels showed clear separation in the β-diversity of the intestinal microbial community, which was confirmed by non-metric multidimensional scaling (NMDS) analysis. Proteobacteria were identified as the core phylum across all communities. Network analysis indicated that the microbial network, whose structure was modulated by differential dietary Zn levels, conformed to the “small world” characteristic. In conclusion, dietary Zn deficiency resulted in liver lipid deposition and impaired glucose metabolism, whereas dietary Zn excess impaired the growth performance. Furthermore, both dietary Zn deficiency and dietary Zn excess disrupted intestinal homeostasis, while adequate Zn group mitigated these abnormalities.