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

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 gene (gs) decreased and gluconeogenesis-related genes (pepck and g6p) were disrupted, leading to reduced liver glycogen level and hepatic metabolic disorder. Dietary Zn excess group increased the glucose metabolism-related genes expression (gs, pepck, and g6p) and liver glycogen. Dietary Zn deficiency group caused liver lipid accumulation, while dietary Zn excess group alleviated liver lipid metabolism. 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 release was significantly elevated in the Zn deficiency group ( P  > 0.05) but significantly decreased in the Zn excess group ( P  > 0.05). By analyzing physical barrier-related genes expression of genes (occludin, claudin3 and claudin15), we found that both dietary Zn deficiency and excess induced intestinal physical barrier impaired. High-throughput sequencing of intestinal microbiota revealed that dietary Zn levels significantly altered the β-diversity of the intestinal microbial community ( P  > 0.05), which was confirmed by non-metric multidimensional scaling (NMDS) analysis. Proteobacteria was 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.