Xianping Shao

Zinc (Zn) is an essential trace element that plays important roles in growth, digestion, antioxidant defense, immunity, and inflammation regulation in fish. This study investigated the effects of graded dietary Zn levels on growth performance, serum biochemistry, digestive enzyme activity, zinc transporter expression, antioxidant capacity, immune responses, and inflammatory regulation in juvenile black carp (Mylopharyngodon piceus). Six isonitrogenous and isoenergetic diets were formulated to contain 27.95, 34.38, 44.90, 66.52, 116.14, and 199.56 mg/kg Zn by supplementing ZnSO₄·7H₂O. Juvenile fish with an initial weight of 2.88 ± 0.12 g were fed the experimental diets for 60 days in triplicate tanks. Growth performance increased with dietary Zn and then plateaued at 44.90–199.56 mg/kg; broken-line regression estimated the optimal dietary Zn requirement at 44.6 mg/kg. Adequate Zn supplementation also reduced whole-body lipid content, increased digestive enzyme activities, improved serum HDL-C and ALP levels, and decreased AST and ALT activities. In addition, adequate dietary Zn (44.90 mg/kg) significantly modulated the expression of zinc transporter genes in the liver and intestine. Adequate dietary Zn supplementation enhanced antioxidant capacity by activating the Nrf2/Keap1 signaling pathway, improved intestinal immunity, and strengthened barrier function by increasing the expression of tight junction proteins and mucins. Moreover, adequate dietary Zn could alleviate inflammatory responses by upregulating anti-inflammatory factors and downregulating pro-inflammatory cytokines via the MAPK14 signaling pathway. These findings suggest that dietary zinc at 44.60 mg/kg is sufficient to promote growth, antioxidant status, immune function, and intestinal health in juvenile black carp.

Copper is an essential trace element for fish, yet defining its optimal dietary levels remains a challenge in aquaculture nutrition. This meta-analysis quantitatively evaluated the effects of dietary copper supplementation on fish growth performance, superoxide dismutase activity, tissue copper levels, and body composition. Significant benefits in terms of fish survival, weight gain, hepatic Cu–Zn superoxide dismutase activity, and copper concentrations in the whole body, liver, and intestine were observed following supplementation with varying levels of copper, while excessive copper intake (> 25 mg/Kg) led to trade-offs in feed conversion, protein efficiency, and condition factor. Meta-regression identified that dietary copper levels, source of copper, feeding duration, and main protein content in the diet significantly moderated effect sizes of weight gain. Piecewise regression showed that the optimal dietary copper concentration determined to be 5.7 mg/kg. Structural equation models revealed that increased dietary protein and feeding duration enhance effect sizes of weight gain through elevated copper and crude protein levels in the body. This study provides a nuanced understanding of dietary copper supplementation effects on fish physiology, offering valuable insights for formulating diets that enhance aquaculture productivity while maintaining fish health.

This study evaluated effects of high starch (20%) on hematological variations, glucose and lipid metabolism, antioxidant ability, inflammatory responses, and histopathological lesions in largemouth bass. Results showed hepatic crude lipid and triacylglycerol (TAG) contents were notably increased in fish fed high starch. High starch could increase counts of neutrophils, lymphocytes, monocytes, eosinophils, and basophils and serum contents of TAG, TBA, BUN, and LEP (p < 0.05). There were increasing trends in levels of GLUT2, glycolysis, gluconeogenesis, and LDH in fish fed high starch through the AKT/PI3K signal pathway. Meanwhile, high starch not only triggered TAG and cholesterol synthesis, but mediated cholesterol accumulation by reducing ABCG5, ABCG8, and NPC1L1. Significant increases in lipid droplets and vacuolization were also shown in hepatocytes of D3–D7 groups fed high starch. In addition, high starch could decrease levels of mitochondrial Trx2, TrxR2, and Prx3, while increasing ROS contents. Moreover, high starch could notably increase amounts of inflammatory factors (IL-1β, TNF-α, etc.) by activating NLRP3 inflammasome key molecules (GSDME, caspase 1, etc.). In conclusion, high starch could not only induce metabolic disorders via gluconeogenesis and accumulation of glycogen, TAG, and cholesterol, but could disturb redox homeostasis and cause inflammatory responses by activating the NLRP3 inflammasome in largemouth bass.