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This study was conducted to investigate the influence of zinc (Zn) supplementation on growth performance, intestinal development and intestinal barrier function in Pekin ducks. A total of 480, one-day-old male Pekin ducks were divided into 6 groups with 8 replicates: 0 mg/kg Zn, 0 mg/kg Zn +0.5 mg/kg lipopolysaccharide (LPS), 30 mg/kg Zn, 30 mg/kg Zn +0.5 mg/kg LPS, 120 mg/kg Zn, 120 mg/kg Zn +0.5 mg/kg LPS. The duck primary intestinal epithelial cells (DIECs) were divided into 6 groups: D-Zn (Zinc deficiency, treated with 2 µmol/L zinc Chelator TPEN), A-Zn (Adequate Zinc, basal medium), H-Zn (High level of Zn, supplemented with 20 µmol/L Zn), D-Zn + 20 µg/mL LPS, A-Zn + 20 µg/mL LPS, H-Zn + 20 µg/mL LPS. The results were as follows: in vivo, with Zn supplementation of 120 mg/kg reduced LPS-induced decrease of growth performance and intestine damage (P < 0.05), and increased intestinal digestive enzyme activity of Pekin ducks (P < 0.05). In addition, Zn supplementation also attenuated LPS-induced intestinal epithelium permeability (P < 0.05), inhibited LPS-induced the expression of proinflammatory cytokines and apoptosis-related genes (P < 0.05), as well as reduced LPS-induced the intestinal stem cells mobilization of Pekin ducks (P < 0.05). In vitro, 20 µmol/L Zn inhibited LPS-induced expression of inflammatory factors and apoptosis-related genes (P < 0.05), promoted the expression of cytoprotection-related genes, and attenuated LPS-induced intestinal epithelium permeability in DIECs (P < 0.05). Mechanistically, 20 µmol/L Zn enhanced tight junction protein markers including CLDN-1, OCLD, and ZO-1 both at protein and mRNA levels (P < 0.05), and also increased the level of phosphorylation of TOR protein (P < 0.05) and activated the TOR signaling pathway. In conclusion, Zn improves growth performance, digestive enzyme activity, and intestinal barrier function of Pekin ducks. Importantly, Zn also reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins and activating the TOR signaling pathway. [ABSTRACT FROM AUTHOR]

Manganese (Mn) is a trace element present in all tissues and is essential for animal growth and health; it also has an antioxidant capacity in tissues. The effect of Mn on meat quality and the mechanism of fat deposition of the breast muscle is still unclear. Therefore, the present study aimed to investigate the effect of Mn supplementation on the growth performance, meat quality, the activity and transcription of antioxidant enzymes, and fatty acid profile in the breast muscle, and the Mn deposition in tissues of Pekin ducks. A total of 896 one-day-old Pekin ducks were allocated into 7 groups, with 8 replicates, each replicate containing 16 ducks. The treatment diets consisted of basal diet supplemented with manganese sulfate at levels 30, 60, 90, 120, 150, 240 mg/kg (as Mn). Results showed that ducks fed diets supplemented with Mn had no effect on the growth performance but decrease in the feed-to-gain ratio of day 1–14 (P < 0.01). Dietary Mn increased significantly the a∗ (redness) value of the duck breast meat at 24 h and intramuscular fat (P < 0.05), and decreased drip loss and shear force of the breast meat (P < 0.05). Manganese supplement significantly reduced the malondialdehyde content (P < 0.05), and significantly increased the mRNA expressions of manganese superoxide dismutase, thioredoxin 2, peroxiredoxin 3, and catalase (P < 0.05). About the fatty acid profile, dietary Mn increased (P < 0.05) the proportions of the C20 family. Manganese accumulation in the heart, breast muscle, and tibia was increased with Mn supplementation (P < 0.05), and Mn content of the heart conforms to the quadratic curve. Besides, Mn supplementation notably increased mRNA expression in genes involved in lipogenesis and deposition and decreased in genes associated with lipolytic in the breast muscle. These findings reveal that dietary Mn could improve meat quality and enhance antioxidant activity and intramuscular fat, which via regulated gene expression involved in lipogenesis and lipolytic. [ABSTRACT FROM AUTHOR]