ArticleJournal of animal science and biotechnology2024
Zinc glycine chelate ameliorates DSS-induced intestinal barrier dysfunction via attenuating TLR4/NF-κB pathway in meat ducks.
Article in Journal of animal science and biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Effects of commercial direct-fed microbials and zinc-methionine supplements on growth performance in preweaning Holstein calves under commercial rearing conditions.Veterinary and animal science · 2026Article
- Food-Derived Zinc-Chelating Peptides: Coordination Chemistry, Intestinal Transport, and Nutritional Functionality.Nutrients · 2026Review
- Physicochemical properties of raw potato starch and its protective effect on bone quality in meat ducks with enteritis.Poultry science · 2026Article
- Bariatric and metabolic surgery improves glycolipid metabolism via bile acid regulation and intestinal barrier repair in T2DM patients.Journal of medical biochemistry · 2026Article
- Zinc gluconate ameliorates antibiotics/PGN-induced intestinal injury via modulating the gut barrier, macrophages immunity and gut microbiota.Frontiers in microbiology · 2026Article
- Intestinal inflammation disrupts energy metabolism in layer pullets: insights into energy partitioning and intestinal metabolomic profiling.Journal of animal science and biotechnology · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundZinc glycine chelate (Zn-Gly) has anti-inflammation and growth-promoting properties; however, the mechanism of Zn-Gly contribution to gut barrier function in Cherry Valley ducks during intestinal inflammation is unknown. Three-hundred 1-day-old ducks were divided into 5 groups (6 replicates and 10 ducks per replicate) in a completely randomized design: the control and dextran sulfate sodium (DSS) groups were fed a corn-soybean meal basal diet, and experimental groups received supplements of 70, 120 or 170 mg/kg Zn in form of Zn-Gly. The DSS and treatment groups were given 2 mL of 0.45 g/mL DSS daily during d 15-21, and the control group received normal saline. The experiment lasted 21 d.
resultsCompared with DSS group, 70, 120 and 170 mg/kg Zn significantly increased body weight (BW), villus height and the ratio of villus to crypt, and significantly decreased the crypt depth of jejunum at 21 d. The number of goblet cells in jejunal villi in the Zn-Gly group was significantly increased by periodic acid-Schiff staining. Compared with control, the content of intestinal permeability marker D-lactic acid (D-LA) and fluxes of fluorescein isothiocyanate (FITC-D) in plasma of DSS group significantly increased, and 170 mg/kg Zn supplementation significantly decreased the D-LA content and FITC-D fluxes. Compared with control, contents of plasma, jejunum endotoxin and jejunum pro-inflammatory factors IL-1β, IL-6 and TNF-α were significantly increased in DSS group, and were significantly decreased by 170 mg/kg Zn supplementation. Dietary Zn significantly increased the contents of anti-inflammatory factors IL-10, IL-22 and sIgA and IgG in jejunum. Real-time PCR and Western blot results showed that 170 mg/kg Zn supplementation significantly increased mRNA expression levels of CLDN-1 and expression of OCLN protein in jejunum, and decreased gene and protein expression of CLDN-2 compared with DSS group. The 120 mg/kg Zn significantly promoted the expressions of IL-22 and IgA. Dietary Zn-Gly supplementation significantly decreased pro-inflammatory genes IL-8 and TNF-α expression levels and TNF-α protein expression in jejunum. Additionally, Zn significantly reduced the gene and protein expression of TLR4, MYD88 and NF-κB p65.
conclusionsZn-Gly improved duck BW and alleviated intestinal injury by regulating intestinal morphology, barrier function and gut inflammation-related signal pathways TLR4/MYD88/NF-κB p65.
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