Hu, Xiuchuan, Wang, Rui, Kille, Peter ![]() Item availability restricted. |
![]() |
PDF
- Accepted Post-Print Version
Restricted to Repository staff only until 26 March 2026 due to copyright restrictions. Download (832kB) |
Abstract
Zinc and several physiologically relevant ligands of the Aryl Hydrocarbon Receptor (AHR) are nutrients that promote intestinal barrier function. We have identified that AHR activation upregulates the expression of zinc importers in the intestinal epithelium to increase intracellular zinc concentrations, which leads to improved epithelial barrier function. Here, we investigated if an amino acid chelate of zinc, in cooperation with AHR activation, can improve the barrier function of a differentiated Caco-2 cell epithelium. Functional assays of the Caco-2 cell epithelium demonstrate that both ZnSO and a lysine and glutamic acid chelate of Zn, in combination with the physiological AHR agonist 6-formylindolo[3,2-b]carbazole (FICZ), increase expression of tight junction proteins at the mRNA and protein levels. FICZ increases uptake of zinc into the epithelium in the presence of ZnSO or the amino acid Zn chelate in the medium to equal extents. We conclude that the lysine and glutamic acid chelate of Zn is as efficacious as ZnSO in reducing permeability of the Caco-2 cell epithelium in the presence of FICZ. The results suggest that dietary supplementation with bioavailable forms of zinc together with nutritional AHR agonists may be beneficial in improving gut barrier function and help prevent inflammatory bowel disease (IBD). [Abstract copyright: Copyright © 2025. Published by Elsevier Inc.]
Item Type: | Article |
---|---|
Date Type: | Published Online |
Status: | In Press |
Schools: | Schools > Biosciences |
Publisher: | Elsevier |
ISSN: | 0955-2863 |
Date of First Compliant Deposit: | 11 April 2025 |
Date of Acceptance: | 21 March 2025 |
Last Modified: | 11 Apr 2025 12:00 |
URI: | https://orca.cardiff.ac.uk/id/eprint/177608 |
Actions (repository staff only)
![]() |
Edit Item |