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Sodium-iodide symporter mediates iodide secretion in rat gastric mucosa in vitro.

Josefsson, Malin LU ; Evilevitch, Lena LU ; Weström, Björn LU ; Grunditz, Torsten LU and Ekblad, Eva LU (2006) In Experimental Biology and Medicine 231(3). p.277-281
Abstract
In vivo studies on rats have demonstrated that considerable amounts of iodide are transported from the bloodstream into the gastric lumen. The mechanisms for and functional significance of this transport are poorly understood. Active (driven by Na+/K+-ATPase) iodide transport into thyroid follicular cells is mediated by the sodium-iodide symporter (NIS), which is also abundantly expressed in gastric mucosa. We aimed to further investigate the iodide transport in gastric mucosa and the possible role of NIS in this transport process. Iodide transport in rat gastric mucosa was studied in vitro in an Ussing chamber system using 125I as a marker. The system allows measurements in both directions over a mucosal specimen. A considerable transport... (More)
In vivo studies on rats have demonstrated that considerable amounts of iodide are transported from the bloodstream into the gastric lumen. The mechanisms for and functional significance of this transport are poorly understood. Active (driven by Na+/K+-ATPase) iodide transport into thyroid follicular cells is mediated by the sodium-iodide symporter (NIS), which is also abundantly expressed in gastric mucosa. We aimed to further investigate the iodide transport in gastric mucosa and the possible role of NIS in this transport process. Iodide transport in rat gastric mucosa was studied in vitro in an Ussing chamber system using 125I as a marker. The system allows measurements in both directions over a mucosal specimen. A considerable transport of iodide (from the serosal to the mucosal side) was established across the gastric mucosa, whereas in the opposite direction (mucosa to serosa), iodide transport was negligible. Sodium perchlorate (NaClO4), a competitive inhibitor of NIS, and ouabain, an inhibitor of the Na+/K+-ATPase, both attenuated gastric iodide transport from the serosal to the mucosal side. To investigate a possible neuroendocrine regulation of the iodide transport identified to occur from the serosal to the mucosal side of the stomach, thyroid-stimulating hormone (TSH), thyrotropin-releasing hormone (TRH), vasoactive intestinal peptide (VIP), histamine, or nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) was added. None of these substances influenced the iodide transport. We conclude that iodide is actively transported into the gastric lumen and that this transport is at least partly mediated by NIS. Additional investigations are needed to understand the regulation and significance of this transport. (Less)
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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
gastric NIS, gastric iodide secretion, ouabain, sodium perchlorate, Ussing chamber
in
Experimental Biology and Medicine
volume
231
issue
3
pages
277 - 281
publisher
SAGE Publications
external identifiers
  • wos:000236017900006
  • pmid:16514173
  • scopus:33644687190
ISSN
1535-3702
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuroendocrine Cell Biology (013212008), Functional Zoology (432112239), Oto-Rhino-Laryngology (013243500), Diabetes, Metabolism and Endocrinology (LUR000004), Department of Biology (000016100)
id
76cc9865-d564-404a-869e-86d3a6cab0ce (old id 154828)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16514173&dopt=Abstract
date added to LUP
2016-04-01 11:51:55
date last changed
2021-06-30 05:15:28
@article{76cc9865-d564-404a-869e-86d3a6cab0ce,
  abstract     = {In vivo studies on rats have demonstrated that considerable amounts of iodide are transported from the bloodstream into the gastric lumen. The mechanisms for and functional significance of this transport are poorly understood. Active (driven by Na+/K+-ATPase) iodide transport into thyroid follicular cells is mediated by the sodium-iodide symporter (NIS), which is also abundantly expressed in gastric mucosa. We aimed to further investigate the iodide transport in gastric mucosa and the possible role of NIS in this transport process. Iodide transport in rat gastric mucosa was studied in vitro in an Ussing chamber system using 125I as a marker. The system allows measurements in both directions over a mucosal specimen. A considerable transport of iodide (from the serosal to the mucosal side) was established across the gastric mucosa, whereas in the opposite direction (mucosa to serosa), iodide transport was negligible. Sodium perchlorate (NaClO4), a competitive inhibitor of NIS, and ouabain, an inhibitor of the Na+/K+-ATPase, both attenuated gastric iodide transport from the serosal to the mucosal side. To investigate a possible neuroendocrine regulation of the iodide transport identified to occur from the serosal to the mucosal side of the stomach, thyroid-stimulating hormone (TSH), thyrotropin-releasing hormone (TRH), vasoactive intestinal peptide (VIP), histamine, or nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) was added. None of these substances influenced the iodide transport. We conclude that iodide is actively transported into the gastric lumen and that this transport is at least partly mediated by NIS. Additional investigations are needed to understand the regulation and significance of this transport.},
  author       = {Josefsson, Malin and Evilevitch, Lena and Weström, Björn and Grunditz, Torsten and Ekblad, Eva},
  issn         = {1535-3702},
  language     = {eng},
  number       = {3},
  pages        = {277--281},
  publisher    = {SAGE Publications},
  series       = {Experimental Biology and Medicine},
  title        = {Sodium-iodide symporter mediates iodide secretion in rat gastric mucosa in vitro.},
  url          = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16514173&dopt=Abstract},
  volume       = {231},
  year         = {2006},
}