Evidence map›Paper›PMID 23006481›Full record

ArticleThe Journal of physiology2012

Dietary iodide controls its own absorption through post-transcriptional regulation of the intestinal Na+/I- symporter.

Juan Pablo Nicola, Andrea Reyna-Neyra, Nancy Carrasco, Ana Maria Masini-Repiso

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04492657 (Study on the Compensatory Mechanism of Iodine Nutrition and the Optimal Intake Level of Lactating Women), which is not on this map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04492657 unknown statusnot on this mapstarted 2020, after this paper: background citation

Study on the Compensatory Mechanism of Iodine Nutrition and the Optimal Intake Level of Lactating Women

TypeobservationalSponsorTianjin Medical UniversityRan2020 to 2024Enrolled600ConditionsNutritional RequirementsArmsno intervention
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Combined Vorinostat and Chloroquine Inhibit Sodium-Iodide Symporter Endocytosis and Enhance Radionuclide Uptake In Vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Implications of NaJournal of the Endocrine Society · 2019
    Review
  10. Na+ coordination at the Na2 site of the Na+/I- symporter.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Sodium/Iodide Symporter Mutant V270E Causes Stunted Growth but No Cognitive Deficiency.The Journal of clinical endocrinology and metabolism · 2015
    Article
  12. Review
  13. Article
  14. Article
  15. Iodide transport: implications for health and disease.International journal of pediatric endocrinology · 2014
    Article
  16. Article
  17. Asn441 plays a key role in folding and function of the Na+/I- symporter (NIS).FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Juan Pablo NicolaCentro de Investigaciones en Bioquímica Clínica e Inmunología-Consejo Nacional de Investigaciones Científicas y Técnicas (CIBICI-CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Haya de la Torre y Medina Allende, X5000HUA, Córdoba, Argentina.
Andrea Reyna-Neyra
Nancy Carrasco
Ana Maria Masini-Repiso
Yale University · USConsejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

THYROID SODIUM I/ SYMPORTERR01DK041544 · NIDDK · YESHIVA UNIVERSITY · PI ABBOTT, GEOFFREY W, CARRASCO, NANCY · 1989 to 2017
$5.6M
NIDDK NIH HHS DK-41544NIDDK NIH HHS R01 DK041544
6 · The paper itself

Abstract

Dietary I(-) absorption in the gastrointestinal tract is the first step in I(-) metabolism. Given that I(-) is an essential constituent of the thyroid hormones, its concentrating mechanism is of significant physiological importance. We recently described the expression of the Na(+)/I(-) symporter (NIS) on the apical surface of the intestinal epithelium as a central component of the I(-) absorption system and reported reduced intestinal NIS expression in response to an I(-)-rich diet in vivo. Here, we evaluated the mechanism involved in the regulation of NIS expression by I(-) itself in enterocytes. Excess I(-) reduced NIS-mediated I(-) uptake in IEC-6 cells in a dose- and time-dependent fashion, which was correlated with a reduction of NIS expression at the plasma membrane. Perchlorate, a competitive inhibitor of NIS, prevented these effects, indicating that an increase in intracellular I(-) regulates NIS. Iodide induced rapid intracellular recruitment of plasma membrane NIS molecules and NIS protein degradation. Lower NIS mRNA levels were detected in response to I(-) treatment, although no transcriptional effect was observed. Interestingly, I(-) decreased NIS mRNA stability, affecting NIS translation. Heterologous green fluorescent protein-based reporter constructs revealed a significant repressive effect of the I(-)-targeting NIS mRNA 3 untranslated region. In conclusion, excess I(-) downregulates NIS expression in enterocytes by virtue of a complex mechanism. Our data suggest that I(-) regulates intestinal NIS mRNA expression at the post-transcriptional level as part of an autoregulatory effect of I(-) on its own metabolism.

Indexed as

AnimalsCell LineDietEnterocytesIntestinal AbsorptionIntestinal MucosaMalePotassium IodideRatsRats, Sprague-DawleySodium-Iodide SymportersSymportersTranscription, GeneticPotassium IodideSodium-Iodide SymportersSymporters

Identifiers

PMID23006481
PMCPMC3530113
OpenAlexW1525135940

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.