Cited by 79Thyroid Disorders and TreatmentsChemical Analysis and Environmental ImpactGrowth Hormone and Insulin-like Growth Factors

Regional physiological adaptation of the central nervous system deiodinases to iodine deficiency

Peeters, Robin, Fekete, Csaba, Goncalves, Carla, Legradi, Gabor, Tu, Helen M., Harney, John W., Bianco, Antonio C., Lechan, Ronald M. +1 more·2001·American Journal of Physiology-Endocrinology and Metabolism

Abstract

The goal of the present investigation was to analyze the types 2 (D2) and 3 (D3) iodothyronine deiodinases in various structures within the central nervous system (CNS) in response to iodine deficiency. After 5-6 wk of low-iodine diet (LID) or LID + 2 microg potassium iodide/ml (LID + KI; control), rats' brains were processed for in situ hybridization histochemistry for D2 and D3 mRNA or dissected, frozen in liquid nitrogen, and processed for D2 and D3 activities. LID did not affect weight gain or serum triiodothyronine, but plasma thyroxine (T4) was undetectable. In the LID + KI animals, D3 activities were highest in the cerebral cortex (CO) and hippocampus (HI), followed by the olfactory bulb and was lowest in cerebellum (CE). Iodine deficiency decreased D3 mRNA expression in all CNS regions, and these changes were accompanied by three- to eightfold decreases in D3 activity. In control animals, D2 activity in the medial basal hypothalamus (MBH) was similar to that in pituitary gland. Of the CNS D2-expressing regions analyzed, the two most responsive to iodine deficiency were the CO and HI, in which an approximately 20-fold increase in D2 activity occurred. Other regions, i.e., CE, lateral hypothalamus, MBH, and pituitary gland, showed smaller increases. The distribution of and changes in D2 mRNA were similar to those of D2 activity. Our results indicate that decreases in the expression of D3 and increases in D2 are an integral peripheral component of the physiological respo…

Integrity signals

Registry

Crossref · 10.1152/ajpendo.2001.281.1.e54

Cites

6 of 6 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • A reduction in plasma T3 could in theory be compensated for by a homeostatic acceleration of the D2 pathway, increasing locally produced T3.

    “A reduction in plasma T3 could in theory be compensated for by a homeostatic acceleration of the D2 pathway, increasing locally produced T3 (44).”

    From Treatment Preferences in Patients With Hypothyroidism (2025) · cites this paper as [44]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Peeters, R., Fekete, C., Goncalves, C., Legradi, G., Tu, H. M., Harney, J. W., Bianco, A. C., Lechan, R. M., & Larsen, P. R.
Affiliations
  • Brigham and Women's Hospital (US)
  • Tufts University (US)
  • Division of Endocrinology, Diabetes, Metabolism and Molecular Medicine, Department of Medicine, New England Medical Center-Tufts University School of Medicine, Boston, Massachusetts 02111
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
2001-07-01
Volume
281
Issue
1
Pages
E54-E61
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2206735333
Cited by
79
References
6
Citations by year
2025: 3 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 3 · 2014: 4 · 2013: 2 · 2012: 5
FWCI
2.07
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK044128, R01 DK 44128)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Chemical Analysis and Environmental Impact
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
Keywords
iodine deficiency, central nervous system, low iodine diet, cerebral cortex, hippocampus, cerebellum, olfactory bulb, medial basal hypothalamus, pituitary gland, thyroid hormone metabolism
MeSH terms
Adaptation, Physiological, Animals, Central Nervous System, Diet, Iodide Peroxidase, Iodine, Isoenzymes, Male, Organ Size, RNA, Messenger, Thyroid Gland, Thyroid Hormones, Rats, Sprague-Dawley, In Situ Hybridization, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review