Evidence map›Paper›PMID 11306605›Full record

ArticleThe Journal of clinical investigation2001

Critical role for thyroid hormone receptor beta2 in the regulation of paraventricular thyrotropin-releasing hormone neurons.

E D Abel, R S Ahima, M E Boers, J K Elmquist, F E Wondisford

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Review
  3. Review
  4. Article
  5. Regulation of Thyroid Hormone Levels by Hypothalamic Thyrotropin-Releasing Hormone Neurons.Thyroid : official journal of the American Thyroid Association · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Thyroid hormone receptor phosphorylation regulates acute fasting-induced suppression of the hypothalamic-pituitary-thyroid axis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Review
  11. Article
  12. Role of thyroid hormones in craniofacial development.Nature reviews. Endocrinology · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Noncanonical thyroid hormone signaling mediates cardiometabolic effects in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. The actions of thyroid hormone signaling in the nucleus.Molecular and cellular endocrinology · 2017
    Review
  20. Review
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

5 authors.

E D AbelDivision of Endocrinology, Metabolism and Diabetes, University of Utah School of Medicine 15 North 2030 East, Building 533, Room 3410B, Salt Lake City, UT 84112, USA. dale.abel@hmbg.utah.edu
R S Ahima
M E Boers
J K Elmquist
F E Wondisford

Funding

THYROID HORMONE ACTION IN THE PITUITARYR01DK049126 · NIDDK · UNIVERSITY OF CHICAGO · PI WONDISFORD, FREDRIC E. · 1995 to 2016
$3.8M
NIDDK NIH HHS DK-02485NIDDK NIH HHS DK-49126NIDDK NIH HHS R01 DK049126
6 · The paper itself

Abstract

Thyroid hormone thyroxine (T(4)) and tri-iodothyronine (T(3)) production is regulated by feedback inhibition of thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) synthesis in the pituitary and hypothalamus when T(3) binds to thyroid hormone receptors (TRs) interacting with the promoters of the genes for the TSH subunit and TRH. All of the TR isoforms likely participate in the negative regulation of TSH production in vivo, but the identity of the specific TR isoforms that negatively regulate TRH production are less clear. To clarify the role of the TR-beta2 isoform in the regulation of TRH gene expression in the hypothalamic paraventricular nucleus, we examined preprothyrotropin-releasing hormone (prepro-TRH) expression in mice lacking the TR-beta2 isoform under basal conditions, after the induction of hypothyroidism with propylthiouracil, and in response to T(3) administration. Prepro-TRH expression was increased in hypothyroid wild-type mice and markedly suppressed after T(3) administration. In contrast, basal TRH expression was increased in TR-beta2-null mice to levels seen in hypothyroid wild-type mice and did not change significantly in response to induction of hypothyroidism or T(3) treatment. However, the suppression of TRH mRNA expression in response to leptin reduction during fasting was preserved in TR-beta2-null mice. Thus TR-beta2 is the key TR isoform responsible for T(3)-mediated negative-feedback regulation by hypophysiotropic TRH neurons.

Indexed as

AnimalsFastingLeptinMiceMice, KnockoutNeuronsParaventricular Hypothalamic NucleusProtein IsoformsReceptors, Thyroid HormoneThyrotropinThyrotropin-Releasing HormoneThyroxineLeptinProtein IsoformsReceptors, Thyroid HormoneThyrotropinThyrotropin-Releasing HormoneThyroxine

Identifiers

PMID11306605
PMCPMC199552

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.