Evidence map›Paper›PMID 11481455›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Brain glucose utilization in mice with a targeted mutation in the thyroid hormone alpha or beta receptor gene.

Y Itoh, T Esaki, M Kaneshige, H Suzuki, M Cook, L Sokoloff, S Y Cheng, J Nunez

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.9field-weighted citation impact, top 6% 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.

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

26 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. The Clinical Spectrum of Resistance to Thyroid Hormone Alpha in Children and AdultsJournal of clinical research in pediatric endocrinology · 2021
    Review
  5. Article
  6. Article
  7. Nuclear receptors and the Warburg effect in cancer.International journal of cancer · 2015
    Review
  8. Resistance to thyroid hormone due to defective thyroid receptor alpha.Best practice & research. Clinical endocrinology & metabolism · 2015
    Review
  9. Review
  10. Review
  11. Review
  12. Genome-wide analysis of thyroid hormone receptors shared and specific functions in neural cells.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Thyroid hormone and cerebellar development.Cerebellum (London, England) · 2008
    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

8 authors at 3 institutions in 1 country.

Y ItohLaboratory of Cerebral Metabolism, National Institute of Mental Health, and National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4030, USA.
T Esaki
M Kaneshige
H Suzuki
M Cook
L Sokoloff
S Y Cheng
J Nunez
National Cancer Institute · USNational Institute of Mental Health · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain glucose utilization is markedly depressed in adult rats made cretinous after birth. To ascertain which subtype of thyroid hormone (TH) receptors, TRalpha1 or TRbeta, is involved in the regulation of glucose utilization during brain development, we used the 2-[(14)C]deoxyglucose method in mice with a mutation in either their TRalpha or TRbeta gene. A C insertion produced a frameshift mutation in their carboxyl terminus. These mutants lacked TH binding and transactivation activities and exhibited potent dominant negative activity. Glucose utilization in the homozygous TRbetaPV mutant mice and their wild-type siblings was almost identical in 19 brain regions, whereas it was markedly reduced in all brain regions of the heterozygous TRalpha1PV mice. These suggest that the alpha1 receptor mediates the TH effects in brain. Inasmuch as local cerebral glucose utilization is closely related to local synaptic activity, we also examined which thyroid hormone receptor is involved in the expression of synaptotagmin-related gene 1 (Srg1), a TH-positively regulated gene involved in the formation and function of synapses [Thompson, C. C. (1996) J. Neurosci. 16, 7832-7840]. Northern analysis showed that Srg1 expression was markedly reduced in the cerebellum of TRalpha(PV/+) mice but not TRbeta(PV/PV) mice. These results show that the same receptor, TRalpha1, is involved in the regulation by TH of both glucose utilization and Srg1 expression.

Indexed as

Age FactorsAnimalsBrainCerebellumCerebral CortexDeoxyglucoseEnergy MetabolismFrameshift MutationGene Expression RegulationGene TargetingGlucoseGlycolysisMembrane ProteinsMiceMice, KnockoutMutagenesis, InsertionalDeoxyglucoseGlucoseMembrane ProteinsNerve Tissue ProteinsProtein IsoformsReceptors, Thyroid HormoneSytl1 protein, mouseThyroid HormonesVesicular Transport Proteins

Identifiers

PMID11481455
PMCPMC55552
OpenAlexW1539467957

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.