Evidence map›Paper›PMID 26499800›Full record

ArticleThe Journal of biological chemistry2015

Coupling between Nutrient Availability and Thyroid Hormone Activation.

Lattoya J Lartey, João Pedro Werneck-de-Castro, InSug O-Sullivan, Terry G Unterman, Antonio C Bianco

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

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  15. The association between serum TSH concentration whithin the normal range and nutritional status in euthyroid pregnant women at the first trimester of gestation.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2021
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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 at 4 institutions in 2 countries.

Lattoya J LarteyFrom the Department of Molecular and Cellular Pharmacology, University of Miami, Miller School of Medicine, Miami, Florida 33136.
João Pedro Werneck-de-Castrothe Department of Internal Medicine, Division of Endocrinology and Metabolism, Rush University Medical Center, Chicago, Illinois 60612, the Carlos Chagas Filho Biophysics Institute and School of Physical Education and Sports, Federal University of Rio de Janeiro, Rio de Janeiro 21941-599, Brazil, and.
InSug O-Sullivanthe Jesse Brown Veterans Affairs Medical Center and the Department of Medicine, University of Illinois at Chicago College of Medicine, Chicago, Illinois 60612.
Terry G Untermanthe Jesse Brown Veterans Affairs Medical Center and the Department of Medicine, University of Illinois at Chicago College of Medicine, Chicago, Illinois 60612.
Antonio C Biancothe Department of Internal Medicine, Division of Endocrinology and Metabolism, Rush University Medical Center, Chicago, Illinois 60612, abianco@deiodinase.org.
Rush University Medical Center · USJesse Brown VA Medical Center · USUniversity of Illinois Chicago · USUniversity of Miami · US

Funding

Metabolic and Xenobiotic Control of Thyroid Hormone MetabolismR01DK077148 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ANTONIO C BIANCO · 2007 to 2026
$4.5M
Thyroid-adrenergic synergism and adaptive thermogenesisR01DK065055 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIANCO, ANTONIO C · 2005 to 2021
$4.4M
NIDDK NIH HHS DK65055NIDDK NIH HHS R01 DK065055NIDDK NIH HHS R01 DK077148
6 · The paper itself

Abstract

The activity of the thyroid gland is stimulated by food availability via leptin-induced thyrotropin-releasing hormone/thyroid-stimulating hormone expression. Here we show that food availability also stimulates thyroid hormone activation by accelerating the conversion of thyroxine to triiodothyronine via type 2 deiodinase in mouse skeletal muscle and in a cell model transitioning from 0.1 to 10% FBS. The underlying mechanism is transcriptional derepression of DIO2 through the mTORC2 pathway as defined in rictor knockdown cells. In cells kept in 0.1% FBS, there is DIO2 inhibition via FOXO1 binding to the DIO2 promoter. Repression of DIO2 by FOXO1 was confirmed using its specific inhibitor AS1842856 or adenoviral infection of constitutively active FOXO1. ChIP studies indicate that 4 h after 10% FBS-containing medium, FOXO1 binding markedly decreases, and the DIO2 promoter is activated. Studies in the insulin receptor FOXO1 KO mouse indicate that insulin is a key signaling molecule in this process. We conclude that FOXO1 represses DIO2 during fasting and that derepression occurs via nutritional activation of the PI3K-mTORC2-Akt pathway.

Indexed as

AnimalsFastingForkhead Box Protein O1Forkhead Transcription FactorsIodide PeroxidaseIodothyronine Deiodinase Type IIMaleMechanistic Target of Rapamycin Complex 2MiceMice, KnockoutMultiprotein ComplexesMuscle, SkeletalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionThyroxineForkhead Box Protein O1Forkhead Transcription FactorsFOXO1 protein, humanIodide PeroxidaseIodothyronine Deiodinase Type IIMechanistic Target of Rapamycin Complex 2Multiprotein ComplexesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktThyroxineTOR Serine-Threonine KinasesTriiodothyronineFOXO1insulinmTOR complex (mTORC)signalingsignal transductionthyroid hormonetype 2 deiodinase

Identifiers

PMID26499800
PMCPMC4683275
OpenAlexW2341045533

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.