Evidence map›Paper›PMID 23305647›Full record

ArticleDiabetes2013

Thyroid hormone promotes postnatal rat pancreatic β-cell development and glucose-responsive insulin secretion through MAFA.

Cristina Aguayo-Mazzucato, Ann Marie Zavacki, Alejandra Marinelarena, Jennifer Hollister-Lock, Ilham El Khattabi, Alessandro Marsili, Gordon C Weir, Arun Sharma, P Reed Larsen, Susan Bonner-Weir

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

94 citing papers in PubMed, 140 citations in OpenAlex.

  1. Review
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  7. Type 2 Diabetes From the Perspective of Telomere Biology.Endocrinology, diabetes & metabolism · 2026
    Review
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34 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Cristina Aguayo-MazzucatoSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, USA.
Ann Marie Zavacki
Alejandra Marinelarena
Jennifer Hollister-Lock
Ilham El Khattabi
Alessandro Marsili
Gordon C Weir
Arun Sharma
P Reed Larsen
Susan Bonner-Weir
Harvard University · USJoslin Diabetes Center · USBrigham and Women's Hospital · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
PHYSIOLOGICAL ROLE OF THYROXINE-BINDING PROTEINSR01DK036256 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI LARSEN, PHILIP REED · 1986 to 2011
$4.7M
RIPE3b1, An Important Insulin Gene Transcription FactorR01DK060127 · NIDDK · JOSLIN DIABETES CENTER · PI SHARMA, ARUN J · 2003 to 2010
$2.5M
Physiological Factors Driving Maturation of Neonatal Beta CellsR01DK093909 · NIDDK · JOSLIN DIABETES CENTER · PI BONNER-WEIR, SUSAN · 2011 to 2015
$1.8M
Role of Deiodinases in Thyroid Hormone HomeostasisR01DK076117 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI ZAVACKI, ANN M · 2006 to 2010
$1.5M
Phenotypic Analysis of Young and Old Beta CellsR01DK066056 · NIDDK · JOSLIN DIABETES CENTER · PI BONNER-WEIR, SUSAN · 2005 to 2008
$1.1M
NIDDK NIH HHS DK 076117NIDDK NIH HHS DK 36256NIDDK NIH HHS DK 93909NIDDK NIH HHS P30 DK036836NIDDK NIH HHS P30 DK36836NIDDK NIH HHS R01 DK036256NIDDK NIH HHS R01 DK060127NIDDK NIH HHS R01 DK066056NIDDK NIH HHS R01 DK076117NIDDK NIH HHS R01 DK093909NIDDK NIH HHS R01 DK 60127NIDDK NIH HHS R01 DK 66056
6 · The paper itself

Abstract

Neonatal β cells do not secrete glucose-responsive insulin and are considered immature. We previously showed the transcription factor MAFA is key for the functional maturation of β cells, but the physiological regulators of this process are unknown. Here we show that postnatal rat β cells express thyroid hormone (TH) receptor isoforms and deiodinases in an age-dependent pattern as glucose responsiveness develops. In vivo neonatal triiodothyronine supplementation and TH inhibition, respectively, accelerated and delayed metabolic development. In vitro exposure of immature islets to triiodothyronine enhanced the expression of Mafa, the secretion of glucose-responsive insulin, and the proportion of responsive cells, all of which are effects that were abolished in the presence of dominant-negative Mafa. Using chromatin immunoprecipitation and electrophoretic mobility shift assay, we show that TH has a direct receptor-ligand interaction with the Mafa promoter and, using a luciferase reporter, that this interaction was functional. Thus, TH can be considered a physiological regulator of functional maturation of β cells via its induction of Mafa.

Indexed as

Cell DifferentiationAnimalsAnimals, NewbornBlood GlucoseCell NucleusGene Expression Regulation, DevelopmentalGenes, ReporterInsulinInsulin-Secreting CellsInsulin SecretionIodide PeroxidaseIslets of LangerhansPromoter Regions, GeneticProtein IsoformsProtein TransportProto-Oncogene Proteins c-mafBlood GlucoseInsulinIodide PeroxidaseMaf protein, ratProtein IsoformsProto-Oncogene Proteins c-mafReceptors, Thyroid HormoneRecombinant ProteinsTriiodothyronine

Identifiers

PMID23305647
PMCPMC3636623
OpenAlexW2168963689

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.