Evidence map›Paper›PMID 21952247›Full record

ArticleEndocrinology2011

Loss of Foxd3 results in decreased β-cell proliferation and glucose intolerance during pregnancy.

Jennifer L Plank, Audrey Y Frist, Alison W LeGrone, Mark A Magnuson, Patricia A Labosky

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Beta-cell compensation and gestational diabetes.The Journal of biological chemistry · 2023
    Review
  3. Article
  4. Modelling gestational diabetes mellitus: large animals hold great promise.Reviews in endocrine & metabolic disorders · 2021
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. β-Cell adaptation in pregnancy.Diabetes, obesity & metabolism · 2016
    Review
  12. Article
  13. Article
  14. The prolactin receptor: Diverse and emerging roles in pathophysiology.Journal of clinical & translational endocrinology · 2015
    Review
  15. High-fat diet-induced β-cell proliferation occurs prior to insulin resistance in C57Bl/6J male mice.American journal of physiology. Endocrinology and metabolism · 2015
    Article
  16. Review
  17. Advancements and challenges in generating accurate animal models of gestational diabetes mellitus.American journal of physiology. Endocrinology and metabolism · 2013
    Review
  18. Article
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 1 institution in 1 country.

Jennifer L PlankDepartment of Cell and Developmental Biology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-0494, USA.
Audrey Y Frist
Alison W LeGrone
Mark A Magnuson
Patricia A Labosky
Vanderbilt University Medical Center · US

Funding

Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Transcriptional networks of pancreas endocrine cell differentiationU19DK042502 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2001 to 2010
$21.5M
MULTIDISCIPLINARY TRAINING IN MOLECULAR ENDOCRINOLOGYT32DK007563 · NIDDK · VANDERBILT UNIVERSITY · PI Richard M O'Brien · 1988 to 2026
$15.9M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Genetic control of pancreatic endocrine cell developmentU01DK089523 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2010 to 2014
$5.3M
Neural crest formation and maintenance of multipotencyR01HD036720 · NICHD · VANDERBILT UNIVERSITY · PI LABOSKY, PATRICIA A · 1999 to 2009
$2.9M
NICHD NIH HHS R01 HD036720NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIDDK NIH HHS P60 DK59637NIDDK NIH HHS T32 DK007563NIDDK NIH HHS T32 DK07563-10NIDDK NIH HHS U01 DK089523NIDDK NIH HHS U19 DK042502NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

A complete molecular understanding of β-cell mass expansion will be useful for the improvement of therapies to treat diabetic patients. During normal periods of metabolic challenges, such as pregnancy, β-cells proliferate, or self-renew, to meet the new physiological demands. The transcription factor Forkhead box D3 (Foxd3) is required for maintenance and self-renewal of several diverse progenitor cell lineages, and Foxd3 is expressed in the pancreatic primordium beginning at 10.5 d postcoitum, becoming localized predominantly to β-cells after birth. Here, we show that mice carrying a pancreas-specific deletion of Foxd3 have impaired glucose tolerance, decreased β-cell mass, decreased β-cell proliferation, and decreased β-cell size during pregnancy. In addition, several genes known to regulate proliferation, Foxm1, Skp2, Ezh2, Akt2, and Cdkn1a, are misregulated in islets isolated from these Foxd3 mutant mice. Together, these data place Foxd3 upstream of several pathways critical for β-cell mass expansion in vivo.

Indexed as

Cell ProliferationAnimalsCell SizeFemaleForkhead Transcription FactorsGene Expression RegulationGlucose IntoleranceInsulin-Secreting CellsMicePancreasPregnancyRepressor ProteinsSequence DeletionForkhead Transcription FactorsFoxd3 protein, mouseRepressor Proteins

Identifiers

PMID21952247
PMCPMC3230055
OpenAlexW2031955501

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.