Evidence map›Paper›PMID 19574445›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2009

The transcriptional response of the islet to pregnancy in mice.

Sebastian Rieck, Peter White, Jonathan Schug, Alan J Fox, Olga Smirnova, Nan Gao, Rana K Gupta, Zhao V Wang, Philipp E Scherer, Mark P Keller and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
9.1field-weighted citation impact, top 2% 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

114 citing papers in PubMed, 161 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Cafeteria diet compromises natural adaptations of islet cell transdifferentiation and turnover in pregnancy.Diabetic medicine : a journal of the British Diabetic Association · 2025
    Article
  8. Review
  9. Article
  10. Isolated hypoprolactinemia: The rarest of the rare?Reviews in endocrine & metabolic disorders · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. β-Cell Heterogeneity and Plasticity.Advances in anatomy, embryology, and cell biology · 2024
    Review
  16. Review
  17. Beta-cell compensation and gestational diabetes.The Journal of biological chemistry · 2023
    Review
  18. Article
  19. Article
  20. Article

54 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

12 authors at 3 institutions in 1 country.

Sebastian RieckDepartment of Genetics and Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6145, USA.
Peter White
Jonathan Schug
Alan J Fox
Olga Smirnova
Nan Gao
Rana K Gupta
Zhao V Wang
Philipp E Scherer
Mark P Keller
Alan D Attie
Klaus H Kaestner
University of Pennsylvania · USThe University of Texas Southwestern Medical Center · USUniversity of Wisconsin–Madison · US

Funding

TRANSCRIPTIONAL CONTROL OF PANCREATIC DEVELOPMENTR01DK055342 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KAESTNER, KLAUS H · 1998 to 2013
$4.7M
NIDDK NIH HHS DK 055342NIDDK NIH HHS DK5 58037NIDDK NIH HHS DK5 66369NIDDK NIH HHS R01 DK055342
6 · The paper itself

Abstract

The inability of the ss-cell to meet the demand for insulin brought about by insulin resistance leads to type 2 diabetes. In adults, ss-cell replication is one of the mechanisms thought to cause the expansion of ss-cell mass. Efforts to treat diabetes require knowledge of the pathways that drive facultative ss-cell proliferation in vivo. A robust physiological stimulus of ss-cell expansion is pregnancy and identifying the mechanisms underlying this stimulus may provide therapeutic leads for the treatment of type 2 diabetes. The peak in ss-cell proliferation during pregnancy occurs on d 14.5 of gestation in mice. Using advanced genomic approaches, we globally characterize the gene expression signature of pancreatic islets on d 14.5 of gestation during pregnancy. We identify a total of 1907 genes as differentially expressed in the islet during pregnancy. The islet's ability to compensate for relative insulin deficiency during metabolic stress is associated with the induction of both proliferative and survival pathways. A comparison of the genes induced in three different models of islet expansion suggests that diverse mechanisms can be recruited to expand islet mass. The identification of many novel genes involved in islet expansion during pregnancy provides an important resource for diabetes researchers to further investigate how these factors contribute to the maintenance of not only islet mass, but ultimately ss-cell mass.

Indexed as

Transcription, GeneticAnimalsCell ProliferationCell SizeCell SurvivalDisease Models, AnimalFemaleGene Expression ProfilingGene Expression RegulationHypertrophyInsulin-Secreting CellsMiceObesityPregnancySignal TransductionTime Factors

Identifiers

PMID19574445
PMCPMC2754894
OpenAlexW2008114808

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.