Evidence map›Paper›PMID 21818396›Full record

ArticlePloS one2011

Postnatal development of numbers and mean sizes of pancreatic islets and beta-cells in healthy mice and GIPR(dn) transgenic diabetic mice.

Nadja Herbach, Martina Bergmayr, Burkhard Göke, Eckhard Wolf, Ruediger Wanke

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
3.5field-weighted citation impact, top 8% 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, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Effect of the Taste Receptor Protein T1R3 on the Development of Islet Tissue of the Murine Pancreas.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. A synopsis of factors regulating beta cell development and beta cell mass.Cellular and molecular life sciences : CMLS · 2016
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Pancreatic β-cell proliferation in obesity.Advances in nutrition (Bethesda, Md.) · 2014
    Review
  15. Review
  16. Article
  17. Article
  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 2 institutions in 1 country.

Nadja HerbachInstitute of Veterinary Pathology, Center for Clinical Veterinary Medicine, LMU Munich, Germany. herbach@patho.vetmed.uni-muenchen.de
Martina Bergmayr
Burkhard Göke
Eckhard Wolf
Ruediger Wanke
Ludwig-Maximilians-Universität München · DELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to examine postnatal islet and beta-cell expansion in healthy female control mice and its disturbances in diabetic GIPR(dn) transgenic mice, which exhibit an early reduction of beta-cell mass. Pancreata of female control and GIPR(dn) transgenic mice, aged 10, 45, 90 and 180 days were examined, using state-of-the-art quantitative-stereological methods. Total islet and beta-cell volumes, as well as their absolute numbers increased significantly until 90 days in control mice, and remained stable thereafter. The mean islet volumes of controls also increased slightly but significantly between 10 and 45 days of age, and then remained stable until 180 days. The total volume of isolated beta-cells, an indicator of islet neogenesis, and the number of proliferating (BrdU-positive) islet cells were highest in 10-day-old controls and declined significantly between 10 and 45 days. In GIPR(dn) transgenic mice, the numbers of islets and beta-cells were significantly reduced from 10 days of age onwards vs. controls, and no postnatal expansion of total islet and beta-cell volumes occurred due to a reduction in islet neogenesis whereas early islet-cell proliferation and apoptosis were unchanged as compared to control mice. Insulin secretion in response to pharmacological doses of GIP was preserved in GIPR(dn) transgenic mice, and serum insulin to pancreatic insulin content in response to GLP-1 and arginine was significantly higher in GIPR(dn) transgenic mice vs. controls. We could show that the increase in islet number is mainly responsible for expansion of islet and beta-cell mass in healthy control mice. GIPR(dn) transgenic mice show a disturbed expansion of the endocrine pancreas, due to perturbed islet neogenesis.

Indexed as

Cell SizeHealthAnimalsAnimals, NewbornApoptosisCell CountCell ProliferationCell SeparationCyclic AMPDiabetes Mellitus, ExperimentalFemaleGlucose Tolerance TestIncretinsInsulinInsulin ResistanceInsulin-Secreting CellsCyclic AMPgastric inhibitory polypeptide receptorIncretinsInsulinReceptors, Gastrointestinal Hormone

Identifiers

PMID21818396
PMCPMC3144241
OpenAlexW2102458347

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.