Evidence map›Paper›PMID 22926403›Full record

ArticleDiabetologia2012

The role of Raf-1 kinase inhibitor protein in the regulation of pancreatic beta cell proliferation in mice.

F N Pardo, J Altirriba, M Pradas-Juni, A García, U Ahlgren, A Barberà, J C Slebe, A J Yáñez, R Gomis, R Gasa

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Lack of CFTR alters the ferret pancreatic ductal epithelial secretome and cellular proteome: Implications for exocrine/endocrine signaling.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2022
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Metastasis suppressors: functional pathways.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

10 authors at 4 institutions in 3 countries.

F N PardoLaboratory of Diabetes and Obesity, IDIBAPS, Centre Esther Koplowitz, Rosselló 153, Barcelona, Spain.
J Altirriba
M Pradas-Juni
A García
U Ahlgren
A Barberà
J C Slebe
A J Yáñez
R Gomis
R Gasa
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESAustral University of Chile · CLUmeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisManoeuvres aimed at increasing beta cell mass have been proposed as regenerative medicine strategies for diabetes treatment. Raf-1 kinase inhibitor protein 1 (RKIP1) is a common regulatory node of the mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways and therefore may be involved in regulation of beta cell homeostasis. The aim of this study was to investigate the involvement of RKIP1 in the control of beta cell mass and function.

methodsRkip1 (also known as Pebp1) knockout (Rkip1 (-/-)) mice were characterised in terms of pancreatic and glucose homeostasis, including morphological and functional analysis. Glucose tolerance and insulin sensitivity were examined, followed by assessment of glucose-induced insulin secretion in isolated islets and beta cell mass quantification through morphometry. Further characterisation included determination of endocrine and exocrine proliferation, apoptosis, MAPK activation and whole genome gene expression assays. Capacity to reverse a diabetic phenotype was assessed in adult Rkip1 (-/-) mice after streptozotocin treatment.

resultsRkip1 (-/-) mice exhibit a moderately larger pancreas and increased beta cell mass and pancreatic insulin content, which correlate with an overall improvement in whole body glucose tolerance. This phenotype is established in young postnatal stages and involves enhanced cellular proliferation without significant alterations in cell death. Importantly, adult Rkip1 (-/-) mice exhibit rapid reversal of streptozotocin-induced diabetes compared with control mice. CONCLUSIONS/

interpretationThese data implicate RKIP1 in the regulation of pancreatic growth and beta cell expansion, thus revealing RKIP1 as a potential pharmacological target to promote beta cell regeneration.

Indexed as

AnimalsBlotting, WesternCell ProliferationDiabetes Mellitus, ExperimentalFluorescent Antibody TechniqueHomeostasisInsulin-Secreting CellsMaleMiceMice, KnockoutNF-kappa BPhenotypePhosphatidylethanolamine Binding ProteinPhosphorylationNF-kappa BPhosphatidylethanolamine Binding Protein

Identifiers

PMID22926403
OpenAlexW2164967518

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.