Evidence map›Paper›PMID 26236746›Full record

ArticleJournal of diabetes research2015

Delta Cell Hyperplasia in Adult Goto-Kakizaki (GK/MolTac) Diabetic Rats.

Lukáš Alán, Tomáš Olejár, Monika Cahová, Jaroslav Zelenka, Zuzana Berková, Magdalena Smětáková, František Saudek, Radoslav Matěj, Petr Ježek

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. 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

9 authors at 4 institutions in 1 country.

Lukáš AlánDepartment No. 75, Institute of Physiology, Academy of Sciences, 14220 Prague, Czech Republic.
Tomáš OlejárDepartment No. 75, Institute of Physiology, Academy of Sciences, 14220 Prague, Czech Republic.
Monika CahováInstitute of Clinical & Experimental Medicine, 14021 Prague, Czech Republic.
Jaroslav ZelenkaDepartment No. 75, Institute of Physiology, Academy of Sciences, 14220 Prague, Czech Republic.
Zuzana BerkováInstitute of Clinical & Experimental Medicine, 14021 Prague, Czech Republic.
Magdalena SmětákováTeaching Thomayer Hospital and Third Medical School, Charles University, 14059 Prague, Czech Republic.
František SaudekInstitute of Clinical & Experimental Medicine, 14021 Prague, Czech Republic.
Radoslav MatějTeaching Thomayer Hospital and Third Medical School, Charles University, 14059 Prague, Czech Republic.
Petr JežekDepartment No. 75, Institute of Physiology, Academy of Sciences, 14220 Prague, Czech Republic.
Institute of Clinical and Experimental Medicine · CZCharles University · CZCzech Academy of Sciences · CZCzech Academy of Sciences, Institute of Physiology · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reduced beta cell mass in pancreatic islets (PI) of Goto-Kakizaki (GK) rats is frequently observed in this diabetic model, but knowledge on delta cells is scarce. Aiming to compare delta cell physiology/pathology of GK to Wistar rats, we found that delta cell number increased over time as did somatostatin mRNA and delta cells distribution in PI is different in GK rats. Subtle changes in 6-week-old GK rats were found. With maturation and aging of GK rats, disturbed cytoarchitecture occurred with irregular beta cells accompanied by delta cell hyperplasia and loss of pancreatic polypeptide (PPY) positivity. Unlike the constant glucose-stimulation index for insulin PI release in Wistar rats, this index declined with GK age, whereas for somatostatin it increased with age. A decrease of GK rat PPY serum levels was found. GK rat body weight decreased with increasing hyperglycemia. Somatostatin analog octreotide completely blocked insulin secretion, impaired proliferation at low autocrine insulin, and decreased PPY secretion and mitochondrial DNA in INS-1E cells. In conclusion, in GK rats PI, significant local delta cell hyperplasia and suspected paracrine effect of somatostatin diminish beta cell viability and contribute to the deterioration of beta cell mass. Altered PPY-secreting cells distribution amends another component of GK PI's pathophysiology.

Indexed as

AgingInsulin ResistanceAnimalsCell Line, TumorCell ProliferationCell SurvivalDiabetes Mellitus, Type 2Gene Expression Regulation, DevelopmentalHyperplasiaImmunohistochemistryInsulinInsulin AntagonistsInsulin-Secreting CellsInsulin SecretionOctreotidePancreatic PolypeptideInsulinInsulin AntagonistsOctreotidePancreatic PolypeptideRNA, MessengerSomatostatin

Identifiers

PMID26236746
PMCPMC4506919
OpenAlexW1608470099

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.