Evidence map›Paper›PMID 17016695›Full record

ArticleDiabetologia2006

Increased islet beta cell replication adjacent to intrapancreatic gastrinomas in humans.

J J Meier, A E Butler, R Galasso, R A Rizza, P C Butler

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
7.6field-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

26 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Review
  3. Pancreatic β-cell heterogeneity in health and diabetes: classes, sources, and subtypes.American journal of physiology. Endocrinology and metabolism · 2021
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Pantoprazole may improve beta cell function and diabetes mellitus.Journal of endocrinological investigation · 2014
    Article
  11. Article
  12. Article
  13. Islet neogenesis: a possible pathway for beta-cell replenishment.The review of diabetic studies : RDS · 2012
    Review
  14. Article
  15. Review
  16. Review
  17. FoxM1 is up-regulated by obesity and stimulates beta-cell proliferation.Molecular endocrinology (Baltimore, Md.) · 2010
    Article
  18. Pancreatic β-Cell Mass as a Pharmacologic Target in Diabetes.McGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students · 2009
    Article
  19. Review
  20. 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.

J J MeierLarry Hillblom Islet Research Center, UCLA David Geffen School of Medicine, 24-130 Warren Hall, 900 Veteran Avenue, Los Angeles, CA 90095-7073, USA.
A E Butler
R Galasso
R A Rizza
P C Butler
Mayo Clinic in Arizona · USUniversity of California, Los Angeles · US

Funding

Role of IAPP in Islet Dysfunction in DiabetesR01DK059579 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BUTLER, PETER CAWOOD · 2001 to 2019
$7.5M
Role of Pulsatile Insulin Secretion.R01DK061539 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BUTLER, PETER CAWOOD · 2002 to 2012
$4.1M
NIDDK NIH HHS DK 59579NIDDK NIH HHS DK61539
6 · The paper itself

Abstract

aims/hypothesisType 1 and type 2 diabetes are characterised by a beta cell deficit. Islet hyperplasia has been described in patients with Zollinger-Ellison syndrome secondary to gastrin-producing tumours (gastrinomas), and gastrin therapy has increased beta cell mass in rodents and human islets in vitro. In the present studies we addressed the following questions: (1) In pancreas specimens from gastrinoma cases, is the fractional beta cell area increased? (2) If so, is this restricted to tumour-adjacent islets or also present in tumour-distant islets? (3) Is new beta cell formation (beta cell replication and islet neogenesis) increased and beta cell apoptosis decreased in pancreas specimens from gastrinoma cases?

methodsPancreas was obtained at surgery from four patients with Zollinger-Ellison syndrome caused by pancreatic gastrinomas and 15 control subjects at autopsy.

resultsIslet fractional beta cell area (p<0.001), islet size (p<0.001) and beta cell replication (Ki67 staining) (p<0.05) were increased in islets adjacent to the tumours, but not in tumour-distant pancreas, compared with control subjects. We did not observe any differences in beta cell apoptosis or in the number of insulin-positive cells in ducts either adjacent to or distant from the tumour. CONCLUSIONS/

interpretationOne or more factors released by human gastrinomas increase beta cell replication in islets immediately adjacent to the tumour, but not in tumour-distant islets. While these findings demonstrate that adult human beta cells can be driven into the cell cycle, they caution against the therapeutic usefulness of gastrin, since islets located >1 cm away from the gastrinomas did not exhibit changes in beta cell turnover, despite markedly elevated systemic gastrin levels sufficient to cause severe gastrointestinal symptoms.

Indexed as

Body Mass IndexCell DivisionDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2GastrinomaGastrinsHumansInsulin-Secreting CellsIslets of LangerhansMiddle AgedPancreatic NeoplasmsZollinger-Ellison SyndromeGastrins

Identifiers

PMID17016695
OpenAlexW2167213847

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.