Evidence map›Paper›PMID 27813705›Full record

ArticleThe Journal of clinical endocrinology and metabolism2017

Increased Proliferation of the Pancreatic Duct Gland Compartment in Type 1 Diabetes.

Abu Saleh Md Moin, Peter C Butler, Alexandra E Butler

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
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  8. Single-cell resolution analysis of the human pancreatic ductal progenitor cell niche.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Review
  10. Review
  11. Article
  12. Pancreatic Progenitors: There and Back Again.Trends in endocrinology and metabolism: TEM · 2019
    Review
  13. Article
  14. Article
  15. Increased Chromogranin A-Positive Hormone-Negative Cells in Chronic Pancreatitis.The Journal of clinical endocrinology and metabolism · 2018
    Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Abu Saleh Md MoinLarry L. Hillblom Islet Research Center, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, California 90095.
Peter C ButlerLarry L. Hillblom Islet Research Center, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, California 90095.
Alexandra E ButlerLarry L. Hillblom Islet Research Center, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, California 90095.
University 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
Capacity and Mechanisms of Beta Cell Regeneration in HumansR01DK077967 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BUTLER, PETER CAWOOD · 2008 to 2016
$2.5M
NIDDK NIH HHS R01 DK059579NIDDK NIH HHS R01 DK077967
6 · The paper itself

Abstract

Context: Pancreatic duct glands (PDGs) have been proposed as a source of regeneration in response to exocrine pancreas injury, and thus may serve as an organ stem cell niche. There is evidence to suggest ongoing β-cell formation in longstanding type 1 diabetes (T1D), but the source is unknown. Objective: To investigate the PDG compartment of the pancreas in humans with T1D for evidence of an active regenerative signature (presence of progenitor cells and increased proliferation) and, in particular, as a potential source of β-cells. Design, Setting, and Participants: Pancreases from 46 brain dead organ donors (22 with T1D, 24 nondiabetic controls) were investigated for activation (increased proliferation) and markers of pancreatic exocrine and endocrine progenitors. Results: PDG cell replication was increased in T1D (6.3% ± 1.6% vs 0.6% ± 0.1%, P < 0.001, T1D vs nondiabetic), most prominently in association with pancreatic inflammation. There were increased progenitor-like cells in PDGs of T1D, but predominantly with an exocrine fate. Conclusion: The PDG compartment is activated in T1D consistent with a response to ongoing inflammation, and via resulting ductal hyperplasia may contribute to local obstructive pancreatitis and eventual pancreatic atrophy characteristic of T1D. However, there is no evidence of effective endocrine cell formation from PDGs.

Indexed as

Cell ProliferationAdolescentAdultAgedAged, 80 and overBiomarkersCase-Control StudiesChildChild, PreschoolDiabetes Mellitus, Type 1FemaleFollow-Up StudiesHumansIslets of LangerhansMaleMiddle AgedBiomarkers

Identifiers

PMID27813705
PMCPMC5413103
OpenAlexW2548273592

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.