Evidence map›Paper›PMID 23524641›Full record

ArticleDiabetes2013

Marked expansion of exocrine and endocrine pancreas with incretin therapy in humans with increased exocrine pancreas dysplasia and the potential for glucagon-producing neuroendocrine tumors.

Alexandra E Butler, Martha Campbell-Thompson, Tatyana Gurlo, David W Dawson, Mark Atkinson, Peter C Butler

Registry-linked trialOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02244164 (Pathophysiological Study of the Increase in Pancreatic Volume in Type 2 Diabetes Treatments.), which is not on this map. Cited by 190 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 9 pooled it
79.6field-weighted citation impact, top 1% 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.

NCT02244164 naterminatednot on this mapstarted 2014, after this paper: background citation

Pathophysiological Study of the Increase in Pancreatic Volume in Type 2 Diabetes Treatments.

TypeinterventionalSponsorErasme University HospitalRan2014 to 2023Enrolled5ConditionsType 2 Diabetes, Incretinomimetics, PancreasArmsIncretinomimetics, DPP-4 inhibitors
3 · Its place in the literature

Who cites it

190 citing papers in PubMed, 9 syntheses or guidelines pooled it, 446 citations in OpenAlex.

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  4. American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2022
    Guideline
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130 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Alexandra E ButlerDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA. aebutler@mednet.ucla.edu
Martha Campbell-Thompson
Tatyana Gurlo
David W Dawson
Mark Atkinson
Peter C Butler
University of California, Los Angeles · USUniversity of Florida · 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
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 DK-059579NIDDK NIH HHS DK-061539NIDDK NIH HHS DK-077967NIDDK NIH HHS R01 DK059579NIDDK NIH HHS R01 DK061539NIDDK NIH HHS R01 DK077967
6 · The paper itself

Abstract

Controversy exists regarding the potential regenerative influences of incretin therapy on pancreatic β-cells versus possible adverse pancreatic proliferative effects. Examination of pancreata from age-matched organ donors with type 2 diabetes mellitus (DM) treated by incretin therapy (n = 8) or other therapy (n = 12) and nondiabetic control subjects (n = 14) reveals an ∼40% increased pancreatic mass in DM treated with incretin therapy, with both increased exocrine cell proliferation (P < 0.0001) and dysplasia (increased pancreatic intraepithelial neoplasia, P < 0.01). Pancreata in DM treated with incretin therapy were notable for α-cell hyperplasia and glucagon-expressing microadenomas (3 of 8) and a neuroendocrine tumor. β-Cell mass was reduced by ∼60% in those with DM, yet a sixfold increase was observed in incretin-treated subjects, although DM persisted. Endocrine cells costaining for insulin and glucagon were increased in DM compared with non-DM control subjects (P < 0.05) and markedly further increased by incretin therapy (P < 0.05). In conclusion, incretin therapy in humans resulted in a marked expansion of the exocrine and endocrine pancreatic compartments, the former being accompanied by increased proliferation and dysplasia and the latter by α-cell hyperplasia with the potential for evolution into neuroendocrine tumors.

Indexed as

AdenomaAdolescentAdultAgedCell ProliferationDiabetes Mellitus, Type 2Dipeptidyl-Peptidase IV InhibitorsFemaleHumansHyperplasiaIncretinsInsulin-Secreting CellsMaleMiddle AgedNeuroendocrine TumorsOrgan SizeDipeptidyl-Peptidase IV InhibitorsIncretinsPyrazinesSitagliptin PhosphateTriazoles

Identifiers

PMID23524641
PMCPMC3712065
OpenAlexW2137982063

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.