Evidence map›Paper›PMID 31748811›Full record

ArticleThe Journal of clinical endocrinology and metabolism2020

In Situ Analysis Reveals That CFTR Is Expressed in Only a Small Minority of β-Cells in Normal Adult Human Pancreas.

Michael G White, Rashmi R Maheshwari, Scott J Anderson, Rolando Berlinguer-Palmini, Claire Jones, Sarah J Richardson, Pavana G Rotti, Sarah L Armour, Yuchun Ding, Natalio Krasnogor and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

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  5. The endocrine complications of cystic fibrosis.Nature reviews. Endocrinology · 2026
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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

14 authors at 5 institutions in 2 countries.

Michael G WhiteDiabetes Regenerative Medicine Research Group, Institute of Cellular Medicine, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne, UK.
Rashmi R MaheshwariDiabetes Regenerative Medicine Research Group, Institute of Cellular Medicine, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne, UK.
Scott J AndersonDiabetes Regenerative Medicine Research Group, Institute of Cellular Medicine, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne, UK.
Rolando Berlinguer-PalminiBio-imaging Unit, Newcastle University, Newcastle Upon Tyne, UK.
Claire JonesMolecular Pathology Node Proximity Laboratory, Royal Victoria Infirmary, Newcastle upon Tyne, UK.
Sarah J RichardsonInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, Exeter, UK.
Pavana G RottiFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA, US.
Sarah L ArmourDiabetes Regenerative Medicine Research Group, Institute of Cellular Medicine, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne, UK.
Yuchun DingInterdisciplinary Computing and Complex Biosystems (ICOS) Research Group, School of Computing, Newcastle University, Newcastle upon Tyne, UK.
Natalio KrasnogorInterdisciplinary Computing and Complex Biosystems (ICOS) Research Group, School of Computing, Newcastle University, Newcastle upon Tyne, UK.
John F EngelhardtFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA, US.
Mike A GrayEpithelial Research Group, Institute for Cell and Molecular Biosciences, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Noel G MorganInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, Exeter, UK.
James A M ShawDiabetes Regenerative Medicine Research Group, Institute of Cellular Medicine, Newcastle University Medical School, Framlington Place, Newcastle upon Tyne, UK.
Newcastle University · GBUniversity of Exeter · GBUniversity of Iowa · USNewcastle upon Tyne Hospitals NHS Foundation Trust · GBRoyal Victoria Infirmary · GB

Funding

Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Brandi Janssen · 1990 to 2026
$40.5M
Vector Core-Core 2P30DK054759 · NIDDK · UNIVERSITY OF IOWA · PI Alejandro Antonio Pezzulo · 1998 to 2026
$30.5M
Department of HealthMedical Research Council MR/R014132/1NIDDK NIH HHS P30 DK054759NIEHS NIH HHS P30 ES005605
6 · The paper itself

Abstract

contextAlthough diabetes affects 40% to 50% of adults with cystic fibrosis, remarkably little is known regarding the underlying mechanisms leading to impaired pancreatic β-cell insulin secretion. Efforts toward improving the functional β-cell deficit in cystic fibrosis-related diabetes (CFRD) have been hampered by an incomplete understanding of whether β-cell function is intrinsically regulated by cystic fibrosis transmembrane conductance regulator (CFTR). Definitively excluding meaningful CFTR expression in human β-cells in situ would contribute significantly to the understanding of CFRD pathogenesis.

objectiveTo determine CFTR messenger ribonucleic acid (mRNA) and protein expression within β-cells in situ in the unmanipulated human pancreas of donors without any known pancreatic pathology.

designIn situ hybridization for CFTR mRNA expression in parallel with insulin immunohistochemical staining and immunofluorescence co-localization of CFTR with insulin and the ductal marker, Keratin-7 (KRT7), were undertaken in pancreatic tissue blocks from 10 normal adult, nonobese deceased organ donors over a wide age range (23-71 years) with quantitative image analysis.

resultsCFTR mRNA was detectable in a mean 0.45% (range 0.17%-0.83%) of insulin-positive cells. CFTR protein expression was co-localized with KRT7. One hundred percent of insulin-positive cells were immunonegative for CFTR.

conclusionsFor the first time, in situ CFTR mRNA expression in the unmanipulated pancreas has been shown to be present in only a very small minority (<1%) of normal adult β-cells. These data signal a need to move away from studying endocrine-intrinsic mechanisms and focus on elucidation of exocrine-endocrine interactions in human cystic fibrosis.

Indexed as

AdultAgedAnimalsAnimals, Genetically ModifiedAnimals, NewbornAutopsyCell CountCystic Fibrosis Transmembrane Conductance RegulatorFemaleFerretsGene Knockout TechniquesHumansInsulin-Secreting CellsMaleMiddle AgedPancreasCFTR protein, humanCystic Fibrosis Transmembrane Conductance Regulatorcystic fibrosis related diabetescystic fibrosis transmembrane regulatorin situ hybridization

Identifiers

PMID31748811
PMCPMC7341165
OpenAlexW2991267152

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.