Evidence map›Paper›PMID 26283735›Full record

ArticleDiabetes2015

The ΔF508 Mutation in the Cystic Fibrosis Transmembrane Conductance Regulator Is Associated With Progressive Insulin Resistance and Decreased Functional β-Cell Mass in Mice.

Ghislaine Fontés, Julien Ghislain, Isma Benterki, Bader Zarrouki, Dominique Trudel, Yves Berthiaume, Vincent Poitout

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06322446 (Effects of a Strength Exercise Program on Muscular Health in People With CF Treated With Modulators of the Cystic Fibrosis Transmembrane Conductance Regulator Receptor), which is not on this map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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.

NCT06322446 naactive not recruitingnot on this mapstarted 2024, after this paper: background citation

Effects of a Strength Exercise Program on Muscular Health in People With CF Treated With Modulators of the Cystic Fibrosis Transmembrane Conductance Regulator Receptor (CFTR)

TypeinterventionalSponsorUniversidad Politecnica de MadridRan2024 to 2026Enrolled48ConditionsCystic FibrosisArmsExercise
3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Role of Ion-Transporting Proteins in Human Disease.International journal of molecular sciences · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Islet Function in the Pathogenesis of Cystic Fibrosis-Related Diabetes Mellitus.Clinical medicine insights. Endocrinology and diabetes · 2021
    Review
  13. Free fatty acid receptor 3 differentially contributes to β-cell compensation under high-fat diet and streptozotocin stress.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Cystic Fibrosis-Related Diabetes: Pathophysiology and Therapeutic Challenges.Clinical medicine insights. Endocrinology and diabetes · 2019
    Review
  18. Article
  19. Review
  20. Review
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

7 authors at 1 institution in 1 country.

Ghislaine FontésMontreal Diabetes Research Center, University of Montreal, Quebec, Canada University of Montreal Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada.
Julien GhislainMontreal Diabetes Research Center, University of Montreal, Quebec, Canada University of Montreal Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada.
Isma BenterkiMontreal Diabetes Research Center, University of Montreal, Quebec, Canada University of Montreal Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada Department of Biochemistry and Molecular Medicine, University of Montreal, Montreal, Quebec, Canada.
Bader ZarroukiMontreal Diabetes Research Center, University of Montreal, Quebec, Canada University of Montreal Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada.
Dominique TrudelUniversity of Montreal Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada Department of Pathology and Cell Biology, University of Montreal, Montreal, Quebec, Canada.
Yves BerthiaumeUniversity of Montreal Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada Department of Medicine, University of Montreal, Montreal, Quebec, Canada.
Vincent PoitoutMontreal Diabetes Research Center, University of Montreal, Quebec, Canada University of Montreal Hospital Research Centre, University of Montreal, Montreal, Quebec, Canada Department of Biochemistry and Molecular Medicine, University of Montreal, Montreal, Quebec, Canada Department of Medicine, University of Montreal, Montreal, Quebec, Canada vincent.poitout@umontreal.ca.
Université de Montréal · CA

Funding

Neutral lipid dysregulation of the pancreatic beta-cellR01DK058096 · NIDDK · UNIVERSITY OF MONTREAL HOSPITAL · PI POITOUT, VINCENT · 2001 to 2020
$3.9M
NIDDK NIH HHS R01 DK058096
6 · The paper itself

Abstract

Cystic fibrosis (CF) is the result of mutations in the cystic fibrosis transmembrane conductance regulator (CFTR). CF-related diabetes affects 50% of adult CF patients. How CFTR deficiency predisposes to diabetes is unknown. Herein, we examined the impact of the most frequent cftr mutation in humans, deletion of phenylalanine at position 508 (ΔF508), on glucose homeostasis in mice. We compared ΔF508 mutant mice with wild-type (WT) littermates. Twelve-week-old male ΔF508 mutants had lower body weight, improved oral glucose tolerance, and a trend toward higher insulin tolerance. Glucose-induced insulin secretion was slightly diminished in ΔF508 mutant islets, due to reduced insulin content, but ΔF508 mutant islets were not more sensitive to proinflammatory cytokines than WT islets. Hyperglycemic clamps confirmed an increase in insulin sensitivity with normal β-cell function in 12- and 18-week-old ΔF508 mutants. In contrast, 24-week-old ΔF508 mutants exhibited insulin resistance and reduced β-cell function. β-Cell mass was unaffected at 11 weeks of age but was significantly lower in ΔF508 mutants versus controls at 24 weeks. This was not associated with gross pancreatic pathology. We conclude that the ΔF508 CFTR mutation does not lead to an intrinsic β-cell secretory defect but is associated with insulin resistance and a β-cell mass deficit in aging mutants.

Indexed as

AgingInsulin ResistanceMutationAnimalsCrosses, GeneticCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDiabetes MellitusDown-RegulationFemaleHumansImmunohistochemistryInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorInsulin

Identifiers

PMID26283735
PMCPMC4876763
OpenAlexW2172574503

What OpenQuestion holds

Textmetadata
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.