Evidence map›Paper›PMID 25025956›Full record

ArticleNature communications2014

Glucose-induced electrical activities and insulin secretion in pancreatic islet β-cells are modulated by CFTR.

Jing Hui Guo, Hui Chen, Ye Chun Ruan, Xue Lian Zhang, Xiao Hu Zhang, Kin Lam Fok, Lai Ling Tsang, Mei Kuen Yu, Wen Qing Huang, Xiao Sun and 4 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04379726 (Characterization of β-cell Function and Insulin Sensitivity in Pre-transplant Patients With Cystic Fibrosis), which is not on this map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
13.2field-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.

NCT04379726 unknown statusnot on this mapstarted 2020, after this paper: background citation

Characterization of β-cell Function and Insulin Sensitivity in Pre-transplant Patients With Cystic Fibrosis

TypeobservationalSponsorFondazione IRCCS Ca' Granda, Ospedale Maggiore PoliclinicoRan2020 to 2023Enrolled150ConditionsCystic Fibrosis-related DiabetesArmstherapeutic optimization
3 · Its place in the literature

Who cites it

97 citing papers in PubMed, 151 citations in OpenAlex.

  1. Impact of Genetics on Endocrine Manifestations of Cystic Fibrosis.Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2026
    Review
  2. Review
  3. Article
  4. CFTR mediates ClNature communications · 2026
    Article
  5. Article
  6. The endocrine complications of cystic fibrosis.Nature reviews. Endocrinology · 2026
    Review
  7. Article
  8. Observational
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. CFTR Modulates Hypothalamic Neuron Excitability to Maintain Female Cycle.International journal of molecular sciences · 2023
    Article
  18. Review
  19. Article
  20. Review

37 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Jing Hui GuoEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Hui ChenEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Ye Chun Ruan1] Epithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China [2] Sichuan University-The Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine, Key Laboratory of Obstetric, Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education of China, West China Second University Hospital, Sichuan University, Chengdu 610041, China [3] Lui Che Woo Institute of Innovative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Xue Lian ZhangDepartment of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Xiao Hu ZhangEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Kin Lam FokEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Lai Ling TsangEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Mei Kuen YuEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Wen Qing HuangEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Xiao SunEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Yiu Wa ChungEpithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Xiaohua Jiang1] Epithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China [2] Sichuan University-The Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine, Key Laboratory of Obstetric, Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education of China, West China Second University Hospital, Sichuan University, Chengdu 610041, China [3] Lui Che Woo Institute of Innovative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Yoshiro SohmaDepartment of Pharmacology, Keio University School of Medicine, Shinjuku, Tokyo 160-8582, Japan.
Hsiao Chang Chan1] Epithelial Cell Biology Research Center, Key Laboratory of Regenerative Medicine of Ministry of Education of China, CUHK-SJTU Joint Center for Human Reproduction and Related Disease, Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China [2] Sichuan University-The Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine, Key Laboratory of Obstetric, Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education of China, West China Second University Hospital, Sichuan University, Chengdu 610041, China [3] Lui Che Woo Institute of Innovative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Chinese University of Hong Kong · CNBeijing Tongren Hospital · CNCapital Medical University · CNKeio University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cause of insulin insufficiency remains unknown in many diabetic cases. Up to 50% adult patients with cystic fibrosis (CF), a disease caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR), develop CF-related diabetes (CFRD) with most patients exhibiting insulin insufficiency. Here we show that CFTR is a regulator of glucose-dependent electrical acitivities and insulin secretion in β-cells. We demonstrate that glucose elicited whole-cell currents, membrane depolarization, electrical bursts or action potentials, Ca(2+) oscillations and insulin secretion are abolished or reduced by inhibitors or knockdown of CFTR in primary mouse β-cells or RINm5F β-cell line, or significantly attenuated in CFTR mutant (DF508) mice compared with wild-type mice. VX-809, a newly discovered corrector of DF508 mutation, successfully rescues the defects in DF508 β-cells. Our results reveal a role of CFTR in glucose-induced electrical activities and insulin secretion in β-cells, shed light on the pathogenesis of CFRD and possibly other idiopathic diabetes, and present a potential treatment strategy.

Indexed as

AnimalsCystic Fibrosis Transmembrane Conductance RegulatorEnzyme-Linked Immunosorbent AssayGlucoseInsulinInsulin-Secreting CellsInsulin SecretionMaleMembrane PotentialsMiceMice, Inbred C57BLPatch-Clamp TechniquesCystic Fibrosis Transmembrane Conductance RegulatorGlucoseInsulin

Identifiers

PMID25025956
PMCPMC4104438
OpenAlexW2147821592

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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.