Evidence map›Paper›PMID 30738804›Full record

ArticleJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society2019

Incretin dysfunction and hyperglycemia in cystic fibrosis: Role of acyl-ghrelin.

Xingshen Sun, Yaling Yi, Bo Liang, Yu Yang, Nan He, Katie Larson Ode, Aliye Uc, Kai Wang, Katherine N Gibson-Corley, John F Engelhardt and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 54% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Endocrine Complications of Cystic Fibrosis.Clinics in chest medicine · 2022
    Review
  5. 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

11 authors at 1 institution in 1 country.

Xingshen SunDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, USA.
Yaling YiDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, USA.
Bo LiangDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, USA.
Yu YangDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, USA.
Nan HeDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, USA.
Katie Larson OdeFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA; Department of Pediatrics, University of Iowa, Iowa City, IA 52242, USA.
Aliye UcFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA; Department of Pediatrics, University of Iowa, Iowa City, IA 52242, USA.
Kai WangDepartment of Biostatistics, University of Iowa, Iowa City, IA 52242, USA.
Katherine N Gibson-CorleyFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA; Department of Pathology, University of Iowa, Iowa City, IA 52242, USA.
John F EngelhardtDepartment of Anatomy and Cell Biology, University of Iowa, Iowa City, IA 52242, USA; Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA. Electronic address: john-engelhardt@uiowa.edu.
Andrew W NorrisFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA; Department of Pediatrics, University of Iowa, Iowa City, IA 52242, USA; Department of Biochemistry, University of Iowa, Iowa City, IA 52242, USA. Electronic address: andrew-norris@uiowa.edu.
University of Iowa · US

Funding

Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Jong Sung Kim · 1990 to 2026
$40.5M
Vector Core-Core 2P30DK054759 · NIDDK · UNIVERSITY OF IOWA · PI Alejandro Antonio Pezzulo · 1998 to 2026
$30.5M
Early Pathogenesis of Cystic Fibrosis Related DiabetesR24DK096518 · NIDDK · UNIVERSITY OF IOWA · PI ENGELHARDT, JOHN F, MORAN, ANTOINETTE M. · 2012 to 2018
$10.1M
National Ferret Resource and Research Center on Lung DiseaseR24HL123482 · NHLBI · UNIVERSITY OF IOWA · PI ENGELHARDT, JOHN F · 2014 to 2018
$3.8M
Splanchno-Hormonal Mechanisms of Cystic Fibrosis Related DiabetesR01DK115791 · NIDDK · UNIVERSITY OF IOWA · PI ENGELHARDT, JOHN F, NORRIS, ANDREW W · 2018 to 2021
$1.9M
Fatty Acid Defects & Oxidative Stress Modulate Islet Function in Cystic FibrosisR01DK097820 · NIDDK · UNIVERSITY OF IOWA · PI NORRIS, ANDREW W, UC, ALIYE · 2012 to 2016
$1.9M
NHLBI NIH HHS R24 HL123482NIDDK NIH HHS P30 DK054759NIDDK NIH HHS R01 DK097820NIDDK NIH HHS R01 DK115791NIDDK NIH HHS R24 DK096518NIEHS NIH HHS P30 ES005605
6 · The paper itself

Abstract

backgroundInsulin secretion is insufficient in cystic fibrosis (CF), even before diabetes is present, though the mechanisms involved remain unclear. Acyl-ghrelin (AG) can diminish insulin secretion and is elevated in humans with CF.

methodsWe tested the hypothesis that elevated AG contributes to reduced insulin secretion and hyperglycemia in CF ferrets.

resultsFasting AG was elevated in CF versus non-CF ferrets. Similar to its effects in other species, AG administration in non-CF ferrets acutely reduced insulin, increased growth hormone, and induced hyperglycemia. During oral glucose tolerance testing, non-CF ferrets had responsive insulin, glucagon like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) levels and maintained normal glucose levels, whereas CF ferrets had insufficient responses and became hyperglycemic. Interestingly in wild-type ferrets, the acyl-ghrelin receptor antagonist [D-Lys3]-GHRP-6 impaired glucose tolerance, and abolished insulin, GLP-1, and GIP responses during glucose tolerance testing. By contrast, in CF ferrets [D-Lys3]-GHRP-6 improved glucose tolerance, enhanced the insulin-to-glucose ratio, but did not impact the already low GLP-1 and GIP levels.

conclusionsThese results suggest a mechanism by which elevated AG contributes to CF hyperglycemia through inhibition of insulin secretion, an effect magnified by low GLP-1 and GIP. Interventions that lower ghrelin, ghrelin action, and/or raise GLP-1 or GIP might improve glycemia in CF.

Indexed as

Insulin SecretionAnimalsCystic FibrosisDisease Models, AnimalFemaleFerretsGhrelinHyperglycemiaIncretinsMaleGhrelinIncretinsCystic fibrosis related diabetes[D-Lys3]-GHRP-6Glucagon-like peptide-1Glucose-dependent insulinotropic peptideGrowth hormone secretagogue receptor

Identifiers

PMID30738804
PMCPMC6591024
OpenAlexW2912137655

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.