Evidence map›Paper›PMID 25299696›Full record

ArticleInternational journal of molecular sciences2014

FOXO1 content is reduced in cystic fibrosis and increases with IGF-I treatment.

Arianna Smerieri, Luisa Montanini, Luigi Maiuri, Sergio Bernasconi, Maria E Street

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

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  6. High expression of P4HA3 in obesity: a potential therapeutic target for type 2 diabetes.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022
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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

5 authors at 2 institutions in 1 country.

Arianna SmerieriDepartment of Pediatrics, University Hospital of Parma, Via Gramsci 14, 43126 Parma, Italy. arianna.smerieri@unipr.it.
Luisa MontaniniDepartment of Pediatrics, University Hospital of Parma, Via Gramsci 14, 43126 Parma, Italy. luisa.montanini@unipr.it.
Luigi MaiuriEuropean Institute for Research in Cystic Fibrosis, San Raffaele Scientific Institute, Via Olgettina 60, 20132 Milan, Italy. maiuri@unina.it.
Sergio BernasconiDepartment of Pediatrics, University Hospital of Parma, Via Gramsci 14, 43126 Parma, Italy. SBernasconi@ao.pr.it.
Maria E StreetDepartment of Pediatrics, University Hospital of Parma, Via Gramsci 14, 43126 Parma, Italy. mariaelisabeth.street@unipr.it.
University of Parma · ITUniversity of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis-related diabetes is to date the most frequent complication in cystic fibrosis (CF). The mechanisms underlying this condition are not well understood, and a possible role of insulin resistance is debated. We investigated insulin signal transduction in CF. Total insulin receptor, IRS1, p85 PI3K, and AKT contents were substantially normal in CF cells (CFBE41o-), whereas winged helix forkhead (FOX)O1 contents were reduced both in baseline conditions and after insulin stimulation. In addition, CF cells showed increased ERK1/2, and reduced β2 arrestin contents. No significant change in SOCS2 was observed. By using a CFTR inhibitor and siRNA, changes in FOXO1 were related to CFTR loss of function. In a CF-affected mouse model, FOXO1 content was reduced in the muscle while no significant difference was observed in liver and adipose tissue compared with wild-type. Insulin-like growth factor 1 (IGF-I) increased FOXO1 content in vitro and in vivo in muscle and adipose tissue. In conclusion; we present the first description of reduced FOXO1 content in CF, which is compatible with reduced gluconeogenesis and increased adipogenesis, both features of insulin insensitivity. IGF-I treatment was effective in increasing FOXO1, thereby suggesting that it could be considered as a potential treatment in CF patients possibly to prevent and treat cystic fibrosis-related diabetes.

Indexed as

Adipose TissueAnimalsCell LineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorFemaleForkhead Box Protein O1Forkhead Transcription FactorsInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsMiceMice, Inbred CFTRMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Muscle, SkeletalPhosphatidylinositol 3-KinasesCystic Fibrosis Transmembrane Conductance RegulatorForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRecombinant ProteinsSocs2 protein, mouseSuppressor of Cytokine Signaling Proteins

Identifiers

PMID25299696
PMCPMC4227201
OpenAlexW2025636347

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.