Evidence map›Paper›PMID 38047107›Full record

ArticleFrontiers in endocrinology2023

E47 as a novel glucocorticoid-dependent gene mediating lipid metabolism in patients with endogenous glucocorticoid excess.

Wei Zhang, Hanna Nowotny, Marily Theodoropoulou, Julia Simon, Charlotte M Hemmer, Martin Bidlingmaier, Matthias K Auer, Martin Reincke, Henriette Uhlenhaut, Nicole Reisch

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

10 authors at 4 institutions in 1 country.

Wei ZhangMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Hanna NowotnyMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Marily TheodoropoulouMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Julia SimonMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Charlotte M HemmerMolecular Endocrinology, Institutes for Diabetes and Obesity & Diabetes and Cancer IDO & IDC, Helmholtz Zentrum Muenchen (HMGU) and German Center for Diabetes Research (DZD), Munich, Germany.
Martin BidlingmaierMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Matthias K AuerMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Martin ReinckeMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Henriette UhlenhautMolecular Endocrinology, Institutes for Diabetes and Obesity & Diabetes and Cancer IDO & IDC, Helmholtz Zentrum Muenchen (HMGU) and German Center for Diabetes Research (DZD), Munich, Germany.
Nicole ReischMedizinische Klinik and Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Ludwig-Maximilians-Universität München · DELMU Klinikum · DEGerman Center for Diabetes Research · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: E47 has been identified as a modulating transcription factor of glucocorticoid receptor target genes, its loss protecting mice from metabolic adverse effects of glucocorticoids. We aimed to analyze the role of E47 in patients with endogenous glucocorticoid excess [Cushing's syndrome (CS)] and its association with disorders of lipid and glucose metabolism. Methods: This is a prospective cohort study including 120 female patients with CS (ACTH-dependent = 79; ACTH-independent = 41) and 26 healthy female controls. Morning whole blood samples after an overnight fast were used to determine E47 mRNA expression levels in patients with overt CS before and 6-12 months after curative surgery. Expression levels were correlated with the clinical phenotype of the patients. Control subjects underwent ACTH stimulation tests and dexamethasone suppression tests to analyze short-term regulation of E47. Results: E47 gene expression showed significant differences in patient cohorts with overt CS vs. patients in remission ( Conclusion: E47 is a GC-dependent gene that is upregulated in GC excess potentially aiming at reducing metabolic glucocorticoid side effects such as dyslipidemia.

Indexed as

Cushing SyndromeGlucocorticoidsAdrenocorticotropic HormoneAnimalsBasic Helix-Loop-Helix ProteinsCholesterolDexamethasoneFemaleHumansHydrocortisoneLipid MetabolismMiceProspective StudiesRNA, MessengerAdrenocorticotropic HormoneBasic Helix-Loop-Helix ProteinsCholesterolDexamethasoneGlucocorticoidsHydrocortisoneRNA, MessengerTCF3 protein, humanACTHcomorbiditycortisolCushing’s diseaseCushing’s syndromedyslipidemiatranscription factor 3

Identifiers

PMID38047107
PMCPMC10691538
OpenAlexW4388797090

What OpenQuestion holds

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LicenceCC BY
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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.