Evidence map›Paper›PMID 29203512›Full record

ArticleDiabetes2018

Glucocorticoids Reprogram β-Cell Signaling to Preserve Insulin Secretion.

Nicholas H F Fine, Craig L Doig, Yasir S Elhassan, Nicholas C Vierra, Piero Marchetti, Marco Bugliani, Rita Nano, Lorenzo Piemonti, Guy A Rutter, David A Jacobson and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Diabetes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
  2. Mifepristone Improves Adipose Tissue Insulin Sensitivity in Insulin Resistant Individuals.The Journal of clinical endocrinology and metabolism · 2021
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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

12 authors at 4 institutions in 3 countries.

Nicholas H F FineInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, U.K.
Craig L DoigInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, U.K.
Yasir S ElhassanInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, U.K.
Nicholas C VierraDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN.
Piero MarchettiDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Marco BuglianiDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Rita NanoDiabetes Research Institute, San Raffaele Scientific Institute, Milan, Italy.
Lorenzo PiemontiDiabetes Research Institute, San Raffaele Scientific Institute, Milan, Italy.ORCID 0000-0002-2172-2198
Guy A RutterSection of Cell Biology and Functional Genomics, Department of Medicine, Imperial College London, London, U.K.ORCID 0000-0001-6360-0343
David A JacobsonDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN.
Gareth G LaveryInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, U.K.
David J HodsonInstitute of Metabolism and Systems Research, University of Birmingham, Edgbaston, U.K. d.hodson@bham.ac.uk.ORCID 0000-0002-8641-8568
The Edgbaston Hospital · GBUniversity of Pisa · ITVanderbilt University · USImperial College London · GB

Funding

Two-Pore-Domain Potassium Channels as Novel Targets for Modulating Islet Hormone SecretionR01DK097392 · NIDDK · VANDERBILT UNIVERSITY · PI JACOBSON, DAVID AARON · 2013 to 2022
$3.3M
Designing selective TALK-1 inhibitors to reduce beta-cell dysfunction in diabetesR01DK115620 · NIDDK · VANDERBILT UNIVERSITY · PI JACOBSON, DAVID AARON · 2018 to 2021
$1.6M
Biotechnology and Biological Sciences Research Council BB/J015873/1Diabetes UK 11/0004210Diabetes UK 12/0004431Medical Research Council MC_PC_14100Medical Research Council MR/K001981/1Medical Research Council MR/K023667/1Medical Research Council MR/L02036X/1Medical Research Council MR/M012646/1Medical Research Council MR/N00275X/1Medical Research Council MR/N020472/1Medical Research Council MR/R010676/1NIDDK NIH HHS R01 DK097392NIDDK NIH HHS R01 DK115620Wellcome TrustWellcome Trust 104612/Z/14/ZWellcome Trust WT098424AIA
6 · The paper itself

Abstract

Excessive glucocorticoid exposure has been shown to be deleterious for pancreatic β-cell function and insulin release. However, glucocorticoids at physiological levels are essential for many homeostatic processes, including glycemic control. We show that corticosterone and cortisol and their less active precursors 11-dehydrocorticosterone (11-DHC) and cortisone suppress voltage-dependent Ca

Indexed as

Calcium Signaling11-beta-Hydroxysteroid Dehydrogenase Type 1AnimalsBiomarkersCalcium ChannelsCell DifferentiationCorticosteroneCortisoneCyclic AMPGlucocorticoidsGlucoseHumansHydrocortisoneInsulinInsulin-Secreting CellsInsulin Secretion11-beta-Hydroxysteroid Dehydrogenase Type 111-dehydrocorticosteroneBiomarkersCalcium ChannelsCorticosteroneCortisoneCyclic AMPGlucocorticoidsGlucoseHydrocortisoneInsulin

Identifiers

PMID29203512
PMCPMC5780059
OpenAlexW2773672092

What OpenQuestion 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 OpenQuestion graph.