Evidence map›Paper›PMID 40622517›Full record

ArticleJournal of endocrinological investigation2025

Dose-dependent and tissue-specific adverse effects of exogenous glucocorticoids: insights for optimizing clinical practice.

Riccardo Pofi, Nantia Othonos, Thomas Marjot, Ilaria Bonaventura, Amy Barrett, Sarah White, Hamish Miller, Tom Potter, Maíra Bailey, Richard Eastell and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of endocrinological investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. 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

15 authors.

Riccardo PofiOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Nantia OthonosOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Thomas MarjotOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Ilaria BonaventuraDepartment of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena, 324, Rome, 00161, Italy.
Amy BarrettOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Sarah WhiteOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Hamish MillerOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Tom PotterOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Maíra BaileyOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Richard EastellMellanby Centre for Musculoskeletal Research, Division of Clinical Medicine, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, SR10 2RX, UK.
Fatma GossielMellanby Centre for Musculoskeletal Research, Division of Clinical Medicine, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, SR10 2RX, UK.
Conor WoodsDepartment of Diabetes & Endocrinology, St James Hospital, Dublin, Ireland.
Jonathan M HazlehurstInstitute of Applied Health Research, University of Birmingham, Edgbaston, Birmingham, UK.
Leanne HodsonOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK.
Jeremy W TomlinsonOxford Centre for Diabetes, Endocrinology and Metabolism, NIHR Oxford Biomedical Research Centre, University of Oxford, Churchill Hospital, Oxford, OX3 7LJ, UK. jeremy.tomlinson@ocdem.ox.ac.uk.ORCID http://orcid.org/0000-0002-3170-8533

Funding

Bioscientifica BioscientificaBritish Heart Foundation FS/15/56/31645British Heart Foundation FS/SBSRF/21/31013European Society of Endocrinology Short Term FellowshipEuropean Union of Medical Specialists Exchange in Endocrinology Expertise programmeMedical Research Council MR/N024591/1Medical Research Council MR/W015455/1NIHR Oxford Biomedical Research Centre Principal Investigator award
6 · The paper itself

Abstract

purposeThere is limited data on dose-specific metabolic effects of exogenous glucocorticoids (GC) doses. This study aimed to investigate the differential tissue-specific and dose-dependent effects of low-to-intermediate prednisolone doses on insulin sensitivity and bone metabolism in healthy individuals.

methodsWe performed a post-hoc pooled analysis of three independent clinical trials, each administering one week of daily prednisolone at 10 mg, 15 mg, or 20 mg, in a total of 30 different healthy male volunteers (aged 18-65; BMI 20-35 kg/m²; normal kidney function). Outcome measures included: changes in liver (endogenous glucose production-EGP, β-hydroxybutyrate-OHB), muscle (M/I value, Glucose disposal-Gd) and adipose tissue (NEFA, glycerol) insulin sensitivity assessed across a hyperinsulinemic-euglycemic clamp. Bone turnover was evaluated through osteocalcin levels.

resultsPrednisolone 10 mg had minimal impact on metabolic parameters. 15 mg and 20 mg caused similar reductions (no dose effects) in liver (time effect p < 0.05 for EGP and OHB) and skeletal muscle (time effect p < 0.05 for M/I and Gd) insulin sensitivity. However, detrimental effects on adipose tissue were dose dependent (dose*time interaction p < 0.05 for NEFA and glycerol). Osteocalcin levels decreased similarly after both 15 mg and 20 mg of prednisolone (p = 0.199).

conclusionsPrednisolone-induced insulin resistance exhibits tissue-specific and dose-dependent effects. While 15 mg daily for 7 days appears to induce clinically relevant metabolic changes in this population, the dose-dependent effects observed in adipose tissue suggest tissue-specific variability in response. These findings highlight the importance of dose selection in GC therapy, particularly in individuals predisposed to metabolic complications, though further studies are needed in populations with underlying metabolic disorders.

Indexed as

Adipose TissueGlucocorticoidsInsulin ResistanceMuscle, SkeletalPrednisoloneAdolescentAdultAgedBone and BonesDose-Response Relationship, DrugHealthy VolunteersHumansLiverMaleMiddle AgedYoung AdultGlucocorticoidsPrednisoloneBone healthDiabetesGlucose metabolismPrednisoloneSide effects

Identifiers

PMID40622517
PMCPMC12398475

What OpenQuestion holds

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Registered trials

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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.