Evidence map›Paper›PMID 33435513›Full record

ReviewInternational journal of molecular sciences2021

Molecular Mechanisms of Glucocorticoid-Induced Insulin Resistance.

Carine Beaupere, Alexandrine Liboz, Bruno Fève, Bertrand Blondeau, Ghislaine Guillemain

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 5 pooled it
19.6field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 5 syntheses or guidelines pooled it, 242 citations in OpenAlex.

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67 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Carine BeaupereINSERM UMR_S938, Saint-Antoine Research Center, Hospitalo-Universitary Institute, Sorbonne Université, ICAN, 75012 Paris, France.ORCID 0000-0002-7220-4892
Alexandrine LibozINSERM UMR_S938, Saint-Antoine Research Center, Hospitalo-Universitary Institute, Sorbonne Université, ICAN, 75012 Paris, France.
Bruno FèveINSERM UMR_S938, Saint-Antoine Research Center, Hospitalo-Universitary Institute, Sorbonne Université, ICAN, 75012 Paris, France.
Bertrand BlondeauINSERM UMR_S938, Saint-Antoine Research Center, Hospitalo-Universitary Institute, Sorbonne Université, ICAN, 75012 Paris, France.
Ghislaine GuillemainINSERM UMR_S938, Saint-Antoine Research Center, Hospitalo-Universitary Institute, Sorbonne Université, ICAN, 75012 Paris, France.
Inserm · FR

Funding

Aide aux jeunes diabétiques Blondeau 2018Fondation pour la Recherche Médicale EQU201903007868Société Francophone du Diabète Blondeau 2019
6 · The paper itself

Abstract

Glucocorticoids (GCs) are steroids secreted by the adrenal cortex under the hypothalamic-pituitary-adrenal axis control, one of the major neuro-endocrine systems of the organism. These hormones are involved in tissue repair, immune stability, and metabolic processes, such as the regulation of carbohydrate, lipid, and protein metabolism. Globally, GCs are presented as 'flight and fight' hormones and, in that purpose, they are catabolic hormones required to mobilize storage to provide energy for the organism. If acute GC secretion allows fast metabolic adaptations to respond to danger, stress, or metabolic imbalance, long-term GC exposure arising from treatment or Cushing's syndrome, progressively leads to insulin resistance and, in fine, cardiometabolic disorders. In this review, we briefly summarize the pharmacological actions of GC and metabolic dysregulations observed in patients exposed to an excess of GCs. Next, we describe in detail the molecular mechanisms underlying GC-induced insulin resistance in adipose tissue, liver, muscle, and to a lesser extent in gut, bone, and brain, mainly identified by numerous studies performed in animal models. Finally, we present the paradoxical effects of GCs on beta cell mass and insulin secretion by the pancreas with a specific focus on the direct and indirect (through insulin-sensitive organs) effects of GCs. Overall, a better knowledge of the specific action of GCs on several organs and their molecular targets may help foster the understanding of GCs' side effects and design new drugs that possess therapeutic benefits without metabolic adverse effects.

Indexed as

Insulin ResistanceAdipose TissueAnimalsGlucocorticoidsHumansInsulinInsulin SecretionLiverMuscle, SkeletalPancreasSignal TransductionGlucocorticoidsInsulinadipose tissueglucocorticoidsinsulin resistancelivermusclepancreatic beta cellssignaling pathway

Identifiers

PMID33435513
PMCPMC7827500
OpenAlexW3118708823

What Socratic 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 Socratic graph.