Evidence map›Paper›PMID 28177189›Full record

Trial reportDiabetes, obesity & metabolism2017

Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct.

Roland H Stimson, Anna J Anderson, Lynne E Ramage, David P Macfarlane, Andrew C de Beaux, Damian J Mole, Ruth Andrew, Brian R Walker

Open access · hybridAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Diabetes, obesity & metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Roland H StimsonCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.ORCID 0000-0002-9002-6188
Anna J AndersonCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Lynne E RamageCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
David P MacfarlaneCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Andrew C de BeauxDepartment of Upper GI Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK.
Damian J MoleDepartment of Upper GI Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK.
Ruth AndrewCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
Brian R WalkerCentre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK.
The Queen's Medical Research Institute · GBEdinburgh Royal Infirmary · GB

Funding

British Heart Foundation RG/11/4/28734Medical Research Council G0901697Medical Research Council MR/K010271/1Medical Research Council MR/P008887/1
6 · The paper itself

Abstract

BACKGROUND AND

aimsThe effects of glucocorticoids on fuel metabolism are complex. Acute glucocorticoid excess promotes lipolysis but chronic glucocorticoid excess causes visceral fat accumulation. We hypothesized that interactions between cortisol and insulin and adrenaline account for these conflicting results. We tested the effect of cortisol on lipolysis and glucose production with and without insulin and adrenaline in humans both in vivo and in vitro. MATERIALS AND

methodsA total of 20 healthy men were randomized to low and high insulin groups (both n = 10). Subjects attended on 3 occasions and received low (c. 150 nM), medium (c. 400 nM) or high (c. 1400 nM) cortisol infusion in a randomized crossover design. Deuterated glucose and glycerol were infused intravenously along with a pancreatic clamp (somatostatin with replacement of glucagon, insulin and growth hormone) and adrenaline. Subcutaneous adipose tissue was obtained for analysis. In parallel, the effect of cortisol on lipolysis was tested in paired primary cultures of human subcutaneous and visceral adipocytes.

resultsIn vivo, high cortisol increased lipolysis only in the presence of high insulin and/or adrenaline but did not alter glucose kinetics. High cortisol increased adipose mRNA levels of ATGL, HSL and CGI-58 and suppressed G0S2. In vitro, high cortisol increased lipolysis in the presence of insulin in subcutaneous, but not visceral, adipocytes.

conclusionsThe acute lipolytic effects of cortisol require supraphysiological concentrations, are dependent on insulin and adrenaline and are observed only in subcutaneous adipose tissue. The resistance of visceral adipose tissue to cortisol's lipolytic effects may contribute to the central fat accumulation observed with chronic glucocorticoid excess.

Indexed as

AdultAgedCross-Over StudiesDouble-Blind MethodEpinephrineGlucocorticoidsGlucoseGlycerolHealthy VolunteersHumansHydrocortisoneInfusions, IntravenousInsulinLipolysisMaleMiddle AgedEpinephrineGlucocorticoidsGlucoseGlycerolHydrocortisoneInsulinadipose tissueadrenalinebody compositiondrug mechanismglucocorticoidglucoseinsulin resistancemetabolism

Identifiers

PMID28177189
PMCPMC5484992
OpenAlexW2586800742

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.