Evidence map›Paper›PMID 33045434›Full record

ArticleMolecular metabolism2020

Skeletal glucocorticoid signalling determines leptin resistance and obesity in aging mice.

Holger Henneicke, Sarah Kim, Michael M Swarbrick, Jingbao Li, Sylvia J Gasparini, Joanne Thai, Daphne Foong, Lauryn L Cavanagh, Colette Fong-Yee, Elisabeth Karsten and 4 more

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

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
  7. The Glucocorticoid Receptor in Osterix-Expressing Cells Regulates Bone Mass, Bone Marrow Adipose Tissue, and Systemic Metabolism in Female Mice During Aging.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
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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

14 authors at 1 institution in 3 countries.

Holger HenneickeBone Research Program, ANZAC Research Institute, The University of Sydney, Australia; Center for Regenerative Therapies TU Dresden, Technische Universität Dresden, Germany; Department of Medicine III, Technische Universität Dresden, Germany; Center for Healthy Aging, Technische Universität Dresden, Germany. Electronic address: holger.henneicke@tu-dresden.de.
Sarah KimBone Research Program, ANZAC Research Institute, The University of Sydney, Australia; Concord Clinical School, The University of Sydney, Australia. Electronic address: sarah.kim1@sydney.edu.au.
Michael M SwarbrickBone Research Program, ANZAC Research Institute, The University of Sydney, Australia; Concord Clinical School, The University of Sydney, Australia. Electronic address: michael.swarbrick@sydney.edu.au.
Jingbao LiBone Research Program, ANZAC Research Institute, The University of Sydney, Australia; Key Laboratory for Space Bioscience & Biotechnology, Institute of Special Environmental Biophysics, School of Life Sciences, Northwestern Polytechnical University, China. Electronic address: lijingbao@nwpu.edu.cn.
Sylvia J GaspariniBone Research Program, ANZAC Research Institute, The University of Sydney, Australia. Electronic address: sylvia.gasparini@tu-dresden.de.
Joanne ThaiBone Research Program, ANZAC Research Institute, The University of Sydney, Australia. Electronic address: joanne.thai@sydney.edu.au.
Daphne FoongBone Research Program, ANZAC Research Institute, The University of Sydney, Australia. Electronic address: daphne.foong@sydney.edu.au.
Lauryn L CavanaghBone Research Program, ANZAC Research Institute, The University of Sydney, Australia. Electronic address: lauryn.cavanagh@sydney.edu.au.
Colette Fong-YeeBone Research Program, ANZAC Research Institute, The University of Sydney, Australia. Electronic address: colette.fong-yee@sydney.edu.au.
Elisabeth KarstenKolling Institute of Medical Research, The University of Sydney, Australia. Electronic address: elisabeth@sanguibio.com.
Ruby C Y LinCentre for Infectious Diseases and Microbiology, Westmead Institute for Medical Research, The University of Sydney, Australia; School of Medical Sciences, University of New South Wales Sydney, Australia. Electronic address: ruby.lin@sydney.edu.au.
Mark S CooperConcord Clinical School, The University of Sydney, Australia. Electronic address: mark.cooper@sydney.edu.au.
Hong ZhouBone Research Program, ANZAC Research Institute, The University of Sydney, Australia; Concord Clinical School, The University of Sydney, Australia. Electronic address: h.zhou@sydney.edu.au.
Markus J SeibelBone Research Program, ANZAC Research Institute, The University of Sydney, Australia; Concord Clinical School, The University of Sydney, Australia. Electronic address: markus.seibel@sydney.edu.au.
The University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAging and chronic glucocorticoid excess share a number of critical features, including the development of central obesity, insulin resistance and osteoporosis. Previous studies have shown that skeletal glucocorticoid signalling increases with aging and that osteoblasts mediate the detrimental skeletal and metabolic effects of chronic glucocorticoid excess. Here, we investigated whether endogenous glucocorticoid action in the skeleton contributes to metabolic dysfunction during normal aging.

methodsMice lacking glucocorticoid signalling in osteoblasts and osteocytes (HSD2

resultsAs they aged, wild-type mice became obese and insulin-resistant. In contrast, HSD2

conclusionsSkeletal glucocorticoid signalling is critical for the development of leptin resistance, obesity and insulin resistance during aging. These findings underscore the skeleton's importance in the regulation of body weight and implicate osteoblastic/osteocytic glucocorticoid signalling in the aetiology of aging-related obesity and metabolic disease.

Indexed as

Adipose TissueAge FactorsAgingAnimalsArcuate Nucleus of HypothalamusBody CompositionBody WeightBone and BonesBrainFemaleGlucocorticoidsGlucoseHypothalamusInsulinInsulin ResistanceLeptinGlucocorticoidsGlucoseInsulinLeptinAgingAppetiteGlucocorticoidLeptinObesityOsteoblastOsteocyte

Identifiers

PMID33045434
PMCPMC7596342
OpenAlexW3092048450

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.