Evidence map›Paper›PMID 29559840›Full record

ArticleInternational journal of medical sciences2018

Dexamethasone Down-regulates Osteocalcin in Bone Cells through Leptin Pathway.

Shu-Mei Chen, Yi-Jen Peng, Chih-Chien Wang, Sui-Lung Su, Donald M Salter, Herng-Sheng Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Effects of Anterior Pituitary Adenomas' Hormones on Glucose Metabolism and Its Clinical Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
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

6 authors at 5 institutions in 2 countries.

Shu-Mei ChenDepartment of Pathology and Laboratory Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, ROC.
Yi-Jen PengDepartment of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
Chih-Chien WangDepartment of Orthopedics, Taipei Medical University Hospital, Taipei, Taiwan, ROC.
Sui-Lung SuSchool of Public Health, National Defense Medical Center, Taipei, Taiwan, ROC.
Donald M SalterCentre for Genomic and Molecular Medicine, IGMM, University of Edinburgh, Edinburgh, UK.
Herng-Sheng LeeDepartment of Pathology and Laboratory Medicine, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, ROC.
National Defense Medical Center · TWKaohsiung Veterans General Hospital · TWTaipei Medical University Hospital · TWTri-Service General Hospital · TWUniversity of Edinburgh · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid therapy, especially at higher doses, is associated with significant adverse side effects including osteoporosis. Leptin, secreted from adipose tissue, has diverse effects on bone tissue regulation. As glucocorticoids stimulate leptin synthesis and secretion directly in adipose tissue we hypothesised that dexamethasone (DEX) induced osteoporosis may, in part, be mediated by an osteoblast dependent leptin-leptin receptor pathway. Human bone cells expressed leptin and leptin receptors (Ob-Ra and Ob-Rb). DEX increased leptin, Ob-Ra and Ob-Rb expression in a dose-dependent manner while decreasing expression of osteocalcin. In the presence of leptin, Cbfa1 and osteonectin expression showed no significant change, whereas osteocalcin expression was decreased. Recombinant human quadruple antagonist leptin suppressed DEX-induced osteocalcin downregulation. The signaling pathway involved up-regulation of JAK2. In conclusion, upregulation of leptin and Ob-Rb in human bone cells by DEX is associated with down-regulation of osteocalcin expression. The down regulation of osteocalcin by DEX was partially through a leptin autocrine/paracrine loop. Adverse effects of DEX on the skeleton may be modified by targeting leptin signaling pathways.

Indexed as

Bone and BonesCell Culture TechniquesCore Binding Factor Alpha 1 SubunitDexamethasoneGene Expression RegulationHumansJanus Kinase 2LeptinOsteoblastsOsteocalcinOsteocytesOsteoporosisReceptors, LeptinSignal TransductionCore Binding Factor Alpha 1 SubunitDexamethasoneJAK2 protein, humanJanus Kinase 2LeptinOsteocalcinReceptors, Leptindexamethasoneosteoblastosteocalcin downregulation

Identifiers

PMID29559840
PMCPMC5859774
OpenAlexW2789327203

What OpenQuestion holds

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LicenceCC BY-NC
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.