Evidence map›Paper›PMID 31606738›Full record

ArticleThe Journal of clinical endocrinology and metabolism2020

A Role for Oncostatin M in the Impairment of Glucose Homeostasis in Obesity.

Irene Piquer-Garcia, Laura Campderros, Siri D Taxerås, Aleix Gavaldà-Navarro, Rosario Pardo, María Vila, Silvia Pellitero, Eva Martínez, Jordi Tarascó, Pau Moreno and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

23 authors at 6 institutions in 2 countries.

Irene Piquer-GarciaDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Laura CampderrosDepartment of Biochemistry and Molecular Biomedicine, and Institute of Biomedicine, University of Barcelona, Barcelona, Spain.
Siri D TaxeråsDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Aleix Gavaldà-NavarroDepartment of Biochemistry and Molecular Biomedicine, and Institute of Biomedicine, University of Barcelona, Barcelona, Spain.
Rosario PardoLaboratory of Metabolism and Obesity, Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain.
María VilaLaboratory of Metabolism and Obesity, Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain.
Silvia PelliteroDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Eva MartínezDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Jordi TarascóDepartment of Surgery, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Pau MorenoDepartment of Surgery, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Joan VillarroyaDepartment of Biochemistry and Molecular Biomedicine, and Institute of Biomedicine, University of Barcelona, Barcelona, Spain.
Rubén CereijoDepartment of Biochemistry and Molecular Biomedicine, and Institute of Biomedicine, University of Barcelona, Barcelona, Spain.
Lorena GonzálezDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Marjorie ReyesDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Silvia Rodriguez-FernándezImmunology Section, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Marta Vives-PiBiomedicalResearch Center (Red Fisiopatología de la Diabetes y enfermedades metabólicas) (CIBERDEM), ISCIII, Madrid, Spain.
Carles LerinEndocrinology, Sant Joan de Déu Hospital, Barcelona, Spain.
Carrie M ElksMatrix Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, Louisiana.
Jacqueline M StephensAdipocyte Biology Laboratory, Pennington Biomedical Research Center, Baton Rouge, Louisiana.
Manel Puig-DomingoDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Francesc VillarroyaDepartment of Biochemistry and Molecular Biomedicine, and Institute of Biomedicine, University of Barcelona, Barcelona, Spain.
Josep A VillenaLaboratory of Metabolism and Obesity, Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain.
David Sánchez-InfantesDepartment of Endocrinology and Nutrition, Germans Trias i Pujol Research Institute, Barcelona, Spain.
Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol · ESInstituto de Salud Carlos III · ESUniversitat Autònoma de Barcelona · ESPennington Biomedical Research Center · USHospital de Sant Pau · ESHospital Sant Joan de Déu Barcelona · ES

Funding

The Effects of Oncostatin M on the Adipose Tissue Extracellular MatrixK01DK106307 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI ELKS, CARRIE M · 2016 to 2019
$508k
NIDDK NIH HHS K01 DK106307
6 · The paper itself

Abstract

contextOncostatin M (OSM) plays a key role in inflammation, but its regulation and function during obesity is not fully understood.

objectiveThe aim of this study was to evaluate the relationship of OSM with the inflammatory state that leads to impaired glucose homeostasis in obesity. We also assessed whether OSM immunoneutralization could revert metabolic disturbances caused by a high-fat diet (HFD) in mice.

design28 patients with severe obesity were included and stratified into two groups: (1) glucose levels <100 mg/dL and (2) glucose levels >100 mg/dL. White adipose tissue was obtained to examine OSM gene expression. Human adipocytes were used to evaluate the effect of OSM in the inflammatory response, and HFD-fed C57BL/6J mice were injected with anti-OSM antibody to evaluate its effects.

resultsOSM expression was elevated in subcutaneous and visceral fat from patients with obesity and hyperglycemia, and correlated with Glut4 mRNA levels, serum insulin, homeostatic model assessment of insulin resistance, and inflammatory markers. OSM inhibited adipogenesis and induced inflammation in human adipocytes. Finally, OSM receptor knockout mice had increased Glut4 mRNA levels in adipose tissue, and OSM immunoneutralization resulted in a reduction of glucose levels and Ccl2 expression in adipose tissue from HFD-fed mice.

conclusionsOSM contributes to the inflammatory state during obesity and may be involved in the development of insulin resistance.

Indexed as

HomeostasisAdipocytesAdultAnimalsFemaleGlucoseGlucose Transporter Type 4HumansInsulin ResistanceMaleMiceMice, Inbred C57BLMiddle AgedObesityOncostatin MReceptors, Oncostatin MGlucoseGlucose Transporter Type 4Oncostatin MReceptors, Oncostatin Minflammationinsulin resistanceobesityoncostatin M

Identifiers

PMID31606738
PMCPMC7112982
OpenAlexW2979601037

What OpenQuestion holds

Textmetadata
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.