Evidence map›Paper›PMID 29701083›Full record

ArticleCartilage2019

Elevated Glucose Levels Preserve Glucose Uptake, Hyaluronan Production, and Low Glutamate Release Following Interleukin-1β Stimulation of Differentiated Chondrocytes.

Victoria Rotter Sopasakis, Ruth Wickelgren, Valentina Sukonina, Camilla Brantsing, Emilia Svala, Elisabeth Hansson, Sven Enerbäck, Anders Lindahl, Eva Skiöldebrand

Open access · bronzeAbstract read
In one paragraph

Article in Cartilage, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
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  10. [Research Progress in Glucose Metabolism of Chondrocytes].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Review
  11. 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

9 authors at 2 institutions in 1 country.

Victoria Rotter SopasakisDepartment of Clinical Chemistry and Transfusion Medicine, University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0002-1012-1952
Ruth WickelgrenDepartment of Clinical Chemistry and Transfusion Medicine, University of Gothenburg, Gothenburg, Sweden.
Valentina SukoninaDepartment of Medical Biochemistry and Cell biology, University of Gothenburg, Gothenburg, Sweden.
Camilla BrantsingDepartment of Clinical Chemistry and Transfusion Medicine, University of Gothenburg, Gothenburg, Sweden.
Emilia SvalaDepartment of Biomedical Sciences and Veterinary Public Health, Swedish University of Agricultural Sciences, Gothenburg, Sweden.
Elisabeth HanssonDepartment of Clinical Neuroscience, University of Gothenburg, Gothenburg, Sweden.
Sven EnerbäckDepartment of Medical Biochemistry and Cell biology, University of Gothenburg, Gothenburg, Sweden.
Anders LindahlDepartment of Clinical Chemistry and Transfusion Medicine, University of Gothenburg, Gothenburg, Sweden.
Eva SkiöldebrandDepartment of Clinical Chemistry and Transfusion Medicine, University of Gothenburg, Gothenburg, Sweden.
University of Gothenburg · SESwedish University of Agricultural Sciences · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChondrocytes are responsible for remodeling and maintaining the structural and functional integrity of the cartilage extracellular matrix. Because of the absence of a vascular supply, chondrocytes survive in a relatively hypoxic environment and thus have limited regenerative capacity during conditions of cellular stress associated with inflammation and matrix degradation, such as osteoarthritis (OA). Glucose is essential to sustain chondrocyte metabolism and is a precursor for key matrix components. In this study, we investigated the importance of glucose as a fuel source for matrix repair during inflammation as well as the effect of glucose on inflammatory mediators associated with osteoarthritis.

designTo create an OA model, we used equine chondrocytes from 4 individual horses that were differentiated into cartilage pellets

resultsWe found that elevated glucose levels preserve glucose uptake, hyaluronan synthesis, and matrix integrity, as well as induce anti-inflammatory actions by maintaining low expression of Toll-like receptor-4 and low secretion of glutamate.

conclusionsAdequate supply of glucose to chondrocytes during conditions of inflammation and matrix degradation interrupts the detrimental inflammatory cycle and induces synthesis of hyaluronan, thereby promoting cartilage repair.

Indexed as

AnimalsCartilage, ArticularCell DifferentiationCells, CulturedChondrocytesExtracellular MatrixGene Expression RegulationGlucoseGlutamic AcidGlycolysisHorsesHyaluronan SynthasesHyaluronic AcidInterleukin-1betaGlucoseGlutamic AcidHyaluronan SynthasesHyaluronic AcidInterleukin-1betachondrocyteshyaluronaninflammationmatrixosteoarthritis

Identifiers

PMID29701083
PMCPMC6755873
OpenAlexW2800512571

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.