Evidence map›Paper›PMID 31540443›Full record

ArticleCells2019

Increased Glycolysis and Higher Lactate Production in Hyperglycemic Myotubes.

Jenny Lund, D Margriet Ouwens, Marianne Wettergreen, Siril S Bakke, G Hege Thoresen, Vigdis Aas

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

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  13. Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024
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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

6 authors at 4 institutions in 3 countries.

Jenny LundSection for Pharmacology and Pharmaceutical Biosciences, Department of Pharmacy, University of Oslo, 0316 Oslo, Norway. jenny.lund@farmasi.uio.no.ORCID 0000-0002-0744-8268
D Margriet OuwensGerman Diabetes Center (DDZ), Leibniz Center for Diabetes Research, Heinrich Heine University, Medical Faculty, 40225 Düsseldorf, Germany. Margriet.Ouwens@ddz.de.ORCID 0000-0001-6709-2702
Marianne WettergreenDepartment of Life Sciences and Health, Faculty of Health Sciences, OsloMet - Oslo Metropolitan University, 0130 Oslo, Norway. Marianne.Wettergreen@ahus.no.
Siril S BakkeCenter of Molecular Inflammation Research and Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, 7491 Trondheim, Norway. siril.s.bakke@ntnu.no.
G Hege ThoresenSection for Pharmacology and Pharmaceutical Biosciences, Department of Pharmacy, University of Oslo, 0316 Oslo, Norway. hege.thoresen@farmasi.uio.no.
Vigdis AasDepartment of Life Sciences and Health, Faculty of Health Sciences, OsloMet - Oslo Metropolitan University, 0130 Oslo, Norway. vigdisaa@oslomet.no.
OsloMet – Oslo Metropolitan University · NOUniversity of Oslo · NOGhent University Hospital · BENorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that chronic hyperglycemia impairs glucose and fatty acid oxidation in cultured human myotubes. To further study the hyperglycemia-induced suppression of oxidation, lactate oxidation, mitochondrial function and glycolytic rate were evaluated. Further, we examined the intracellular content of reactive oxygen species (ROS), production of lactate and conducted pathway-ANOVA analysis on microarray data. In addition, the roles of the pentose phosphate pathway (PPP) and the hexosamine pathway were evaluated. Lactic acid oxidation was suppressed in hyperglycemic versus normoglycaemic myotubes. No changes in mitochondrial function or ROS concentration were observed. Pathway-ANOVA analysis indicated several upregulated pathways in hyperglycemic cells, including glycolysis and PPP. Functional studies showed that glycolysis and lactate production were higher in hyperglycemic than normoglycaemic cells. However, there were no indications of involvement of PPP or the hexosamine pathway. In conclusion, hyperglycemia reduced substrate oxidation while increasing glycolysis and lactate production in cultured human myotubes.

Indexed as

GlycolysisAdultCells, CulturedFemaleHealthy VolunteersHumansHyperglycemiaLactic AcidMaleMuscle Fibers, SkeletalYoung AdultLactic Acidglycolysishyperglycemialactatemyotubespathway analysissubstrate oxidation

Identifiers

PMID31540443
PMCPMC6770141
OpenAlexW2974093802

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.