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dc.date.accessioned2020-05-16T18:39:03Z
dc.date.available2020-05-16T18:39:03Z
dc.date.created2020-01-14T09:31:41Z
dc.date.issued2019
dc.identifier.citationLund, Jenny Ouwens, DM Wettergreen, Marianne Bakke, Siril Skaret Thoresen, G. Hege Aas, Vigdis . Increased glycolysis and higher lactate production in hyperglycemic myotubes. Cells. 2019, 8(9)
dc.identifier.urihttp://hdl.handle.net/10852/75799
dc.description.abstractPrevious 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.
dc.languageEN
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleIncreased glycolysis and higher lactate production in hyperglycemic myotubes
dc.typeJournal article
dc.creator.authorLund, Jenny
dc.creator.authorOuwens, DM
dc.creator.authorWettergreen, Marianne
dc.creator.authorBakke, Siril Skaret
dc.creator.authorThoresen, G. Hege
dc.creator.authorAas, Vigdis
cristin.unitcode185,15,23,30
cristin.unitnameFarmakologi og farmasøytisk biovitenskap
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1772006
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Cells&rft.volume=8&rft.spage=&rft.date=2019
dc.identifier.jtitleCells
dc.identifier.volume8
dc.identifier.issue9
dc.identifier.pagecount14
dc.identifier.doihttps://doi.org/10.3390/cells8091101
dc.identifier.urnURN:NBN:no-78860
dc.type.documentTidsskriftartikkel
dc.type.peerreviewedPeer reviewed
dc.source.issn2073-4409
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/75799/2/cells-08-01101%2B%25281%2529.pdf
dc.type.versionPublishedVersion
cristin.articleid1101
dc.relation.projectNFR/223255


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