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dc.contributor.authorLund, Jenny
dc.contributor.authorOuwens, DM
dc.contributor.authorWettergreen, Marianne
dc.contributor.authorBakke, Siril Skaret
dc.contributor.authorThoresen, G. Hege
dc.contributor.authorAas, Vigdis
dc.date.accessioned2020-01-29T08:23:11Z
dc.date.available2020-01-29T08:23:11Z
dc.date.created2020-01-14T09:31:41Z
dc.date.issued2019
dc.identifier.citationCells. 2019, 8 (9), .nb_NO
dc.identifier.issn2073-4409
dc.identifier.urihttp://hdl.handle.net/11250/2638460
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.nb_NO
dc.language.isoengnb_NO
dc.publisherMDPInb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleIncreased glycolysis and higher lactate production in hyperglycemic myotubesnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.pagenumber14nb_NO
dc.source.volume8nb_NO
dc.source.journalCellsnb_NO
dc.source.issue9nb_NO
dc.identifier.doi10.3390/cells8091101
dc.identifier.cristin1772006
dc.description.localcode© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).nb_NO
cristin.unitcode194,65,15,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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