Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/62052
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dc.contributorDepartment of Health Technology and Informatics-
dc.creatorSupriya, R-
dc.creatorTam, BT-
dc.creatorPei, XM-
dc.creatorLai, CW-
dc.creatorChan, LW-
dc.creatorYung, BY-
dc.creatorSiu, PM-
dc.date.accessioned2016-12-19T08:58:21Z-
dc.date.available2016-12-19T08:58:21Z-
dc.identifier.urihttp://hdl.handle.net/10397/62052-
dc.language.isoenen_US
dc.publisherFrontiers Research Foundationen_US
dc.rightsCopyright © 2016 Supriya, Tam, Pei, Lai, Chan, Yung and Siu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) (https://creativecommons.org/licenses/by/4.0/). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.en_US
dc.rightsThe following publication Supriya R, Tam BT, Pei XM, Lai CW, Chan LW, Yung BY and Siu PM (2016) Doxorubicin Induces Inflammatory Modulation and Metabolic Dysregulation in Diabetic Skeletal Muscle. Front. Physiol. 7:323,1-13 is available at https://dx.doi.org/10.3389/fphys.2016.00323en_US
dc.subjectAnaerobic glycolysisen_US
dc.subjectAnti-inflammationen_US
dc.subjectCancer chemotherapyen_US
dc.subjectMyotoxicityen_US
dc.subjectPro-inflammationen_US
dc.subjectType 2 diabetes mellitusen_US
dc.titleDoxorubicin induces inflammatory modulation and metabolic dysregulation in diabetic skeletal muscleen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage1en_US
dc.identifier.epage13en_US
dc.identifier.volume7en_US
dc.identifier.doi10.3389/fphys.2016.00323en_US
dcterms.abstractAnti-cancer agent doxorubicin (DOX) has been demonstrated to worsen insulin signaling, engender muscle atrophy, trigger pro-inflammation, and induce a shift to anaerobic glycolytic metabolism in skeletal muscle. The myotoxicity of DOX in diabetic skeletal muscle remains largely unclear. This study examined the effects of DOX on insulin signaling, muscle atrophy, pro-/anti-inflammatory microenvironment, and glycolysis metabolic regulation in skeletal muscle of db/db diabetic and db/+ non-diabetic mice. Non-diabetic db/+ mice and diabetic db/db mice were randomly assigned to the following groups: db/+CON, db/+DOX, db/dbCON, and db/dbDOX. Mice in db/+DOX and db/dbDOX groups were intraperitoneally injected with DOX at a dose of 15 mg per kg body weight whereas mice in db/+CON and db/dbCON groups were injected with the same volume of saline instead of DOX. Gastrocnemius was immediately harvested, weighed, washed with cold phosphate buffered saline, frozen in liquid nitrogen, and stored at -80°C for later analysis. The effects of DOX on diabetic muscle were neither seen in insulin signaling markers (Glut4, pIRS1Ser636/639, and pAktSer473) nor muscle atrophy markers (muscle mass, MuRF1 and MAFbx). However, DOX exposure resulted in enhancement of pro-inflammatory favoring microenvironment (as indicated by TNF-α, HIFα and pNFκBp65) accompanied by diminution of anti-inflammatory favoring microenvironment (as indicated by IL15, PGC1a and pAMPKß1Ser108). Metabolism of diabetic muscle was shifted to anaerobic glycolysis after DOX exposure as demonstrated by our analyses of PDK4, LDH and pACCSer79. Our results demonstrated that there might be a link between inflammatory modulation and the dysregulation of aerobic glycolytic metabolism in DOX-injured diabetic skeletal muscle. These findings help to understand the pathogenesis of DOX-induced myotoxicity in diabetic muscle.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationFrontiers in physiology, 27 July 2016, v. 7, 323, p. 1-13-
dcterms.isPartOfFrontiers in physiology-
dcterms.issued2016-07-27-
dc.identifier.isiWOS:000380314400001-
dc.identifier.scopus2-s2.0-84981525092-
dc.identifier.pmid27512375-
dc.identifier.ros2016000202-
dc.identifier.eissn1664-042Xen_US
dc.identifier.artn323en_US
dc.identifier.rosgroupid2016000201-
dc.description.ros2016-2017 > Academic research: refereed > Publication in refereed journalen_US
dc.description.validate201804_a bcmaen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_IR/PIRAen_US
dc.description.pubStatusPublisheden_US
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