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dc.contributor.authorSishi, Balindiween_US
dc.contributor.authorLoos, Benjaminen_US
dc.contributor.authorEllis, Beverleyen_US
dc.contributor.authorSmith, Wayneen_US
dc.contributor.authorDu Toit, Eugeneen_US
dc.contributor.authorEngelbrecht, Anna-Marten_US
dc.date.accessioned2017-05-03T15:31:45Z
dc.date.available2017-05-03T15:31:45Z
dc.date.issued2011en_US
dc.date.modified2013-05-29T09:36:21Z
dc.identifier.issn09580670en_US
dc.identifier.doi10.1113/expphysiol.2010.054189en_US
dc.identifier.urihttp://hdl.handle.net/10072/38575
dc.description.abstractPro-inflammatory and stress activated signaling pathways are important role players in the pathogenesis of obesity and insulin resistance. Obesity and type II diabetes are associated with chronic, low-grade inflammation and elevated TNF-a levels. There is increasing evidence that TNF-a may play a critical role in skeletal muscle atrophy. However, the effects of obesity-induced insulin resistance on these signaling pathways are poorly understood in skeletal muscle. Therefore, the present study addressed the effects of obesity-induced insulin resistance on the activity of the ubiquitin ligases, NF-?B-, p38 MAPK- and PI3-kinase signaling pathways in the gastrocnemius muscle and compared these with muscle of standard chow-fed control rats. Male Wistar rats were randomly allocated to a control diet group (standard commercial chow - 60% carbohydrates, 30% protein and 10% fat) or a cafeteria diet group (65% carbohydrates, 19% protein and 16% fat) for 16 weeks. Blood analysis was conducted to determine the impact of the model of obesity on circulating insulin, glucose, free fatty acids, TNF-a and angiotensin II concentrations. The experimental animals were 18% heavier and had 68% greater visceral fat mass than their control counterparts and was also dyslipidaemic. Significant increases in the ubiquitin ligase, MURF-1, as well as in caspase-3- and PARP cleavage were observed in the muscle of obese animals compared to the controls. We propose that dyslipidaemia may be a mechanism for the activation of inflammatory/stress activated signaling pathways in obesity and type II diabetes which will lead to apoptosis and atrophy in skeletal muscle.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_US
dc.format.extent1951238 bytes
dc.format.mimetypeapplication/pdf
dc.languageEnglishen_US
dc.language.isoen_US
dc.publisherWiley-Blackwell Publishing Ltden_US
dc.publisher.placeUnited Kingdomen_US
dc.relation.ispartofstudentpublicationNen_US
dc.relation.ispartofpagefrom179en_US
dc.relation.ispartofpageto193en_US
dc.relation.ispartofjournalExperimental Physiologyen_US
dc.relation.ispartofvolume96en_US
dc.rights.retentionYen_US
dc.subject.fieldofresearchPhysiology not elsewhere classifieden_US
dc.subject.fieldofresearchCardiovascular Medicine and Haematology not elsewhere classifieden_US
dc.subject.fieldofresearchMedical Physiology not elsewhere classifieden_US
dc.subject.fieldofresearchcode060699en_US
dc.subject.fieldofresearchcode110299en_US
dc.subject.fieldofresearchcode111699en_US
dc.titleDiet-induced obesity alters signalling pathways and induces atrophy and apoptosis in skeletal muscle in a prediabetic rat modelen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.rights.copyrightCopyright 2010 The Physiological Society. This is the author-manuscript version of the paper. Reproduced in accordance with the copyright policy of the publisher. The definitive version is available at http://onlinelibrary.wiley.com/en_US
gro.date.issued2011
gro.hasfulltextFull Text


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