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dc.contributor.authorCarré, JEen
dc.contributor.authorAffourtit, Cen
dc.date.accessioned2019-06-21T14:00:02Z
dc.date.issued2019-06-05en
dc.identifier.issn1422-0067en
dc.identifier.urihttp://hdl.handle.net/10026.1/14354
dc.description.abstract

<jats:p>Insulin resistance is a key feature of the metabolic syndrome, a cluster of medical disorders that together increase the chance of developing type 2 diabetes and cardiovascular disease. In turn, type 2 diabetes may cause complications such as diabetic kidney disease (DKD). Obesity is a major risk factor for developing systemic insulin resistance, and skeletal muscle is the first tissue in susceptible individuals to lose its insulin responsiveness. Interestingly, lean individuals are not immune to insulin resistance either. Non-obese, non-diabetic subjects with chronic kidney disease (CKD), for example, exhibit insulin resistance at the very onset of CKD, even before clinical symptoms of renal failure are clear. This uraemic insulin resistance contributes to the muscle weakness and muscle wasting that many CKD patients face, especially during the later stages of the disease. Bioenergetic failure has been associated with the loss of skeletal muscle insulin sensitivity in obesity and uraemia, as well as in the development of kidney disease and its sarcopenic complications. In this mini review, we evaluate how mitochondrial activity of different renal cell types changes during DKD progression, and discuss the controversial role of oxidative stress and mitochondrial reactive oxygen species in DKD. We also compare the involvement of skeletal muscle mitochondria in uraemic and obesity-related muscle insulin resistance.</jats:p>

en
dc.format.extent2751 - 2751en
dc.language.isoenen
dc.publisherMDPIen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.titleMitochondrial Activity and Skeletal Muscle Insulin Resistance in Kidney Diseaseen
dc.typeJournal Article
plymouth.issue11en
plymouth.volume20en
plymouth.journalInternational Journal of Molecular Sciencesen
dc.identifier.doi10.3390/ijms20112751en
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/School of Biomedical Sciences
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dcterms.dateAccepted2019-06-04en
dc.rights.embargodate2019-06-28en
dc.identifier.eissn1422-0067en
dc.rights.embargoperiodNot knownen
rioxxterms.versionofrecord10.3390/ijms20112751en
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
rioxxterms.licenseref.startdate2019-06-05en
rioxxterms.typeJournal Article/Reviewen


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