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dc.contributor.authorChowdhury, Subir K. Roy
dc.contributor.authorDobrowsky, Rick T.
dc.contributor.authorFennyhough, Paul
dc.date.accessioned2017-06-22T19:01:59Z
dc.date.available2017-06-22T19:01:59Z
dc.date.issued2011-11-01
dc.identifier.citationRoy Chowdhury, S. K., Dobrowsky, R. T., & Fernyhough, P. (2011). Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes. Mitochondrion, 11(6), 845–854. http://doi.org/10.1016/j.mito.2011.06.007en_US
dc.identifier.urihttp://hdl.handle.net/1808/24581
dc.description.abstractDiabetic neuropathy is a major complication of diabetes that results in the progressive deterioration of the sensory nervous system. Mitochondrial dysfunction has been proposed to play an important role in the pathogenesis of the neurodegeneration observed in diabetic neuropathy. Our recent work has shown that mitochondrial dysfunction occurs in dorsal root ganglia (DRG) sensory neurons in streptozotocin (STZ) induced diabetic rodents. In neurons, the nutrient excess associated with prolonged diabetes may trigger a switching off of AMP kinase (AMPK) and/or silent information regulator T1 (SIRT1) signaling leading to impaired peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α expression/activity and diminished mitochondrial activity. This review briefly summarizes the alterations of mitochondrial function and proteome in sensory neurons of STZ-diabetic rodents. We also discuss the possible involvement of AMPK/SIRT/PGC-1α pathway in other diabetic models and different tissues affected by diabetes.en_US
dc.publisherElsevieren_US
dc.rightsThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.subjectMitochondrial respiratory chainen_US
dc.subjectDiabetic neuropathyen_US
dc.subjectDorsal root gangliaen_US
dc.subjectPGC-1αen_US
dc.subjectAMPKen_US
dc.subjectSIRTen_US
dc.titleNutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetesen_US
dc.typeArticleen_US
kusw.kuauthorDobrowsky, Rick T.
kusw.kudepartmentPharmacyen_US
dc.identifier.doi10.1016/j.mito.2011.06.007en_US
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.identifier.pmidPMC3375692en_US
dc.rights.accessrightsopenAccess


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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Except where otherwise noted, this item's license is described as: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.