Mitochondrial Respiratory Capacity and Content Are Normal in Young Insulin-Resistant Obese Humans

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dc.contributor.authorFisher-Wellman, Kelsey H.
dc.contributor.authorWeber, Todd M.
dc.contributor.authorCathey, Brook L.
dc.contributor.authorBrophy, Patricia
dc.contributor.authorGilliam, Laura A. A.
dc.contributor.authorKane, Constance L.
dc.contributor.authorMaples, Jill M.
dc.contributor.authorGavin, Timothy Patrick
dc.contributor.authorHoumard, Joseph A.
dc.contributor.authorNeufer, P. Darrell
dc.date.accessioned2016-05-26T16:04:16Z
dc.date.available2016-05-26T16:04:16Z
dc.date.issued2014-01
dc.description.abstractConsiderable debate exists about whether alterations in mitochondrial respiratory capacity and/or content play a causal role in the development of insulin resistance during obesity. The current study was undertaken to determine whether such alterations are present during the initial stages of insulin resistance in humans. Young (∼23 years) insulin-sensitive lean and insulin-resistant obese men and women were studied. Insulin resistance was confirmed through an intravenous glucose tolerance test. Measures of mitochondrial respiratory capacity and content as well as H(2)O(2) emitting potential and the cellular redox environment were performed in permeabilized myofibers and primary myotubes prepared from vastus lateralis muscle biopsy specimens. No differences in mitochondrial respiratory function or content were observed between lean and obese subjects, despite elevations in H(2)O(2) emission rates and reductions in cellular glutathione. These findings were apparent in permeabilized myofibers as well as in primary myotubes. The results suggest that reductions in mitochondrial respiratory capacity and content are not required for the initial manifestation of peripheral insulin resistance.en_US
dc.identifier.citationDiabetes; 63:1 p. 132-141en_US
dc.identifier.doi10.2337/db13-0940
dc.identifier.issn0012-1797
dc.identifier.pmidpmc3868052en_US
dc.identifier.urihttp://hdl.handle.net/10342/5399
dc.relation.urihttp://www.ncbi.nlm.nih.gov/pubmed/23974920en_US
dc.titleMitochondrial Respiratory Capacity and Content Are Normal in Young Insulin-Resistant Obese Humansen_US
dc.typeArticleen_US
ecu.journal.issue1en_US
ecu.journal.nameDiabetesen_US
ecu.journal.pages132-141en_US
ecu.journal.volume63en_US

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