Gymnastik- och idrottshögskolan, GIH

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Increased intrinsic mitochondrial respiratory capacity in skeletal muscle from rats with streptozotocin-induced hyperglycemia.
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
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2015 (English)In: Physiological Reports, E-ISSN 2051-817X, Vol. 3, no 7, article id e12467Article in journal (Refereed) Published
Abstract [en]

Type I diabetes mellitus (T1DM) is a chronic disorder, characterized by an almost or complete insulin deficiency. Widespread tissue dysfunction and deleterious diabetes-complications are associated with long-term elevations of blood glucose. The aim of this study was to investigate the effects of type I diabetes, as induced by streptozotocin, on the mitochondria in skeletal muscles that predominantly consist of either slow or fast twitch fibers. Soleus (primarily slow twitch fiber type) and the plantaris muscle (mainly fast twitch fiber type) were removed in order to measure mitochondrial protein expression and integrated mitochondrial respiratory function. Mitochondrial capacity for oxidative phosphorylation (OXPHOS) was found to be higher in the slow (more oxidative) soleus muscle from STZ rats when evaluating lipid and complex I linked OXPHOS capacity, whereas no difference was detected between the groups when evaluating the more physiological complex I and II linked OXPHOS capacity. These findings indicate that chronic hyperglycemia results in an elevated intrinsic mitochondrial respiratory capacity in both soleus and, at varying degree, plantaris muscle, findings that are consistent with human T1DM patients.

Place, publisher, year, edition, pages
2015. Vol. 3, no 7, article id e12467
National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
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URN: urn:nbn:se:gih:diva-3984DOI: 10.14814/phy2.12467PubMedID: 26197936OAI: oai:DiVA.org:gih-3984DiVA, id: diva2:844642
Available from: 2015-08-07 Created: 2015-08-07 Last updated: 2017-12-04Bibliographically approved

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Boushel, Robert

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