Increased intrinsic mitochondrial respiratory capacity in skeletal muscle from rats with streptozotocin‐induced hyperglycemia

Physiological Reports

Steen Larsen¹  Celena Scheede-Bergdahl²  Thomas Whitesell³  Robert Boushel³ 

[1] Centre for Healthy Aging, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark;Department of Kinesiology & Physical Education, McGill University, Montreal, Quebec, Canada;Department of Exercise Science, Concordia University, Montreal, Quebec, Canada

关键词: Hyperglycemia;    mitochondria;    OXPHOS;    skeletal muscle;    streptozotocin;    type I diabetes;   

DOI  :  10.14814/phy2.12467

来源: Wiley

【 摘 要 】

Abstract

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.

【 授权许可】

CC BY   
© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

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