Larsen 2015 Physiol Rep

From Bioblast
Publications in the MiPMap
Larsen S, Scheede-Bergdahl C, Whitesell T, Boushel R, Bergdahl A (2015) Increased intrinsic mitochondrial respiratory capacity in skeletal muscle from rats with streptozotocin-induced hyperglycemia. Physiol Rep 3 pii:e12467.

Β» PMID: 26197936

Larsen S, Scheede-Bergdahl C, Whitesell T, Boushel R, Bergdahl A (2015) Physiol Rep

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. β€’ Keywords: Hyperglycemia, OXPHOS, Mitochondria, Skeletal muscle, Streptozotocin, Type I diabetes

β€’ O2k-Network Lab: CA Montreal Bergdahl A, CA Vancouver Boushel RC, SE Stockholm Boushel RC, DK Copenhagen Dela F, DK Copenhagen Larsen S

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Diabetes 

Organism: Rat  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Coupling state: LEAK, OXPHOS  Pathway: F, N, CIV, NS, Other combinations, ROX  HRR: Oxygraph-2k 

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