RGD Reference Report - Training-induced mitochondrial adaptation: role of peroxisome proliferator-activated receptor gamma coactivator-1alpha, nuclear factor-kappaB and beta-blockade. - Rat Genome Database

RGD Reference Report - Training-induced mitochondrial adaptation: role of peroxisome proliferator-activated receptor gamma coactivator-1alpha, nuclear factor-kappaB and beta-blockade. - Rat Genome Database

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Training-induced mitochondrial adaptation: role of peroxisome proliferator-activated receptor gamma coactivator-1alpha, nuclear factor-kappaB and beta-blockade.
Authors:	Feng, H Kang, C Dickman, JR Koenig, R Awoyinka, I Zhang, Y Ji, LL
Citation:	Feng H, etal., Exp Physiol. 2013 Mar;98(3):784-95. doi: 10.1113/expphysiol.2012.069286. Epub 2012 Oct 26.
RGD ID:	7242021
Pubmed:	PMID:23104933 (View Abstract at PubMed)
DOI:	DOI:10.1113/expphysiol.2012.069286 (Journal Full-text)
Interaction of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) with other cellular signalling pathways plays an important role in training-induced mitochondrial adaptations. The purpose of this study was to examine whether pyrolidine dithiocarbamate (PDTC), a nuclear factor-kappaB inhibitor and antioxidant, and the beta-adrenergic blocker propranolol would affect the PGC-1alpha-induced mitochondrial transcription factors, enzymes and proteins involved in energy metabolism and antioxidant defense in response to endurance training. Female Sprague-Dawley rats (aged 8 weeks) were randomly divided into two groups (n = 24), one subjected to 8 weeks of treadmill training and one remaining sedentary. Each group of rats was subdivided in to three groups that were injected (i.p.) daily with PDTC (50 mg (kg body weight)), propranolol (30 mg kg) or saline as a control 1 h before the daily exercise session. Sedentary PDTC-treated rats showed 75% higher PGC-1alpha content (P < 0.01) but lower mitochondrial transcription factor A and phosphorylated cAMP-responsive element binding protein (p-CREB) than control rats. Training increased PGC-1alpha by 57% (P < 0.01), cytochrome c oxidase 4 by 30% (P < 0.05) and p-CREB by 13% (P < 0.05), whereas the mitochondrial mitofusin-2 level was decreased by 24% (P < 0.01). Treatment with PDTC decreased PGC-1alpha and p-CREB content by 34 and 53% (P < 0.05), respectively, in trained rats and abolished training effects on cytochrome c oxidase 4 and mitochondrial mitofusin-2. None of the training effects was abolished by propranolol treatment. Mitochondrial superoxide dismutase activity was decreased with PDTC, whereas training-induced glutathione peroxidase activity was unaltered by either drug. The data indicates that nuclear factor-kappaB-inhibitory and antioxidant properties of PDTC can attenuate PGC-1alpha-mediated mitochondrial adaptation to endurance training, whereas the beta-adrenergic pathway has little adverse effect.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
Ppargc1a	Rat	response to organic cyclic compound		IEP		pyrrolidine dithiocarbamate	RGD

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Genes (Rattus norvegicus)

Ppargc1a (PPARG coactivator 1 alpha)

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