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Exercise training boosts eNOS-dependent mitochondrial biogenesis in mouse heart: role in adaptation of glucose metabolism.
Am J Physiol Endocrinol Metab. 2014 Mar 01; 306(5):E519-28.AJ

Abstract

Endurance exercise training increases cardiac energy metabolism through poorly understood mechanisms. Nitric oxide (NO) produced by endothelial NO synthase (eNOS) in cardiomyocytes contributes to cardiac adaptation. Here we demonstrate that the NO donor diethylenetriamine-NO (DETA-NO) activated mitochondrial biogenesis and function, as assessed by upregulated peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), nuclear respiratory factor 1, and mitochondrial transcription factor A (Tfam) expression, and by increased mitochondrial DNA content and citrate synthase activity in primary mouse cardiomyocytes. DETA-NO also induced mitochondrial biogenesis and function and enhanced both basal and insulin-stimulated glucose uptake in HL-1 cardiomyocytes. The DETA-NO-mediated effects were suppressed by either PGC-1α or Tfam small-interference RNA in HL-1 cardiomyocytes. Wild-type and eNOS(-/-) mice were subjected to 6 wk graduated swim training. We found that eNOS expression, mitochondrial biogenesis, mitochondrial volume density and number, and both basal and insulin-stimulated glucose uptake were increased in left ventricles of swim-trained wild-type mice. On the contrary, the genetic deletion of eNOS prevented all these adaptive phenomena. Our findings demonstrate that exercise training promotes eNOS-dependent mitochondrial biogenesis in heart, which behaves as an essential step in cardiac glucose transport.

Authors+Show Affiliations

Internal Medicine Unit and Center for the Study and Integrated Treatment of Obesity, Department of Medicine, Padua University, Padua, Italy;No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24381004

Citation

Vettor, Roberto, et al. "Exercise Training Boosts eNOS-dependent Mitochondrial Biogenesis in Mouse Heart: Role in Adaptation of Glucose Metabolism." American Journal of Physiology. Endocrinology and Metabolism, vol. 306, no. 5, 2014, pp. E519-28.
Vettor R, Valerio A, Ragni M, et al. Exercise training boosts eNOS-dependent mitochondrial biogenesis in mouse heart: role in adaptation of glucose metabolism. Am J Physiol Endocrinol Metab. 2014;306(5):E519-28.
Vettor, R., Valerio, A., Ragni, M., Trevellin, E., Granzotto, M., Olivieri, M., Tedesco, L., Ruocco, C., Fossati, A., Fabris, R., Serra, R., Carruba, M. O., & Nisoli, E. (2014). Exercise training boosts eNOS-dependent mitochondrial biogenesis in mouse heart: role in adaptation of glucose metabolism. American Journal of Physiology. Endocrinology and Metabolism, 306(5), E519-28. https://doi.org/10.1152/ajpendo.00617.2013
Vettor R, et al. Exercise Training Boosts eNOS-dependent Mitochondrial Biogenesis in Mouse Heart: Role in Adaptation of Glucose Metabolism. Am J Physiol Endocrinol Metab. 2014 Mar 1;306(5):E519-28. PubMed PMID: 24381004.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exercise training boosts eNOS-dependent mitochondrial biogenesis in mouse heart: role in adaptation of glucose metabolism. AU - Vettor,Roberto, AU - Valerio,Alessandra, AU - Ragni,Maurizio, AU - Trevellin,Elisabetta, AU - Granzotto,Marnie, AU - Olivieri,Massimiliano, AU - Tedesco,Laura, AU - Ruocco,Chiara, AU - Fossati,Andrea, AU - Fabris,Roberto, AU - Serra,Roberto, AU - Carruba,Michele O, AU - Nisoli,Enzo, Y1 - 2013/12/31/ PY - 2014/1/2/entrez PY - 2014/1/2/pubmed PY - 2014/5/3/medline KW - endothelial nitric oxide synthase KW - exercise training KW - glucose uptake KW - heart KW - mitochondrial biogenesis KW - nitric oxide SP - E519 EP - 28 JF - American journal of physiology. Endocrinology and metabolism JO - Am. J. Physiol. Endocrinol. Metab. VL - 306 IS - 5 N2 - Endurance exercise training increases cardiac energy metabolism through poorly understood mechanisms. Nitric oxide (NO) produced by endothelial NO synthase (eNOS) in cardiomyocytes contributes to cardiac adaptation. Here we demonstrate that the NO donor diethylenetriamine-NO (DETA-NO) activated mitochondrial biogenesis and function, as assessed by upregulated peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), nuclear respiratory factor 1, and mitochondrial transcription factor A (Tfam) expression, and by increased mitochondrial DNA content and citrate synthase activity in primary mouse cardiomyocytes. DETA-NO also induced mitochondrial biogenesis and function and enhanced both basal and insulin-stimulated glucose uptake in HL-1 cardiomyocytes. The DETA-NO-mediated effects were suppressed by either PGC-1α or Tfam small-interference RNA in HL-1 cardiomyocytes. Wild-type and eNOS(-/-) mice were subjected to 6 wk graduated swim training. We found that eNOS expression, mitochondrial biogenesis, mitochondrial volume density and number, and both basal and insulin-stimulated glucose uptake were increased in left ventricles of swim-trained wild-type mice. On the contrary, the genetic deletion of eNOS prevented all these adaptive phenomena. Our findings demonstrate that exercise training promotes eNOS-dependent mitochondrial biogenesis in heart, which behaves as an essential step in cardiac glucose transport. SN - 1522-1555 UR - https://www.unboundmedicine.com/medline/citation/24381004/Exercise_training_boosts_eNOS_dependent_mitochondrial_biogenesis_in_mouse_heart:_role_in_adaptation_of_glucose_metabolism_ L2 - http://www.physiology.org/doi/full/10.1152/ajpendo.00617.2013?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -