dc.creatorTroncoso Magñin, Mayarling Francisca
dc.creatorPavez Giani, Mario Gustavo
dc.creatorWilson Rodríguez, Carlos Antonio
dc.creatorLagos Cerón, Daniel Alejandro
dc.creatorDurán Gárate, Javier Andre
dc.creatorRamos, Sebastián
dc.creatorBarrientos Briones, Genaro Christian
dc.creatorSilva, Patricio
dc.creatorLlanos Vidal, Paola Andrea
dc.creatorBasualto Alarcón, Carla Edith
dc.creatorWestenbrink, B. Daan
dc.creatorLavandero González, Sergio Alejandro
dc.creatorEstrada Hormazábal, Manuel Iván
dc.date.accessioned2021-12-14T13:58:27Z
dc.date.accessioned2022-01-27T21:55:10Z
dc.date.available2021-12-14T13:58:27Z
dc.date.available2022-01-27T21:55:10Z
dc.date.created2021-12-14T13:58:27Z
dc.date.issued2021
dc.identifierBiol Res (2021) 54:3
dc.identifier10.1186/s40659-021-00328-4
dc.identifierhttps://repositorio.uchile.cl/handle/2250/183189
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/3317070
dc.description.abstractBackground Testosterone regulates nutrient and energy balance to maintain protein synthesis and metabolism in cardiomyocytes, but supraphysiological concentrations induce cardiac hypertrophy. Previously, we determined that testosterone increased glucose uptake-via AMP-activated protein kinase (AMPK)-after acute treatment in cardiomyocytes. However, whether elevated glucose uptake is involved in long-term changes of glucose metabolism or is required during cardiomyocyte growth remained unknown. In this study, we hypothesized that glucose uptake and glycolysis increase in testosterone-treated cardiomyocytes through AMPK and androgen receptor (AR). Methods Cultured cardiomyocytes were stimulated with 100 nM testosterone for 24 h, and hypertrophy was verified by increased cell size and mRNA levels of beta-myosin heavy chain (beta-mhc). Glucose uptake was assessed by 2-NBDG. Glycolysis and glycolytic capacity were determined by measuring extracellular acidification rate (ECAR). Results Testosterone induced cardiomyocyte hypertrophy that was accompanied by increased glucose uptake, glycolysis enhancement and upregulated mRNA expression of hexokinase 2. In addition, testosterone increased AMPK phosphorylation (Thr172), while inhibition of both AMPK and AR blocked glycolysis and cardiomyocyte hypertrophy induced by testosterone. Moreover, testosterone supplementation in adult male rats by 5 weeks induced cardiac hypertrophy and upregulated beta-mhc, Hk2 and Pfk2 mRNA levels. Conclusion These results indicate that testosterone stimulates glucose metabolism by activation of AMPK and AR signaling which are critical to induce cardiomyocyte hypertrophy.
dc.languageen
dc.publisherBMC
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/us/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States
dc.sourceBiological Research
dc.subjectTestosterone
dc.subjectAMP-activated protein kinase
dc.subjectGlucose transport
dc.subjectGlycolysis
dc.subjectAndrogen receptor
dc.subjectCardiac hypertrophy
dc.titleTestosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy
dc.typeArtículos de revistas


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