Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy
- Autores
- Troncoso, Mayarling Francisca; Pavez, Mario; Wilson Rodriguez, Carlos; Lagos, Daniel; Duran, Javier; Ramos, Sebastián; Barrientos, Genaro; Silva, Patricio; Llanos, Paola; Basualto Alarcón, Carla; Westenbrink, B. Daan; Lavandero, Sergio; Estrada, Manuel
- Año de publicación
- 2021
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Background: 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 β-myosin heavy chain (β-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 β-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.
Fil: Troncoso, Mayarling Francisca. Universidad de Chile; Chile
Fil: Pavez, Mario. Universidad de Chile; Chile
Fil: Wilson Rodriguez, Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina. Universidad de Chile; Chile
Fil: Lagos, Daniel. Universidad de Chile; Chile
Fil: Duran, Javier. Universidad de Chile; Chile
Fil: Ramos, Sebastián. Universidad de Chile; Chile
Fil: Barrientos, Genaro. Universidad de Chile; Chile
Fil: Silva, Patricio. Universidad Central de Chile; Chile
Fil: Llanos, Paola. Universidad de Chile; Chile
Fil: Basualto Alarcón, Carla. Universidad de Chile; Chile. Universidad de Aysén; Chile
Fil: Westenbrink, B. Daan. University of Groningen; Países Bajos
Fil: Lavandero, Sergio. Universidad de Chile; Chile. Texas A&M University; Estados Unidos
Fil: Estrada, Manuel. Universidad de Chile; Chile - Materia
-
AMP-ACTIVATED PROTEIN KINASE
ANDROGEN RECEPTOR
CARDIAC HYPERTROPHY
GLUCOSE TRANSPORT
GLYCOLYSIS
TESTOSTERONE - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/168726
Ver los metadatos del registro completo
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Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophyTroncoso, Mayarling FranciscaPavez, MarioWilson Rodriguez, CarlosLagos, DanielDuran, JavierRamos, SebastiánBarrientos, GenaroSilva, PatricioLlanos, PaolaBasualto Alarcón, CarlaWestenbrink, B. DaanLavandero, SergioEstrada, ManuelAMP-ACTIVATED PROTEIN KINASEANDROGEN RECEPTORCARDIAC HYPERTROPHYGLUCOSE TRANSPORTGLYCOLYSISTESTOSTERONEhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background: 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 β-myosin heavy chain (β-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 β-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.Fil: Troncoso, Mayarling Francisca. Universidad de Chile; ChileFil: Pavez, Mario. Universidad de Chile; ChileFil: Wilson Rodriguez, Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina. Universidad de Chile; ChileFil: Lagos, Daniel. Universidad de Chile; ChileFil: Duran, Javier. Universidad de Chile; ChileFil: Ramos, Sebastián. Universidad de Chile; ChileFil: Barrientos, Genaro. Universidad de Chile; ChileFil: Silva, Patricio. Universidad Central de Chile; ChileFil: Llanos, Paola. Universidad de Chile; ChileFil: Basualto Alarcón, Carla. Universidad de Chile; Chile. Universidad de Aysén; ChileFil: Westenbrink, B. Daan. University of Groningen; Países BajosFil: Lavandero, Sergio. Universidad de Chile; Chile. Texas A&M University; Estados UnidosFil: Estrada, Manuel. Universidad de Chile; ChileSociedad de Biología de Chile2021-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/168726Troncoso, Mayarling Francisca; Pavez, Mario; Wilson Rodriguez, Carlos; Lagos, Daniel; Duran, Javier; et al.; Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy; Sociedad de Biología de Chile; Biological Research; 54; 1; 12-2021; 1-160716-97600717-6287CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1186/s40659-021-00328-4info:eu-repo/semantics/altIdentifier/url/https://biolres.biomedcentral.com/articles/10.1186/s40659-021-00328-4info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:30:30Zoai:ri.conicet.gov.ar:11336/168726instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:30:30.658CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy |
| title |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy |
| spellingShingle |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy Troncoso, Mayarling Francisca AMP-ACTIVATED PROTEIN KINASE ANDROGEN RECEPTOR CARDIAC HYPERTROPHY GLUCOSE TRANSPORT GLYCOLYSIS TESTOSTERONE |
| title_short |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy |
| title_full |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy |
| title_fullStr |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy |
| title_full_unstemmed |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy |
| title_sort |
Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy |
| dc.creator.none.fl_str_mv |
Troncoso, Mayarling Francisca Pavez, Mario Wilson Rodriguez, Carlos Lagos, Daniel Duran, Javier Ramos, Sebastián Barrientos, Genaro Silva, Patricio Llanos, Paola Basualto Alarcón, Carla Westenbrink, B. Daan Lavandero, Sergio Estrada, Manuel |
| author |
Troncoso, Mayarling Francisca |
| author_facet |
Troncoso, Mayarling Francisca Pavez, Mario Wilson Rodriguez, Carlos Lagos, Daniel Duran, Javier Ramos, Sebastián Barrientos, Genaro Silva, Patricio Llanos, Paola Basualto Alarcón, Carla Westenbrink, B. Daan Lavandero, Sergio Estrada, Manuel |
| author_role |
author |
| author2 |
Pavez, Mario Wilson Rodriguez, Carlos Lagos, Daniel Duran, Javier Ramos, Sebastián Barrientos, Genaro Silva, Patricio Llanos, Paola Basualto Alarcón, Carla Westenbrink, B. Daan Lavandero, Sergio Estrada, Manuel |
| author2_role |
author author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
AMP-ACTIVATED PROTEIN KINASE ANDROGEN RECEPTOR CARDIAC HYPERTROPHY GLUCOSE TRANSPORT GLYCOLYSIS TESTOSTERONE |
| topic |
AMP-ACTIVATED PROTEIN KINASE ANDROGEN RECEPTOR CARDIAC HYPERTROPHY GLUCOSE TRANSPORT GLYCOLYSIS TESTOSTERONE |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
Background: 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 β-myosin heavy chain (β-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 β-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. Fil: Troncoso, Mayarling Francisca. Universidad de Chile; Chile Fil: Pavez, Mario. Universidad de Chile; Chile Fil: Wilson Rodriguez, Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina. Universidad de Chile; Chile Fil: Lagos, Daniel. Universidad de Chile; Chile Fil: Duran, Javier. Universidad de Chile; Chile Fil: Ramos, Sebastián. Universidad de Chile; Chile Fil: Barrientos, Genaro. Universidad de Chile; Chile Fil: Silva, Patricio. Universidad Central de Chile; Chile Fil: Llanos, Paola. Universidad de Chile; Chile Fil: Basualto Alarcón, Carla. Universidad de Chile; Chile. Universidad de Aysén; Chile Fil: Westenbrink, B. Daan. University of Groningen; Países Bajos Fil: Lavandero, Sergio. Universidad de Chile; Chile. Texas A&M University; Estados Unidos Fil: Estrada, Manuel. Universidad de Chile; Chile |
| description |
Background: 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 β-myosin heavy chain (β-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 β-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. |
| publishDate |
2021 |
| dc.date.none.fl_str_mv |
2021-12 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
| dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/168726 Troncoso, Mayarling Francisca; Pavez, Mario; Wilson Rodriguez, Carlos; Lagos, Daniel; Duran, Javier; et al.; Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy; Sociedad de Biología de Chile; Biological Research; 54; 1; 12-2021; 1-16 0716-9760 0717-6287 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/168726 |
| identifier_str_mv |
Troncoso, Mayarling Francisca; Pavez, Mario; Wilson Rodriguez, Carlos; Lagos, Daniel; Duran, Javier; et al.; Testosterone activates glucose metabolism through AMPK and androgen signaling in cardiomyocyte hypertrophy; Sociedad de Biología de Chile; Biological Research; 54; 1; 12-2021; 1-16 0716-9760 0717-6287 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
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info:eu-repo/semantics/altIdentifier/doi/10.1186/s40659-021-00328-4 info:eu-repo/semantics/altIdentifier/url/https://biolres.biomedcentral.com/articles/10.1186/s40659-021-00328-4 |
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info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/ |
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openAccess |
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https://creativecommons.org/licenses/by/2.5/ar/ |
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application/pdf application/pdf |
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Sociedad de Biología de Chile |
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Sociedad de Biología de Chile |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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