Cardiac Hypertrophy in obesity: Leptin-TRH interaction

Autores
Aisicovich, Maia; Peres Diaz, Ludmila Soledad; Schuman, Mariano Luis; Landa, Maria Silvina; Garcia, Silvia Ines
Año de publicación
2018
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Cardiac TRH induce left ventricular hypertrophy (LVH) and fibrosis, its inhibition prevent hypertrophy.The adiponectin leptin induces TRH in CNS. We hypothesized that in obesity, the increase of TRH induced by hyperleptinemia is responsible of the LVH, until now mostly attributed to pressure load. We studied obese Agouti mice suffering hypertension with hyperleptinemia and found LVH with increased TRH gene expression. Consequently we found higher (p<0.05) fibrotic and hypertrophic markers vs lean (BL/6J). As pressure could explain results we treated obese mice with diuretic (hydroclorothiazide 20 mg/kg/day) from weaning (n=9), the diuretic group was normotensive in contrast to control obese mice. Nevertheless both groups developed (p<0.05): LVH, higher TRH gene and elevated fibrotic and hypertrophic markers suggesting that LVH is not induced by hypertension. In contrast to Agouti, we studied obese Ob/Ob mice lacking leptin due to a disruption in their gene. Mice are normotensive, without LVH despite their obesity. We treated 2 groups with leptin (sc. 80 ug/kg/day) or saline from weaning for 15 days. Only the group treated with leptin developed LVH (LV weight/tibia length, p< 0.05, n=7) vs saline, pointing out that LVH is leptin dependant. As hypothesized, in this group we found an increase (p<0.05) in cardiac TRH accompanied by higher expression of type III collagen suggesting that leptin-TRH interaction is required for obesity-induced LVH. To confirm cardiac cells TRH´s leptin induction, cardiomyocytes derived cell line H9C2 (n=6) was stimulated with leptin (10 and100 ng/ml). TRH expression (rt-PCR) and peptide (WB) were increased (p<0.05) post leptin at both concentrations. Moreover we developed cardiomiocytes primary culture from neonates, in which leptin stimulus (80 ng/ml, 24 hs) increased (p<0.05) TRH content vs controls confirming the direct TRH induction by leptin in heart cells. Finally, obese-induced LVH is leptin-dependent, who probably stimulates hypertrophy and fibrosis by its TRH induction.
Fil: Aisicovich, Maia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Peres Diaz, Ludmila Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Schuman, Mariano Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Landa, Maria Silvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Garcia, Silvia Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVI Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Mar del Plata
Argentina
Sociedad Argentina de Fisiología
Sociedad Argentina de Inmunología
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Virología
Sociedad Argentina de Nanomedicinas
Materia
LEPTIN
TRH
HEART
HYPERTROPHY
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/269518
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/269518
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Cardiac Hypertrophy in obesity: Leptin-TRH interactionAisicovich, MaiaPeres Diaz, Ludmila SoledadSchuman, Mariano LuisLanda, Maria SilvinaGarcia, Silvia InesLEPTINTRHHEARTHYPERTROPHYhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Cardiac TRH induce left ventricular hypertrophy (LVH) and fibrosis, its inhibition prevent hypertrophy.The adiponectin leptin induces TRH in CNS. We hypothesized that in obesity, the increase of TRH induced by hyperleptinemia is responsible of the LVH, until now mostly attributed to pressure load. We studied obese Agouti mice suffering hypertension with hyperleptinemia and found LVH with increased TRH gene expression. Consequently we found higher (p<0.05) fibrotic and hypertrophic markers vs lean (BL/6J). As pressure could explain results we treated obese mice with diuretic (hydroclorothiazide 20 mg/kg/day) from weaning (n=9), the diuretic group was normotensive in contrast to control obese mice. Nevertheless both groups developed (p<0.05): LVH, higher TRH gene and elevated fibrotic and hypertrophic markers suggesting that LVH is not induced by hypertension. In contrast to Agouti, we studied obese Ob/Ob mice lacking leptin due to a disruption in their gene. Mice are normotensive, without LVH despite their obesity. We treated 2 groups with leptin (sc. 80 ug/kg/day) or saline from weaning for 15 days. Only the group treated with leptin developed LVH (LV weight/tibia length, p< 0.05, n=7) vs saline, pointing out that LVH is leptin dependant. As hypothesized, in this group we found an increase (p<0.05) in cardiac TRH accompanied by higher expression of type III collagen suggesting that leptin-TRH interaction is required for obesity-induced LVH. To confirm cardiac cells TRH´s leptin induction, cardiomyocytes derived cell line H9C2 (n=6) was stimulated with leptin (10 and100 ng/ml). TRH expression (rt-PCR) and peptide (WB) were increased (p<0.05) post leptin at both concentrations. Moreover we developed cardiomiocytes primary culture from neonates, in which leptin stimulus (80 ng/ml, 24 hs) increased (p<0.05) TRH content vs controls confirming the direct TRH induction by leptin in heart cells. Finally, obese-induced LVH is leptin-dependent, who probably stimulates hypertrophy and fibrosis by its TRH induction.Fil: Aisicovich, Maia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Peres Diaz, Ludmila Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Schuman, Mariano Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Landa, Maria Silvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Garcia, Silvia Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaLXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVI Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de FisiologíaMar del PlataArgentinaSociedad Argentina de FisiologíaSociedad Argentina de InmunologíaSociedad Argentina de Investigación ClínicaSociedad Argentina de VirologíaSociedad Argentina de NanomedicinasFundación Revista Medicina2018info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/269518Cardiac Hypertrophy in obesity: Leptin-TRH interaction; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVI Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Mar del Plata; Argentina; 2018; 1-21669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.medicinabuenosaires.com/revistas/vol78-18/s3/vol78supIII.pdfNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-29T11:49:16Zoai:ri.conicet.gov.ar:11336/269518instacron: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:34982025-10-29 11:49:17.019CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Cardiac Hypertrophy in obesity: Leptin-TRH interaction
title Cardiac Hypertrophy in obesity: Leptin-TRH interaction
spellingShingle Cardiac Hypertrophy in obesity: Leptin-TRH interaction
Aisicovich, Maia
LEPTIN
TRH
HEART
HYPERTROPHY
title_short Cardiac Hypertrophy in obesity: Leptin-TRH interaction
title_full Cardiac Hypertrophy in obesity: Leptin-TRH interaction
title_fullStr Cardiac Hypertrophy in obesity: Leptin-TRH interaction
title_full_unstemmed Cardiac Hypertrophy in obesity: Leptin-TRH interaction
title_sort Cardiac Hypertrophy in obesity: Leptin-TRH interaction
dc.creator.none.fl_str_mv Aisicovich, Maia
Peres Diaz, Ludmila Soledad
Schuman, Mariano Luis
Landa, Maria Silvina
Garcia, Silvia Ines
author Aisicovich, Maia
author_facet Aisicovich, Maia
Peres Diaz, Ludmila Soledad
Schuman, Mariano Luis
Landa, Maria Silvina
Garcia, Silvia Ines
author_role author
author2 Peres Diaz, Ludmila Soledad
Schuman, Mariano Luis
Landa, Maria Silvina
Garcia, Silvia Ines
author2_role author
author
author
author
dc.subject.none.fl_str_mv LEPTIN
TRH
HEART
HYPERTROPHY
topic LEPTIN
TRH
HEART
HYPERTROPHY
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Cardiac TRH induce left ventricular hypertrophy (LVH) and fibrosis, its inhibition prevent hypertrophy.The adiponectin leptin induces TRH in CNS. We hypothesized that in obesity, the increase of TRH induced by hyperleptinemia is responsible of the LVH, until now mostly attributed to pressure load. We studied obese Agouti mice suffering hypertension with hyperleptinemia and found LVH with increased TRH gene expression. Consequently we found higher (p<0.05) fibrotic and hypertrophic markers vs lean (BL/6J). As pressure could explain results we treated obese mice with diuretic (hydroclorothiazide 20 mg/kg/day) from weaning (n=9), the diuretic group was normotensive in contrast to control obese mice. Nevertheless both groups developed (p<0.05): LVH, higher TRH gene and elevated fibrotic and hypertrophic markers suggesting that LVH is not induced by hypertension. In contrast to Agouti, we studied obese Ob/Ob mice lacking leptin due to a disruption in their gene. Mice are normotensive, without LVH despite their obesity. We treated 2 groups with leptin (sc. 80 ug/kg/day) or saline from weaning for 15 days. Only the group treated with leptin developed LVH (LV weight/tibia length, p< 0.05, n=7) vs saline, pointing out that LVH is leptin dependant. As hypothesized, in this group we found an increase (p<0.05) in cardiac TRH accompanied by higher expression of type III collagen suggesting that leptin-TRH interaction is required for obesity-induced LVH. To confirm cardiac cells TRH´s leptin induction, cardiomyocytes derived cell line H9C2 (n=6) was stimulated with leptin (10 and100 ng/ml). TRH expression (rt-PCR) and peptide (WB) were increased (p<0.05) post leptin at both concentrations. Moreover we developed cardiomiocytes primary culture from neonates, in which leptin stimulus (80 ng/ml, 24 hs) increased (p<0.05) TRH content vs controls confirming the direct TRH induction by leptin in heart cells. Finally, obese-induced LVH is leptin-dependent, who probably stimulates hypertrophy and fibrosis by its TRH induction.
Fil: Aisicovich, Maia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Peres Diaz, Ludmila Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Schuman, Mariano Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Landa, Maria Silvina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Garcia, Silvia Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVI Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología
Mar del Plata
Argentina
Sociedad Argentina de Fisiología
Sociedad Argentina de Inmunología
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Virología
Sociedad Argentina de Nanomedicinas
description Cardiac TRH induce left ventricular hypertrophy (LVH) and fibrosis, its inhibition prevent hypertrophy.The adiponectin leptin induces TRH in CNS. We hypothesized that in obesity, the increase of TRH induced by hyperleptinemia is responsible of the LVH, until now mostly attributed to pressure load. We studied obese Agouti mice suffering hypertension with hyperleptinemia and found LVH with increased TRH gene expression. Consequently we found higher (p<0.05) fibrotic and hypertrophic markers vs lean (BL/6J). As pressure could explain results we treated obese mice with diuretic (hydroclorothiazide 20 mg/kg/day) from weaning (n=9), the diuretic group was normotensive in contrast to control obese mice. Nevertheless both groups developed (p<0.05): LVH, higher TRH gene and elevated fibrotic and hypertrophic markers suggesting that LVH is not induced by hypertension. In contrast to Agouti, we studied obese Ob/Ob mice lacking leptin due to a disruption in their gene. Mice are normotensive, without LVH despite their obesity. We treated 2 groups with leptin (sc. 80 ug/kg/day) or saline from weaning for 15 days. Only the group treated with leptin developed LVH (LV weight/tibia length, p< 0.05, n=7) vs saline, pointing out that LVH is leptin dependant. As hypothesized, in this group we found an increase (p<0.05) in cardiac TRH accompanied by higher expression of type III collagen suggesting that leptin-TRH interaction is required for obesity-induced LVH. To confirm cardiac cells TRH´s leptin induction, cardiomyocytes derived cell line H9C2 (n=6) was stimulated with leptin (10 and100 ng/ml). TRH expression (rt-PCR) and peptide (WB) were increased (p<0.05) post leptin at both concentrations. Moreover we developed cardiomiocytes primary culture from neonates, in which leptin stimulus (80 ng/ml, 24 hs) increased (p<0.05) TRH content vs controls confirming the direct TRH induction by leptin in heart cells. Finally, obese-induced LVH is leptin-dependent, who probably stimulates hypertrophy and fibrosis by its TRH induction.
publishDate 2018
dc.date.none.fl_str_mv 2018
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Reunión
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/269518
Cardiac Hypertrophy in obesity: Leptin-TRH interaction; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVI Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Mar del Plata; Argentina; 2018; 1-2
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/269518
identifier_str_mv Cardiac Hypertrophy in obesity: Leptin-TRH interaction; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXVI Reunión Anual de la Sociedad Argentina de Inmunología y Reunión Anual de la Sociedad Argentina de Fisiología; Mar del Plata; Argentina; 2018; 1-2
1669-9106
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.medicinabuenosaires.com/revistas/vol78-18/s3/vol78supIII.pdf
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
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rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
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dc.coverage.none.fl_str_mv Nacional
dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
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repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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