Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity

Detalhes bibliográficos
Autor(a) principal: Nascimento, Andre F. [UNESP]
Data de Publicação: 2011
Outros Autores: Luvizotto, Renata A. M. [UNESP], Leopoldo, Andre S. [UNESP], Lima-Leopoldo, Ana P. [UNESP], Seiva, Fabio R. [UNESP], Justulin, Luis A. [UNESP], Silva, Maeli Dal Pai [UNESP], Okoshi, Katashi [UNESP], Wang, Xiang-Dong, Cicogna, Antonio Carlos [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.lfs.2011.03.015
http://hdl.handle.net/11449/11595
Resumo: Aims: Leptin resistance has been associated with cardiac lipotoxicity; however, whether leptin resistance is a risk factor associated with cardiac lipotoxicity at different time points in diet-induced obesity is unclear. The objective of this study was to evaluate this relationship.Main methods: Male Wistar rats were fed a normal chow diet (12% from fat) or a high-fat diet (49% from fat) for 15 and 45 weeks, respectively. The adiposity index, body weight and co-morbidities were evaluated. Heart lipotoxicity was assessed by analyzing cardiac function and morphological changes as well as cardiac triglyceride, ceramide and lipid hydroperoxide accumulations. Cardiac apoptosis was examined using the TUNEL method. Leptin function was determined by examining plasma leptin levels, cardiac leptin receptors (OB-R) and related phosphorylations of AMP-activated kinase protein (AMPK) and Acetyl CoA carboxylase (ACC).Key findings: The diet-induced obesity was characterized by an elevated adiposity index, body weight and leptin levels at both 15 and 45 weeks. There was no difference between groups in the cardiac triglyceride or lipid hydroperoxide levels. Interestingly, ceramide levels decreased in obese animals in both experimental periods. The cardiac morphological and functional parameters were not altered. Although down-regulation of OB-R has occurred in chronic obesity, it did not adversely affect AMPK or ACC phosphorylation.Significance: The development of obesity via long-term feeding of a high-fat diet to rats does not result in cardiac lipotoxicity but promotes the down-regulation of OB-R. However, this does not result in altered levels of AMPK or ACC phosphotylations in this animal model. (C) 2011 Elsevier B.V. All rights reserved.
id UNSP_fd6a86528a4ac6cb2c2bb9e9737a4b76
oai_identifier_str oai:repositorio.unesp.br:11449/11595
network_acronym_str UNSP
network_name_str Repositório Institucional da UNESP
repository_id_str 2946
spelling Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicityCardiac lipotoxicityCardiac leptin receptorDiet-induced obesityHigh-fat dietAims: Leptin resistance has been associated with cardiac lipotoxicity; however, whether leptin resistance is a risk factor associated with cardiac lipotoxicity at different time points in diet-induced obesity is unclear. The objective of this study was to evaluate this relationship.Main methods: Male Wistar rats were fed a normal chow diet (12% from fat) or a high-fat diet (49% from fat) for 15 and 45 weeks, respectively. The adiposity index, body weight and co-morbidities were evaluated. Heart lipotoxicity was assessed by analyzing cardiac function and morphological changes as well as cardiac triglyceride, ceramide and lipid hydroperoxide accumulations. Cardiac apoptosis was examined using the TUNEL method. Leptin function was determined by examining plasma leptin levels, cardiac leptin receptors (OB-R) and related phosphorylations of AMP-activated kinase protein (AMPK) and Acetyl CoA carboxylase (ACC).Key findings: The diet-induced obesity was characterized by an elevated adiposity index, body weight and leptin levels at both 15 and 45 weeks. There was no difference between groups in the cardiac triglyceride or lipid hydroperoxide levels. Interestingly, ceramide levels decreased in obese animals in both experimental periods. The cardiac morphological and functional parameters were not altered. Although down-regulation of OB-R has occurred in chronic obesity, it did not adversely affect AMPK or ACC phosphorylation.Significance: The development of obesity via long-term feeding of a high-fat diet to rats does not result in cardiac lipotoxicity but promotes the down-regulation of OB-R. However, this does not result in altered levels of AMPK or ACC phosphotylations in this animal model. (C) 2011 Elsevier B.V. All rights reserved.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)US Department of AgricultureSão Paulo State Univ UNESP, Botucatu Sch Med, Dept Clin Med, Botucatu, SP, BrazilSão Paulo State Univ UNESP, Inst Biosci, Dept Morphol, Botucatu, SP, BrazilTufts Univ, Jean Mayer USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USATufts Univ, Dept Nutr Sci, Gerald J & Dorothy R Friedman Sch Nutr Sci & Poli, Boston, MA 02111 USASão Paulo State Univ UNESP, Botucatu Sch Med, Dept Clin Med, Botucatu, SP, BrazilSão Paulo State Univ UNESP, Inst Biosci, Dept Morphol, Botucatu, SP, BrazilCNPq: 471256/2007-2US Department of Agriculture: 1950-51000-064SPergamon-Elsevier B.V. LtdUniversidade Estadual Paulista (Unesp)Tufts UnivNascimento, Andre F. [UNESP]Luvizotto, Renata A. M. [UNESP]Leopoldo, Andre S. [UNESP]Lima-Leopoldo, Ana P. [UNESP]Seiva, Fabio R. [UNESP]Justulin, Luis A. [UNESP]Silva, Maeli Dal Pai [UNESP]Okoshi, Katashi [UNESP]Wang, Xiang-DongCicogna, Antonio Carlos [UNESP]2014-05-20T13:33:53Z2014-05-20T13:33:53Z2011-06-06info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1031-1038application/pdfhttp://dx.doi.org/10.1016/j.lfs.2011.03.015Life Sciences. Oxford: Pergamon-Elsevier B.V. Ltd, v. 88, n. 23-24, p. 1031-1038, 2011.0024-3205http://hdl.handle.net/11449/1159510.1016/j.lfs.2011.03.015WOS:000291299300005WOS000291299300005.pdf15909715763094209418970103564137Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengLife Sciences3.2341,071info:eu-repo/semantics/openAccess2024-08-14T17:23:10Zoai:repositorio.unesp.br:11449/11595Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-14T17:23:10Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
title Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
spellingShingle Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
Nascimento, Andre F. [UNESP]
Cardiac lipotoxicity
Cardiac leptin receptor
Diet-induced obesity
High-fat diet
title_short Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
title_full Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
title_fullStr Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
title_full_unstemmed Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
title_sort Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
author Nascimento, Andre F. [UNESP]
author_facet Nascimento, Andre F. [UNESP]
Luvizotto, Renata A. M. [UNESP]
Leopoldo, Andre S. [UNESP]
Lima-Leopoldo, Ana P. [UNESP]
Seiva, Fabio R. [UNESP]
Justulin, Luis A. [UNESP]
Silva, Maeli Dal Pai [UNESP]
Okoshi, Katashi [UNESP]
Wang, Xiang-Dong
Cicogna, Antonio Carlos [UNESP]
author_role author
author2 Luvizotto, Renata A. M. [UNESP]
Leopoldo, Andre S. [UNESP]
Lima-Leopoldo, Ana P. [UNESP]
Seiva, Fabio R. [UNESP]
Justulin, Luis A. [UNESP]
Silva, Maeli Dal Pai [UNESP]
Okoshi, Katashi [UNESP]
Wang, Xiang-Dong
Cicogna, Antonio Carlos [UNESP]
author2_role author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (Unesp)
Tufts Univ
dc.contributor.author.fl_str_mv Nascimento, Andre F. [UNESP]
Luvizotto, Renata A. M. [UNESP]
Leopoldo, Andre S. [UNESP]
Lima-Leopoldo, Ana P. [UNESP]
Seiva, Fabio R. [UNESP]
Justulin, Luis A. [UNESP]
Silva, Maeli Dal Pai [UNESP]
Okoshi, Katashi [UNESP]
Wang, Xiang-Dong
Cicogna, Antonio Carlos [UNESP]
dc.subject.por.fl_str_mv Cardiac lipotoxicity
Cardiac leptin receptor
Diet-induced obesity
High-fat diet
topic Cardiac lipotoxicity
Cardiac leptin receptor
Diet-induced obesity
High-fat diet
description Aims: Leptin resistance has been associated with cardiac lipotoxicity; however, whether leptin resistance is a risk factor associated with cardiac lipotoxicity at different time points in diet-induced obesity is unclear. The objective of this study was to evaluate this relationship.Main methods: Male Wistar rats were fed a normal chow diet (12% from fat) or a high-fat diet (49% from fat) for 15 and 45 weeks, respectively. The adiposity index, body weight and co-morbidities were evaluated. Heart lipotoxicity was assessed by analyzing cardiac function and morphological changes as well as cardiac triglyceride, ceramide and lipid hydroperoxide accumulations. Cardiac apoptosis was examined using the TUNEL method. Leptin function was determined by examining plasma leptin levels, cardiac leptin receptors (OB-R) and related phosphorylations of AMP-activated kinase protein (AMPK) and Acetyl CoA carboxylase (ACC).Key findings: The diet-induced obesity was characterized by an elevated adiposity index, body weight and leptin levels at both 15 and 45 weeks. There was no difference between groups in the cardiac triglyceride or lipid hydroperoxide levels. Interestingly, ceramide levels decreased in obese animals in both experimental periods. The cardiac morphological and functional parameters were not altered. Although down-regulation of OB-R has occurred in chronic obesity, it did not adversely affect AMPK or ACC phosphorylation.Significance: The development of obesity via long-term feeding of a high-fat diet to rats does not result in cardiac lipotoxicity but promotes the down-regulation of OB-R. However, this does not result in altered levels of AMPK or ACC phosphotylations in this animal model. (C) 2011 Elsevier B.V. All rights reserved.
publishDate 2011
dc.date.none.fl_str_mv 2011-06-06
2014-05-20T13:33:53Z
2014-05-20T13:33:53Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1016/j.lfs.2011.03.015
Life Sciences. Oxford: Pergamon-Elsevier B.V. Ltd, v. 88, n. 23-24, p. 1031-1038, 2011.
0024-3205
http://hdl.handle.net/11449/11595
10.1016/j.lfs.2011.03.015
WOS:000291299300005
WOS000291299300005.pdf
1590971576309420
9418970103564137
url http://dx.doi.org/10.1016/j.lfs.2011.03.015
http://hdl.handle.net/11449/11595
identifier_str_mv Life Sciences. Oxford: Pergamon-Elsevier B.V. Ltd, v. 88, n. 23-24, p. 1031-1038, 2011.
0024-3205
10.1016/j.lfs.2011.03.015
WOS:000291299300005
WOS000291299300005.pdf
1590971576309420
9418970103564137
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Life Sciences
3.234
1,071
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 1031-1038
application/pdf
dc.publisher.none.fl_str_mv Pergamon-Elsevier B.V. Ltd
publisher.none.fl_str_mv Pergamon-Elsevier B.V. Ltd
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv
_version_ 1808128153463291904