Long-term high-fat diet-induced obesity decreases the cardiac leptin receptor without apparent lipotoxicity
Autor(a) principal: | |
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Data de Publicação: | 2011 |
Outros Autores: | , , , , , , , , |
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. |
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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 |
|
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1808128153463291904 |