High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses
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/10.1111/j.1464-410X.2010.09704.x http://hdl.handle.net/11449/20884 |
Resumo: | What's known on the subject? and What does the study add?Erectile dysfunction (ED) is defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance. ED has been found in patients with cardiovascular and endocrine-metabolic diseases. Overweight, obesity and weight gain have been shown to be independent risk factors for the development of ED. Clinical studies show that ED should be considered an early clinical manifestation of risk factors for cardiovascular events, including acute myocardial infarction. However, the mechanisms that explains ED associated with obesity are yet to be fully elucidated.Using a mice model of high-fat diet associated with obesity, we have demonstrated that ED is the result of impaired endothelial and nitrergic cavernosal relaxations along with increased contractile responses, favouring penile detumescence.OBJECTIVEObesity induced by high-fat diet (HFD) is one of the most important risk factor for the development of erectile dysfunction (ED) in man. This study aimed to characterize the ED resulting from obesity associated with HFD in mice.MATERIALS and METHODSC57BL/6 mice fed for 10 weeks with either HFD to induce obesity or a standard-chow diet (SD) were used. Corpus cavernosum was surgically dissected free, and strips were mounted in 10-mL organ baths containing Krebs solution.Functional responses to endothelium-dependent and -independent agents, as well as to electrical-field stimulation were measured in the cavernosal tissue. Levels of cGMP in erectile tissue were detected by enzyme immunoassay assay.RESULTSThe potency (pEC(50)) and maximal response (E(max)) to acetylcholine were significantly lower in the HFD group compared with the SD group. A marked decrease in the non-adrenergic non-cholinergic (nitrergic) cavernosal relaxations in the HFD group was also detected. There were no significant differences between the SD and HFD groups for the cavernosal relaxations in response to sodium nitroprusside.The contractile responses elicited by the alpha(1)-adrenoceptor agonist phenylephrine were significantly greater in the HFD group compared with the SD group.Similarly, the electrical-field stimulation (2-8 Hz)-induced adrenergic contractions were markedly greater in HFD mice. The pEC(50) for endothelin-1 was about 6.9-fold higher in the HFD compared with SD group.The basal cGMP content was 47% lower in HFD strips compared with SD group. There were no morphological alterations in erectile tissue of HFD group compared with SD mice.CONCLUSIONObesity associated with HFD favours ED as result of impaired endothelial and nitrergic cavernosal relaxations along with increased contractile responses to adrenergic stimulation and endothelin-1 receptor activation. |
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High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responsesobesitymale impotencenitric oxideendothelin-1noradrenalinecyclic GMPWhat's known on the subject? and What does the study add?Erectile dysfunction (ED) is defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance. ED has been found in patients with cardiovascular and endocrine-metabolic diseases. Overweight, obesity and weight gain have been shown to be independent risk factors for the development of ED. Clinical studies show that ED should be considered an early clinical manifestation of risk factors for cardiovascular events, including acute myocardial infarction. However, the mechanisms that explains ED associated with obesity are yet to be fully elucidated.Using a mice model of high-fat diet associated with obesity, we have demonstrated that ED is the result of impaired endothelial and nitrergic cavernosal relaxations along with increased contractile responses, favouring penile detumescence.OBJECTIVEObesity induced by high-fat diet (HFD) is one of the most important risk factor for the development of erectile dysfunction (ED) in man. This study aimed to characterize the ED resulting from obesity associated with HFD in mice.MATERIALS and METHODSC57BL/6 mice fed for 10 weeks with either HFD to induce obesity or a standard-chow diet (SD) were used. Corpus cavernosum was surgically dissected free, and strips were mounted in 10-mL organ baths containing Krebs solution.Functional responses to endothelium-dependent and -independent agents, as well as to electrical-field stimulation were measured in the cavernosal tissue. Levels of cGMP in erectile tissue were detected by enzyme immunoassay assay.RESULTSThe potency (pEC(50)) and maximal response (E(max)) to acetylcholine were significantly lower in the HFD group compared with the SD group. A marked decrease in the non-adrenergic non-cholinergic (nitrergic) cavernosal relaxations in the HFD group was also detected. There were no significant differences between the SD and HFD groups for the cavernosal relaxations in response to sodium nitroprusside.The contractile responses elicited by the alpha(1)-adrenoceptor agonist phenylephrine were significantly greater in the HFD group compared with the SD group.Similarly, the electrical-field stimulation (2-8 Hz)-induced adrenergic contractions were markedly greater in HFD mice. The pEC(50) for endothelin-1 was about 6.9-fold higher in the HFD compared with SD group.The basal cGMP content was 47% lower in HFD strips compared with SD group. There were no morphological alterations in erectile tissue of HFD group compared with SD mice.CONCLUSIONObesity associated with HFD favours ED as result of impaired endothelial and nitrergic cavernosal relaxations along with increased contractile responses to adrenergic stimulation and endothelin-1 receptor activation.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Univ Campinas UNICAMP, Fac Med Sci, Dept Pharmacol & Internal Med, São Paulo, BrazilUniv São Paulo State UNESP, Dept Phys Educ, São Paulo, BrazilMed Coll Georgia, Dept Pharmacol & Toxicol, Augusta, GA 30912 USAUniv São Paulo State UNESP, Dept Phys Educ, São Paulo, BrazilWiley-BlackwellUniversidade Estadual de Campinas (UNICAMP)Universidade Estadual Paulista (Unesp)Med Coll GeorgiaToque, Haroldo A.da Silva, Fabio H.Calixto, Marina C.Lintomen, LeticiaSchenka, Andre A.Saad, Mario J.Zanesco, Angelina [UNESP]Antunes, Edson2013-09-30T18:49:20Z2014-05-20T13:58:46Z2013-09-30T18:49:20Z2014-05-20T13:58:46Z2011-05-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article1628-1634http://dx.doi.org/10.1111/j.1464-410X.2010.09704.xBju International. Malden: Wiley-blackwell, v. 107, n. 10, p. 1628-1634, 2011.1464-4096http://hdl.handle.net/11449/2088410.1111/j.1464-410X.2010.09704.xWOS:0002898991000164472007237545596Web of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengBju International4.6882,094info:eu-repo/semantics/openAccess2021-10-22T19:32:46Zoai:repositorio.unesp.br:11449/20884Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T18:35:47.069127Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses |
title |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses |
spellingShingle |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses Toque, Haroldo A. obesity male impotence nitric oxide endothelin-1 noradrenaline cyclic GMP |
title_short |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses |
title_full |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses |
title_fullStr |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses |
title_full_unstemmed |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses |
title_sort |
High-fat diet associated with obesity induces impairment of mouse corpus cavernosum responses |
author |
Toque, Haroldo A. |
author_facet |
Toque, Haroldo A. da Silva, Fabio H. Calixto, Marina C. Lintomen, Leticia Schenka, Andre A. Saad, Mario J. Zanesco, Angelina [UNESP] Antunes, Edson |
author_role |
author |
author2 |
da Silva, Fabio H. Calixto, Marina C. Lintomen, Leticia Schenka, Andre A. Saad, Mario J. Zanesco, Angelina [UNESP] Antunes, Edson |
author2_role |
author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual de Campinas (UNICAMP) Universidade Estadual Paulista (Unesp) Med Coll Georgia |
dc.contributor.author.fl_str_mv |
Toque, Haroldo A. da Silva, Fabio H. Calixto, Marina C. Lintomen, Leticia Schenka, Andre A. Saad, Mario J. Zanesco, Angelina [UNESP] Antunes, Edson |
dc.subject.por.fl_str_mv |
obesity male impotence nitric oxide endothelin-1 noradrenaline cyclic GMP |
topic |
obesity male impotence nitric oxide endothelin-1 noradrenaline cyclic GMP |
description |
What's known on the subject? and What does the study add?Erectile dysfunction (ED) is defined as the persistent inability to achieve and/or maintain an erection sufficient for satisfactory sexual performance. ED has been found in patients with cardiovascular and endocrine-metabolic diseases. Overweight, obesity and weight gain have been shown to be independent risk factors for the development of ED. Clinical studies show that ED should be considered an early clinical manifestation of risk factors for cardiovascular events, including acute myocardial infarction. However, the mechanisms that explains ED associated with obesity are yet to be fully elucidated.Using a mice model of high-fat diet associated with obesity, we have demonstrated that ED is the result of impaired endothelial and nitrergic cavernosal relaxations along with increased contractile responses, favouring penile detumescence.OBJECTIVEObesity induced by high-fat diet (HFD) is one of the most important risk factor for the development of erectile dysfunction (ED) in man. This study aimed to characterize the ED resulting from obesity associated with HFD in mice.MATERIALS and METHODSC57BL/6 mice fed for 10 weeks with either HFD to induce obesity or a standard-chow diet (SD) were used. Corpus cavernosum was surgically dissected free, and strips were mounted in 10-mL organ baths containing Krebs solution.Functional responses to endothelium-dependent and -independent agents, as well as to electrical-field stimulation were measured in the cavernosal tissue. Levels of cGMP in erectile tissue were detected by enzyme immunoassay assay.RESULTSThe potency (pEC(50)) and maximal response (E(max)) to acetylcholine were significantly lower in the HFD group compared with the SD group. A marked decrease in the non-adrenergic non-cholinergic (nitrergic) cavernosal relaxations in the HFD group was also detected. There were no significant differences between the SD and HFD groups for the cavernosal relaxations in response to sodium nitroprusside.The contractile responses elicited by the alpha(1)-adrenoceptor agonist phenylephrine were significantly greater in the HFD group compared with the SD group.Similarly, the electrical-field stimulation (2-8 Hz)-induced adrenergic contractions were markedly greater in HFD mice. The pEC(50) for endothelin-1 was about 6.9-fold higher in the HFD compared with SD group.The basal cGMP content was 47% lower in HFD strips compared with SD group. There were no morphological alterations in erectile tissue of HFD group compared with SD mice.CONCLUSIONObesity associated with HFD favours ED as result of impaired endothelial and nitrergic cavernosal relaxations along with increased contractile responses to adrenergic stimulation and endothelin-1 receptor activation. |
publishDate |
2011 |
dc.date.none.fl_str_mv |
2011-05-01 2013-09-30T18:49:20Z 2013-09-30T18:49:20Z 2014-05-20T13:58:46Z 2014-05-20T13:58:46Z |
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/10.1111/j.1464-410X.2010.09704.x Bju International. Malden: Wiley-blackwell, v. 107, n. 10, p. 1628-1634, 2011. 1464-4096 http://hdl.handle.net/11449/20884 10.1111/j.1464-410X.2010.09704.x WOS:000289899100016 4472007237545596 |
url |
http://dx.doi.org/10.1111/j.1464-410X.2010.09704.x http://hdl.handle.net/11449/20884 |
identifier_str_mv |
Bju International. Malden: Wiley-blackwell, v. 107, n. 10, p. 1628-1634, 2011. 1464-4096 10.1111/j.1464-410X.2010.09704.x WOS:000289899100016 4472007237545596 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Bju International 4.688 2,094 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
1628-1634 |
dc.publisher.none.fl_str_mv |
Wiley-Blackwell |
publisher.none.fl_str_mv |
Wiley-Blackwell |
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_ |
1808128954195771392 |