Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.

<h4>Introduction</h4>The role of glucocorticoids in atherosclerosis development is not clearly established. Human studies show a clear association between glucocorticoid excess and cardiovascular disease, whereas most animal models indicate an inhibitory effect of glucocorticoids on athe...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Hanna E Auvinen, Yanan Wang, Hans Princen, Johannes A Romijn, Louis M Havekes, Johannes W A Smit, Onno C Meijer, Nienke R Biermasz, Patrick C N Rensen, Alberto M Pereira
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ccc4dae512d74cce8cb7e2e75a17fc60
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:ccc4dae512d74cce8cb7e2e75a17fc60
record_format	dspace
spelling	oai:doaj.org-article:ccc4dae512d74cce8cb7e2e75a17fc602021-11-18T07:44:39ZBoth transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE3-leiden.CETP mice.1932-620310.1371/journal.pone.0063882https://doaj.org/article/ccc4dae512d74cce8cb7e2e75a17fc602013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23717502/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Introduction</h4>The role of glucocorticoids in atherosclerosis development is not clearly established. Human studies show a clear association between glucocorticoid excess and cardiovascular disease, whereas most animal models indicate an inhibitory effect of glucocorticoids on atherosclerosis development. These animal models, however, neither reflect long-term glucocorticoid overexposure nor display human-like lipoprotein metabolism.<h4>Aim</h4>To investigate the effects of transient and continuous glucocorticoid excess on atherosclerosis development in a mouse model with human-like lipoprotein metabolism upon feeding a Western-type diet.<h4>Methods</h4>Pair-housed female APOE3-Leiden.CETP (E3L.CETP) mice fed a Western-type containing 0.1% cholesterol for 20 weeks were given corticosterone (50 µg/ml) for either 5 (transient group) or 17 weeks (continuous group), or vehicle (control group) in the drinking water. At the end of the study, atherosclerosis severity, lesion area in the aortic root, the number of monocytes adhering to the endothelial wall and macrophage content of the plaque were measured.<h4>Results</h4>Corticosterone treatment increased body weight and food intake for the duration of the treatment and increased gonadal and subcutaneous white adipose tissue weight in transient group by +35% and +31%, and in the continuous group by +140% and 110%. Strikingly, both transient and continuous corticosterone treatment decreased total atherosclerotic lesion area by -39% without lowering plasma cholesterol levels. In addition, there was a decrease of -56% in macrophage content of the plaque with continuous corticosterone treatment, and a similar trend was present with the transient treatment.<h4>Conclusion</h4>Increased corticosterone exposure in mice with human-like lipoprotein metabolism has beneficial, long-lasting effects on atherosclerosis, but negatively affects body fat distribution by promoting fat accumulation in the long-term. This indicates that the increased atherosclerosis observed in humans in states of glucocorticoid excess may not be related to cortisol per se, but might be the result of complex indirect effects of cortisol.Hanna E AuvinenYanan WangHans PrincenJohannes A RomijnLouis M HavekesJohannes W A SmitOnno C MeijerNienke R BiermaszPatrick C N RensenAlberto M PereiraPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 5, p e63882 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hanna E Auvinen Yanan Wang Hans Princen Johannes A Romijn Louis M Havekes Johannes W A Smit Onno C Meijer Nienke R Biermasz Patrick C N Rensen Alberto M Pereira Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.
description	<h4>Introduction</h4>The role of glucocorticoids in atherosclerosis development is not clearly established. Human studies show a clear association between glucocorticoid excess and cardiovascular disease, whereas most animal models indicate an inhibitory effect of glucocorticoids on atherosclerosis development. These animal models, however, neither reflect long-term glucocorticoid overexposure nor display human-like lipoprotein metabolism.<h4>Aim</h4>To investigate the effects of transient and continuous glucocorticoid excess on atherosclerosis development in a mouse model with human-like lipoprotein metabolism upon feeding a Western-type diet.<h4>Methods</h4>Pair-housed female APOE*3-Leiden.CETP (E3L.CETP) mice fed a Western-type containing 0.1% cholesterol for 20 weeks were given corticosterone (50 µg/ml) for either 5 (transient group) or 17 weeks (continuous group), or vehicle (control group) in the drinking water. At the end of the study, atherosclerosis severity, lesion area in the aortic root, the number of monocytes adhering to the endothelial wall and macrophage content of the plaque were measured.<h4>Results</h4>Corticosterone treatment increased body weight and food intake for the duration of the treatment and increased gonadal and subcutaneous white adipose tissue weight in transient group by +35% and +31%, and in the continuous group by +140% and 110%. Strikingly, both transient and continuous corticosterone treatment decreased total atherosclerotic lesion area by -39% without lowering plasma cholesterol levels. In addition, there was a decrease of -56% in macrophage content of the plaque with continuous corticosterone treatment, and a similar trend was present with the transient treatment.<h4>Conclusion</h4>Increased corticosterone exposure in mice with human-like lipoprotein metabolism has beneficial, long-lasting effects on atherosclerosis, but negatively affects body fat distribution by promoting fat accumulation in the long-term. This indicates that the increased atherosclerosis observed in humans in states of glucocorticoid excess may not be related to cortisol per se, but might be the result of complex indirect effects of cortisol.
format	article
author	Hanna E Auvinen Yanan Wang Hans Princen Johannes A Romijn Louis M Havekes Johannes W A Smit Onno C Meijer Nienke R Biermasz Patrick C N Rensen Alberto M Pereira
author_facet	Hanna E Auvinen Yanan Wang Hans Princen Johannes A Romijn Louis M Havekes Johannes W A Smit Onno C Meijer Nienke R Biermasz Patrick C N Rensen Alberto M Pereira
author_sort	Hanna E Auvinen
title	Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.
title_short	Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.
title_full	Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.
title_fullStr	Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.
title_full_unstemmed	Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.
title_sort	both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in apoe*3-leiden.cetp mice.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/ccc4dae512d74cce8cb7e2e75a17fc60
work_keys_str_mv	AT hannaeauvinen bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT yananwang bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT hansprincen bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT johannesaromijn bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT louismhavekes bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT johanneswasmit bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT onnocmeijer bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT nienkerbiermasz bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT patrickcnrensen bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice AT albertompereira bothtransientandcontinuouscorticosteroneexcessinhibitatheroscleroticplaqueformationinapoe3leidencetpmice
_version_	1718423063116120064

Both transient and continuous corticosterone excess inhibit atherosclerotic plaque formation in APOE*3-leiden.CETP mice.

Ejemplares similares