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Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model

BACKGROUND: Lipid dysregulation is a classical risk factor for cardiovascular disease (CVD), yet scanty evidence existed regarding cardiac lipid metabolism that is directly related to heart damage. Recently, the relationship between dyslipidemia and pro-inflammatory insults has led to further unders...

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Autores principales: Han, Qian, Yeung, Sze C., Ip, Mary S. M., Mak, Judith C. W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6237003/
https://www.ncbi.nlm.nih.gov/pubmed/30428911
http://dx.doi.org/10.1186/s12944-018-0905-3
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author Han, Qian
Yeung, Sze C.
Ip, Mary S. M.
Mak, Judith C. W.
author_facet Han, Qian
Yeung, Sze C.
Ip, Mary S. M.
Mak, Judith C. W.
author_sort Han, Qian
collection PubMed
description BACKGROUND: Lipid dysregulation is a classical risk factor for cardiovascular disease (CVD), yet scanty evidence existed regarding cardiac lipid metabolism that is directly related to heart damage. Recently, the relationship between dyslipidemia and pro-inflammatory insults has led to further understanding on the CVD-predisposing effects of dyslipidemia. The aims of the present study were to investigate whether high-fat high-cholesterol (HFHC) diet-induced hyperlipidemia would cause heart damage and to study the potential role of local cardiac lipid dysregulation in the occurrence of cellular injury. METHODS: Male Sprague–Dawley rats were divided into normal chow or HFHC diet groups, and sacrificed after 2 or 4 weeks, respectively. Lipid peroxidation marker level was measured. Lipid parameters in the rat hearts were detected. Cardiac damage was evaluated. RESULTS: HFHC diet increased serum levels of cholesterol and free fatty acids (FFAs) and led to systemic oxidative stress and pro-inflammatory status. Cardiac lipid dysregulation, which was characterized by elevated levels of cholesterol and adipocyte (A)- and heart (H)-fatty acid binding proteins (FABPs), occurred after HFHC diet for 4 weeks. Cardiac damage was further evident with elevated circulating H-FABP levels, increased cardiac interstitial fibrosis and the loss of troponin I. CONCLUSION: Our data demonstrated that HFHC diet led to systemic and cardiac lipid dysregulation, accompanied by systemic oxidative and pro-inflammatory stresses, and these may finally cooperate to cause a series of pathological changes of the heart tissue. Our findings suggest that maintenance of lipid regulation may be essential in the prevention of heart damage.
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spelling pubmed-62370032018-11-23 Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model Han, Qian Yeung, Sze C. Ip, Mary S. M. Mak, Judith C. W. Lipids Health Dis Research BACKGROUND: Lipid dysregulation is a classical risk factor for cardiovascular disease (CVD), yet scanty evidence existed regarding cardiac lipid metabolism that is directly related to heart damage. Recently, the relationship between dyslipidemia and pro-inflammatory insults has led to further understanding on the CVD-predisposing effects of dyslipidemia. The aims of the present study were to investigate whether high-fat high-cholesterol (HFHC) diet-induced hyperlipidemia would cause heart damage and to study the potential role of local cardiac lipid dysregulation in the occurrence of cellular injury. METHODS: Male Sprague–Dawley rats were divided into normal chow or HFHC diet groups, and sacrificed after 2 or 4 weeks, respectively. Lipid peroxidation marker level was measured. Lipid parameters in the rat hearts were detected. Cardiac damage was evaluated. RESULTS: HFHC diet increased serum levels of cholesterol and free fatty acids (FFAs) and led to systemic oxidative stress and pro-inflammatory status. Cardiac lipid dysregulation, which was characterized by elevated levels of cholesterol and adipocyte (A)- and heart (H)-fatty acid binding proteins (FABPs), occurred after HFHC diet for 4 weeks. Cardiac damage was further evident with elevated circulating H-FABP levels, increased cardiac interstitial fibrosis and the loss of troponin I. CONCLUSION: Our data demonstrated that HFHC diet led to systemic and cardiac lipid dysregulation, accompanied by systemic oxidative and pro-inflammatory stresses, and these may finally cooperate to cause a series of pathological changes of the heart tissue. Our findings suggest that maintenance of lipid regulation may be essential in the prevention of heart damage. BioMed Central 2018-11-14 /pmc/articles/PMC6237003/ /pubmed/30428911 http://dx.doi.org/10.1186/s12944-018-0905-3 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Han, Qian
Yeung, Sze C.
Ip, Mary S. M.
Mak, Judith C. W.
Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model
title Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model
title_full Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model
title_fullStr Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model
title_full_unstemmed Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model
title_short Dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model
title_sort dysregulation of cardiac lipid parameters in high-fat high-cholesterol diet-induced rat model
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6237003/
https://www.ncbi.nlm.nih.gov/pubmed/30428911
http://dx.doi.org/10.1186/s12944-018-0905-3
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