Cargando…
Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet
BACKGROUND: Metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD). One important feature underlying the pathophysiology of many types of CVD is microvascular dysfunction. Although components of MetS are themselves CVD risk factors, the risk is increased when the...
Autores principales: | , , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3916304/ https://www.ncbi.nlm.nih.gov/pubmed/24490784 http://dx.doi.org/10.1186/1475-2840-13-31 |
_version_ | 1782302689129922560 |
---|---|
author | Aoqui, Cristiane Chmielewski, Stefan Scherer, Elias Eißler, Ruth Sollinger, Daniel Heid, Irina Braren, Rickmer Schmaderer, Christoph Megens, Remco TA Weber, Christian Heemann, Uwe Tschöp, Matthias Baumann, Marcus |
author_facet | Aoqui, Cristiane Chmielewski, Stefan Scherer, Elias Eißler, Ruth Sollinger, Daniel Heid, Irina Braren, Rickmer Schmaderer, Christoph Megens, Remco TA Weber, Christian Heemann, Uwe Tschöp, Matthias Baumann, Marcus |
author_sort | Aoqui, Cristiane |
collection | PubMed |
description | BACKGROUND: Metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD). One important feature underlying the pathophysiology of many types of CVD is microvascular dysfunction. Although components of MetS are themselves CVD risk factors, the risk is increased when the syndrome is considered as one entity. We aimed to characterize microvascular function and some of its influencing factors in the course of MetS development. METHODS: Development of MetS in C57BL/6 mice on a high-fat diet (HFD, 51% of energy from fat) was studied. The initial phase of MetS (I-MetS) was defined as the first 2 weeks of HFD feeding, with the fully developed phase occurring after 8 weeks of HFD. We characterized these phases by assessing changes in adiposity, blood pressure, and microvascular function. All data are presented as mean ± standard error (SEM). Differences between cumulative dose–response curves of myograph experiments were calculated using non-linear regression analysis. In other experiments, comparisons between two groups were made with Student’s t-test. Comparisons between more than two groups were made using one-way ANOVA with Tukey post-hoc test. A probability value <0.05 was considered statistically significant. RESULTS: I-MetS mice presented with weight gain, blood pressure elevation, and microvascular dysfunction characterized by augmented vasoconstriction. This finding, contrary to those in mice with fully developed MetS, was not associated with endothelial dysfunction, insulin resistance, or systemic inflammation. In the initial phase, perivascular adipose tissue showed no sign of inflammation and had no influence on the pattern of vasoconstriction. These findings suggest that the onset of hypertension in MetS is strongly influenced by vascular smooth muscle cell dysfunction and independent of important factors known to influence microvascular function and consequently blood pressure levels. CONCLUSION: We identified in I-MetS the occurrence of isolated augmented vasoconstriction along with blood pressure elevation, but not the presence of classical MetS components known to influence microvascular function. These findings increase our understanding of the pathophysiology of CVD risk associated with MetS. |
format | Online Article Text |
id | pubmed-3916304 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-39163042014-02-07 Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet Aoqui, Cristiane Chmielewski, Stefan Scherer, Elias Eißler, Ruth Sollinger, Daniel Heid, Irina Braren, Rickmer Schmaderer, Christoph Megens, Remco TA Weber, Christian Heemann, Uwe Tschöp, Matthias Baumann, Marcus Cardiovasc Diabetol Original Investigation BACKGROUND: Metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD). One important feature underlying the pathophysiology of many types of CVD is microvascular dysfunction. Although components of MetS are themselves CVD risk factors, the risk is increased when the syndrome is considered as one entity. We aimed to characterize microvascular function and some of its influencing factors in the course of MetS development. METHODS: Development of MetS in C57BL/6 mice on a high-fat diet (HFD, 51% of energy from fat) was studied. The initial phase of MetS (I-MetS) was defined as the first 2 weeks of HFD feeding, with the fully developed phase occurring after 8 weeks of HFD. We characterized these phases by assessing changes in adiposity, blood pressure, and microvascular function. All data are presented as mean ± standard error (SEM). Differences between cumulative dose–response curves of myograph experiments were calculated using non-linear regression analysis. In other experiments, comparisons between two groups were made with Student’s t-test. Comparisons between more than two groups were made using one-way ANOVA with Tukey post-hoc test. A probability value <0.05 was considered statistically significant. RESULTS: I-MetS mice presented with weight gain, blood pressure elevation, and microvascular dysfunction characterized by augmented vasoconstriction. This finding, contrary to those in mice with fully developed MetS, was not associated with endothelial dysfunction, insulin resistance, or systemic inflammation. In the initial phase, perivascular adipose tissue showed no sign of inflammation and had no influence on the pattern of vasoconstriction. These findings suggest that the onset of hypertension in MetS is strongly influenced by vascular smooth muscle cell dysfunction and independent of important factors known to influence microvascular function and consequently blood pressure levels. CONCLUSION: We identified in I-MetS the occurrence of isolated augmented vasoconstriction along with blood pressure elevation, but not the presence of classical MetS components known to influence microvascular function. These findings increase our understanding of the pathophysiology of CVD risk associated with MetS. BioMed Central 2014-02-03 /pmc/articles/PMC3916304/ /pubmed/24490784 http://dx.doi.org/10.1186/1475-2840-13-31 Text en Copyright © 2014 Aoqui et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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 | Original Investigation Aoqui, Cristiane Chmielewski, Stefan Scherer, Elias Eißler, Ruth Sollinger, Daniel Heid, Irina Braren, Rickmer Schmaderer, Christoph Megens, Remco TA Weber, Christian Heemann, Uwe Tschöp, Matthias Baumann, Marcus Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet |
title | Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet |
title_full | Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet |
title_fullStr | Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet |
title_full_unstemmed | Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet |
title_short | Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet |
title_sort | microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3916304/ https://www.ncbi.nlm.nih.gov/pubmed/24490784 http://dx.doi.org/10.1186/1475-2840-13-31 |
work_keys_str_mv | AT aoquicristiane microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT chmielewskistefan microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT schererelias microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT eißlerruth microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT sollingerdaniel microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT heidirina microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT brarenrickmer microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT schmadererchristoph microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT megensremcota microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT weberchristian microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT heemannuwe microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT tschopmatthias microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet AT baumannmarcus microvasculardysfunctioninthecourseofmetabolicsyndromeinducedbyhighfatdiet |