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

doi:10.1186/1475-2840-13-31

2014

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Title:: Microvascular dysfunction in the course of metabolic syndrome induced by high-fat diet.
Document type:: Journal Article; Research Support, Non-U.S. Gov't; Article
Author(s):: 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
Abstract:: 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.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.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.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.
Journal title abbreviation:: Cardiovasc Diabetol
Year:: 2014
Journal volume:: 13
Pages contribution:: 31
Language:: eng
Fulltext / DOI:: doi:10.1186/1475-2840-13-31
Pubmed ID:: http://view.ncbi.nlm.nih.gov/pubmed/24490784
Print-ISSN:: 1475-2840
TUM Institution:: Fachgebiet Nephrologie (Prof. Heemann); Hals-Nasen-Ohrenklinik und Poliklinik; Kliniken und Institute
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