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Structural and functional microvascular alterations in a rat model of metabolic syndrome induced by a high‐fat diet
Author(s) -
Nascimento Alessandro R.,
Machado Marcus,
Jesus Nathália,
Gomes Fabiana,
Lessa Marcos A.,
Bonomo Isabela T.,
Tibiriçá Eduardo
Publication year - 2013
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20358
Subject(s) - medicine , endocrinology , insulin resistance , skeletal muscle , metabolic syndrome , hypertriglyceridemia , microcirculation , ventricle , muscle hypertrophy , insulin , cholesterol , diabetes mellitus , triglyceride
Objective To investigate microvascular alterations in an experimental model of metabolic syndrome induced by a high‐fat diet (HFD) associated with salt supplementation (0.5% NaCl). Design and Methods Wistar Kyoto rats were fed standard chow (control group, CONT) or HFD for 20 weeks. The functional capillary density (FCD) was assessed using intravital fluorescence videomicroscopy. Results The HFD group presented a higher systolic blood pressure, plasma glucose and insulin levels, total and LDL‐cholesterol levels, triglycerides, and visceral and epididymal fat when compared with the CONT group. When compared with the CONT group, the HFD group showed a lower FCD in the skeletal muscle ( P < 0.05) but not in the skin ( P > 0.05). The HFD group also had a lower capillary‐to‐fiber ratio in the skeletal muscle ( P < 0.01). The capillary volume density‐to‐fiber volume density ratio in the left ventricle of the HFD was also reduced ( P < 0.01). Finally, rats fed with HFD showed ventricular hypertrophy and increased cardiomyocyte diameter ( P < 0.01). Conclusions The long‐term administration of a HFD associated with salt supplementation to rats generates an experimental model of metabolic syndrome characterized by central body fat deposition, insulin resistance, glucose intolerance, hypertriglyceridemia, hypercholesterolemia, arterial hypertension, cardiac remodeling, and rarefaction of the microcirculation in the heart and skeletal muscle.