A 28-week high-fat/high-sucrose diet in rabbits induced metabolic syndrome with concentric LV hypertrophy, ventricular-selective fibrosis, and chamber-specific proteomic changes.
Experimental metabolic syndrome in rabbits drives chamber-specific cardiac remodeling characterized by ventricular-selective fibrosis and metabolic inefficiency, preceding overt systolic or diastolic dysfunction.
Metabolic syndrome (MetS) drives cardiac remodeling and fibrosis, contributing to diastolic dysfunction and heart failure with preserved ejection fraction, but chamber-specific mechanisms remain poorly defined. New Zealand White rabbits were fed a high-fat/high-sucrose diet for 28 weeks to induce experimental MetS. Systemic phenotype, cardiac structure (echocardiography), myocardial fibrosis (Picrosirius red histology), myosin/collagen gene expression (qRT-PCR), and chamber-specific proteomics were assessed across left/right atria and ventricles. The model reproduced central obesity, glucose intolerance, dyslipidemia, and mild hypertension, with concentric left ventricular hypertrophy and selective ventricular fibrosis, as follows: increased collagen in left ventricle (LV) and right ventricle (RV), unchanged in atria. Ventricular α-myosin heavy-chain gene expression was upregulated, while collagen I and α-smooth muscle actin transcripts showed ventricular-specific downregulation. Proteomics revealed atrial metabolic and cytoskeletal adaptations with minimal extracellular matrix involvement; ventricles displayed early profibrotic cues (galectin-3 in LV), metabolic inefficiency (impaired glycolysis/ATP production in LV; lipid oxidation shift in RV), and diminished provisional matrix support. Conclusions: concentric LV hypertrophy and great vessel enlargement occurred without systolic/diastolic dysfunction; ventricular-selective fibrosis, α-myosin heavy-chain upregulation, type I collagen/α-smooth muscle actin downregulation, and chamber-specific proteomic changes showed atrial adaptation versus ventricular early profibrotic/metabolic inefficiency.
Arias-Mutis et al. (Fri,) conducted a other in Experimental Metabolic Syndrome. High-fat/high-sucrose diet was evaluated on Systemic phenotype, cardiac structure, myocardial fibrosis, gene expression, and chamber-specific proteomics. A 28-week high-fat/high-sucrose diet in rabbits induced metabolic syndrome with concentric LV hypertrophy, ventricular-selective fibrosis, and chamber-specific proteomic changes.