Key result
High-fat/high-sucrose diet in rabbits induces metabolic syndrome, concentric LV hypertrophy, and ventricular-selective fibrosis.
Why the study?
Metabolic syndrome drives cardiac remodeling and fibrosis, but chamber-specific mechanisms remain poorly defined.
Experimental metabolic syndrome in rabbits drives chamber-specific cardiac remodeling characterized by ventricular-selective fibrosis and metabolic inefficiency, preceding overt systolic or diastolic dysfunction.
May support chamber-specific targeting in MetS-related HFpEF; leaves open human validation before practice change.
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.
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Arias-Mutis et al. (2026) studied 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.
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