Key result
Quercetin reduces left ventricular mass ~20% and improves cardiac function in obese mice.
Why the study?
Does dietary quercetin supplementation attenuate cardiac dysfunction, adverse myocardial remodelling, and metabolic dysregulation in mice with high-fat diet-induced obesity-related cardiomyopathy?
Does dietary quercetin supplementation attenuate cardiac dysfunction, adverse myocardial remodelling, and metabolic dysregulation in mice with high-fat diet-induced obesity-related cardiomyopathy?
This preclinical proteomic study demonstrates that dietary quercetin attenuates high-fat diet-induced cardiac hypertrophy, fibrosis, oxidative stress, and systolic dysfunction in mice while normalizing myocardial Fabp3, Adipoq, AMPK, and PPARα expression.
Quercetin effects in obese mice do not support clinical use; leaves open translation to human obesity cardiomyopathy.
Obesity-related cardiomyopathy involves metabolic dysregulation, oxidative stress, fibrosis and cardiac dysfunction. We investigated quercetin using tandem mass tag-based cardiac proteomics in high-fat diet (HFD)-fed mice. We identified 180 differentially expressed proteins (DEPs) between HFD and control mice and 303 between quercetin-treated and untreated HFD mice. Pathway analyses implicated lipid metabolism, peroxisome proliferator-activated receptor (PPAR) signalling and branched-chain amino acid degradation. Among 36 overlapping DEPs, 35 exhibited opposite changes across comparisons, highlighting heart-type fatty acid-binding protein 3 (Fabp3) and adiponectin (Adipoq) as candidate response-associated proteins. Western blotting confirmed elevated myocardial Fabp3 and reduced Adipoq with HFD, both shifted toward control levels following quercetin treatment, alongside restored AMP-activated protein kinase (AMPK) phosphorylation and reduced PPARα expression. Qualitative Oil Red O staining showed no overt myocardial neutral-lipid accumulation despite increased hepatic lipid staining in HFD mice. Molecular docking predicted favourable binding poses for quercetin with Fabp3 and Adipoq (− 8.8 and − 8.2 kcal/mol), without establishing direct binding. Quercetin also attenuated oxidative stress, inflammation, collagen deposition and cardiac dysfunction. These findings suggest coordinated Fabp3-, Adipoq-, AMPK- and PPARα-associated responses, warranting causal validation.
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Xu et al. (2026) studied High-fat diet-induced obesity-related cardiomyopathy (n=24). Quercetin vs. Untreated high-fat diet (HFD) and normal-diet control (CONT) was evaluated on Left ventricular mass and heart mass reduction, cardiac function (EF, FS), and myocardial proteomic profile (p=<0.01). Quercetin reduced left ventricular mass by 20.40% and heart mass by 15.57% (p<0.01) while improving cardiac function and shifting Fabp3 and Adipoq toward control levels in high-fat diet-fed mice.
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