BIOCHEMICAL AND INFLAMMATORY MARKERS OF CARDIAC REMODELING IN EXPERIMENTAL METABOLIC OBESITY
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Abstract
Objective: to investigate the biochemical and inflammatory mechanisms underlying myocardial remodeling in a rat model of diet-induced metabolic obesity. Methods: twenty male albino rats were divided into control and high-fat–high-carbohydrate diet (HFD) groups and observed for 12 weeks. Serum lipid profile, oxidative stress markers (MDA, SOD, catalase), and inflammatory mediators (IL-6, TNF-α, CRP) were assessed. Histological analysis of myocardial samples (H&E) included morphometry of cardiomyocyte area, left ventricular wall thickness, and interstitial fibrosis. Statistical and correlation analyses were performed. Results: the HFD group showed marked dyslipidemia — total cholesterol (+42.3%), triglycerides (+58.6%), LDL (+61.9%), and decreased HDL (−27.4%) (p < 0.01). MDA levels increased by +67.8%, while SOD and catalase decreased by 34–30% (p < 0.01). IL-6, TNF-α, and CRP levels were elevated 2.4–2.5-fold versus controls (p < 0.001). Morphometric data revealed cardiomyocyte hypertrophy and 2.6-fold greater interstitial fibrosis. Correlation analysis confirmed strong positive associations between MDA and fibrosis (r = 0.63; p < 0.01) and between IL-6 and fibrosis (r = 0.58; p < 0.01). Conclusion: chronic HFD exposure induces biochemical and inflammatory disbalance that drives oxidative stress, fibrosis, and cardiac remodeling in metabolic obesity. The observed changes may serve as early indicators of metabolic cardiomyopathy and potential therapeutic targets for antioxidant and anti-inflammatory intervention.
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