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<p>Obesity-associated cardiomyopathy (Ob-CM) arises from a complex interaction of systemic metabolic disturbances, myocardial lipid overload, and impaired insulin signalling. This study evaluated the cardiometabolic efficacy of a polyherbal formulation (PHF) comprising <i>Vernonia amygdalina</i>, <i>Cissus quadrangularis</i>, <i>Eryngium foetidum</i>, and <i>Aristolochia indica</i> in a high-fat-diet (HFD)-induced Ob-CM rat model. HFD rats exhibited marked adiposity, dyslipidemia, insulin resistance, inflammatory imbalance, and myocardial triglyceride accumulation. PHF administration significantly reduced body weight, visceral fat, serum lipids, free fatty acids, and HOMA-IR, while restoring adiponectin, reducing pro-inflammatory cytokines, and lowering cardiac injury biomarkers. PHF also attenuated myocardial lipid deposition and preserved cardiac histoarchitecture. Mechanistically, PHF reinstated PI3K/IRS-1/Akt/GLUT4-mediated insulin signalling and corrected PPARα/SREBP-1c-driven lipotoxicity by enhancing AMPK-CPT1-mediated fatty acid oxidation and reducing de novo lipogenesis. These results indicate that PHF confers cardioprotection through coordinated metabolic reprogramming, supporting its potential as an integrative, multi-target therapeutic strategy for obesity-related cardiac dysfunction.</p>

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Polyherbal Formulation Attenuates High-Fat-Diet-Induced Obesity Cardiomyopathy by Modulating PI3K/Akt-IRS1-GLUT4 Insulin Signalling and PPARα/SREBP-Mediated Cardiac Lipotoxicity Pathways

  • 期刊论文

  • 发表日期：

    2026年5月12日

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  • N. Chandrasekharnath,
  • A. Uma,
  • Y. V. Mahalakshmi

摘要

Obesity-associated cardiomyopathy (Ob-CM) arises from a complex interaction of systemic metabolic disturbances, myocardial lipid overload, and impaired insulin signalling. This study evaluated the cardiometabolic efficacy of a polyherbal formulation (PHF) comprising Vernonia amygdalina, Cissus quadrangularis, Eryngium foetidum, and Aristolochia indica in a high-fat-diet (HFD)-induced Ob-CM rat model. HFD rats exhibited marked adiposity, dyslipidemia, insulin resistance, inflammatory imbalance, and myocardial triglyceride accumulation. PHF administration significantly reduced body weight, visceral fat, serum lipids, free fatty acids, and HOMA-IR, while restoring adiponectin, reducing pro-inflammatory cytokines, and lowering cardiac injury biomarkers. PHF also attenuated myocardial lipid deposition and preserved cardiac histoarchitecture. Mechanistically, PHF reinstated PI3K/IRS-1/Akt/GLUT4-mediated insulin signalling and corrected PPARα/SREBP-1c-driven lipotoxicity by enhancing AMPK-CPT1-mediated fatty acid oxidation and reducing de novo lipogenesis. These results indicate that PHF confers cardioprotection through coordinated metabolic reprogramming, supporting its potential as an integrative, multi-target therapeutic strategy for obesity-related cardiac dysfunction.