Identification of an Optimized Quinoa Supplementation Strategy that Protects Against High-Fat Diet-Induced Multi-Organ Injury in Rats: Integrated Biochemical, Bioenergetic and Histopathological Evidence

Abstract

Background: Obesity induced by chronic consumption of a high-fat diet (HFD) is associated with dyslipidemia, oxidative stress, mitochondrial dysfunction, and progressive multi-organ injury. Although Chenopodium quinoa Willd. is recognized as a nutrient-rich functional food with potent antioxidant and hypolipidemic properties, limited information is available regarding the comparative
efficacy of different supplementation levels against obesity-associated metabolic disturbances. Objective: This study aimed to evaluate the protective effects of two supplementation levels of quinoa against HFD-induced obesity and to compare their efficacy with that of a reference hypolipidemic drug. Methods: Thirty male albino rats were randomly assigned to five experimental groups (n = 6/group): normal control, HFD-fed obese control, HFD supplemented with quinoa at the first dose level (HFQ1), HFD supplemented with quinoa at the second dose level (HFQ2), and HFD treated with a reference statin. Obesity was induced by HFD feeding for six weeks. Serum lipid profile, hepatic oxidative stress biomarkers [malondialdehyde (MDA), reduced glutathione (GSH), and oxidized glutathione (GSSG)], hepatic adenine nucleotides (ATP, ADP, and AMP), and histopathological alterations in the liver, kidney, and coronary arteries were evaluated using validated biochemical and histological methods. Results: HFD feeding induced marked dyslipidemia, enhanced lipid peroxidation, depletion of antioxidant defenses, impaired hepatic bioenergetics, and severe hepatic, renal, and vascular lesions compared with the normal control group. Both quinoa supplementation levels significantly (P < 0.05) attenuated these obesity-associated abnormalities; however, the higher supplementation level (HFQ2) produced greater improvements than HFQ1 in lipid homeostasis, oxidative status, tissue energy metabolism, and histopathological architecture. Although the reference statin significantly improved most measured parameters, HFQ2 exhibited comparable or superior protective effects in several biochemical and histopathological outcomes. Conclusion: Quinoa supplementation effectively ameliorated HFD-induced metabolic dysfunction and multi-organ injury through coordinated improvement of lipid metabolism, redox homeostasis, mitochondrial bioenergetics, and tissue integrity. The higher supplementation level (HFQ2) demonstrated the greatest protective efficacy, supporting its potential as a functional food strategy for preventing obesity-associated hepatic, renal, and cardiovascular complications.