Quercetin: Mechanisms of Action, Clinical Evidence in Metabolic Syndrome, and Translational Opportunities in Food Preservation

Quercetin is a plant-derived flavonol positioned at the interface of metabolic health and food preservation. This review integrates quercetin chemistry, plant biosynthesis and metabolism, production-relevant extraction and microbial synthesis, bioavailability, mechanisms of action, preclinical and clinical evidence in metabolic syndrome (MetS), and applications in clean-label food preservation. Experimental studies indicate that quercetin modulates obesity-associated inflammation, dyslipidemia, hepatic steatosis, insulin resistance, hypertension, endothelial dysfunction, and gut-barrier impairment through interconnected Nrf2/HO-1, NF-κB/NLRP3, AMPK/SIRT1, PI3K/Akt, eNOS/NO, lipid metabolism, and microbiota-related pathways. Human evidence is narrower and heterogeneous: modest reductions in systolic blood pressure constitute the most consistent signal, whereas effects on fasting glucose, lipids, inflammatory markers, endothelial function, liver fat, and body weight vary by population, formulation, dose, and duration. In food systems, quercetin has been investigated as an antioxidant, antimicrobial, antibiofilm agent, and photodynamic photosensitizer. It is incorporated into edible films, coatings, freshness indicators, and controlled-release packaging, although most evidence remains laboratory-scale. Key translational challenges include limited aqueous solubility, variable bioavailability, incomplete long-term safety evidence, matrix-dependent efficacy, sensory constraints, manufacturing scale-up, migration, and regulation. Overall, quercetin is promising, but clinical use and industrial deployment require formulation-specific, adequately powered human studies and validation in clinically relevant populations and under commercially realistic processing conditions.