Abstract
Background and Objectives: Metabolic syndrome (MetS) is characterized by a cluster of factors, including dyslipidemia, insulin resistance, central obesity, elevated blood pressure, and impaired fasting glucose, which together elevate the risk of type 2 diabetes and cardiovascular disease. Nutraceuticals containing botanical extracts with antioxidant and metabolic activity have emerged as promising adjunctive strategies in the management of MetS. This study evaluated the clinical effectiveness and biological rationale of a standardized food supplement (QUINOLAM), containing extracts of Cydonia oblonga (quince), Olea europaea (olive leaf), and Amaranthus spp., in adults with metabolic syndrome. Materials and Methods: This was a retrospective, single-center observational study including adults with documented MetS who received one tablet daily of the QUINOLAM-based supplement for at least 12 weeks. The primary endpoint was the change in total cholesterol. Secondary endpoints included LDL-C, HDL-C, triglycerides, fasting glucose, HbA1c, HOMA-IR, CRP, and BMI. In parallel, preclinical studies were conducted using HepG2 cells to investigate QUINOLAM's effects on LDL receptor expression, glucose uptake, antioxidant activity, and cell viability. Results: Thirty patients met the inclusion criteria. A significant reduction in total cholesterol was observed at both 6 and 12 weeks (p < 0.005), accompanied by a significant decline in LDL-C by week 12 (p < 0.05). Among patients with baseline fasting glucose ≥100 mg/dL (n = 19), a significant improvement in glycemia was recorded (p < 0.005). Trends toward improvement were noted in other metabolic indices. In vitro, QUINOLAM enhanced LDL receptor expression (p < 0.05) and glucose uptake (p < 0.01), demonstrated antioxidant activity in the TEAC assay, and showed no cytotoxicity at relevant doses. Conclusions: In a real-world setting, daily supplementation with QUINOLAM was associated with significant improvements in lipid and glycemic control among patients with MetS. Preclinical findings further support its mechanistic plausibility via modulation of LDL handling, glucose metabolism, and oxidative stress. These results warrant confirmation in larger, prospective clinical trials.