Sulforaphane and Broccoli-Derived Preparations in Obesity and Obesity-Related Metabolic Dysfunction: Mechanistic...

Background/Objectives: Obesity is a major global health challenge characterized by adipose tissue dysfunction, insulin resistance, chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, and increased cardiometabolic risk. Despite substantial therapeutic advances, limitations related to cost, adverse effects, and long-term adherence have stimulated interest in complementary nutritional approaches. Sulforaphane, a bioactive isothiocyanate derived primarily from broccoli and other cruciferous vegetables, has attracted considerable attention because of its antioxidant, anti-inflammatory, and metabolic regulatory properties. This narrative review critically evaluates the current evidence regarding the role of sulforaphane and broccoli-derived preparations in obesity and obesity-associated metabolic dysfunction. Methods: A narrative review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar. Eligible publications included in vitro, animal, clinical, observational, and relevant review studies investigating sulforaphane, glucoraphanin, or broccoli-derived preparations in relation to obesity, adiposity, insulin resistance, metabolic syndrome, inflammation, oxidative stress, energy metabolism, and related metabolic abnormalities. Results: In vitro studies consistently demonstrate inhibition of adipocyte differentiation and lipid accumulation, attenuation of oxidative stress and inflammatory signaling, and enhancement of cellular energy metabolism. Animal studies further report reductions in adiposity, insulin resistance, hepatic steatosis, oxidative stress, and chronic inflammation, together with improvements in energy expenditure, metabolic flexibility, and obesity-associated metabolic abnormalities. Mechanistic evidence indicates that sulforaphane exerts pleiotropic metabolic effects through activation of the Nrf2 and AMPK pathways, suppression of NF-κB-mediated inflammation, improvement of mitochondrial function, promotion of thermogenesis and adipose tissue browning, regulation of lipid metabolism, and modulation of gut microbiota composition. Human studies, although limited and heterogeneous, suggest possible improvements in glycemic control, insulin sensitivity, endothelial function, and other surrogate metabolic biomarkers associated with obesity. However, evidence demonstrating clinically meaningful reductions in body weight, adiposity, or body composition remains limited and inconsistent, and improvements in these surrogate biomarkers should not be interpreted as evidence of reduced obesity-related morbidity or clinically meaningful adiposity reduction. Bioavailability, myrosinase activity, food processing, gut microbiota composition, and interindividual variability remain important determinants of efficacy and key translational challenges. Conclusions: Current evidence provides strong mechanistic and preclinical support for sulforaphane as a promising candidate adjunctive nutritional intervention for improving obesity-associated metabolic dysfunction. Nevertheless, current human evidence suggests possible metabolic benefits but does not establish sulforaphane as an effective weight-loss intervention or an evidence-based treatment for obesity. Large, long-term randomized controlled trials employing standardized sulforaphane preparations and comprehensive assessments of body weight, adiposity, body composition, metabolic health, pharmacokinetics, and gut microbiota composition are required to establish its clinical efficacy and define its role within precision nutrition strategies for obesity and obesity-associated metabolic dysfunction.