At the cellular level, we found that: (1) ALE metabolites exert hepatoprotective properties in human hepatocytes by counteracting a fatty acid-induced lipotoxic stress that is commonly observed in hypercholesterolemia [9] and steatohepatitis [10]; (2) ALE metabolites limit adipogenic differentiation and hypertrophy, a cellular feature of obesity and metabolic syndrome [23]; (3) finally, ALE metabolites protect chondrocyte from an IL-1β stimulation that mimics osteo-arthritis inflammatory environment [14]. The gene discussed is IL1B; the disease is Obesity.