The association might be dues to the fact that obesity and abnormal lipid stores down-regulate the ferroportin-1 exporter by hepcidin since obesity and dyslipidemia are associated with chronic, low grade, systemic inflammation by activating different cytokines which in turn up-regulates the transcription of protein hepcidin that results in sequestration of iron within entrecote, hepatocytes, and iron storing macrophages that will reduce iron bioavailability [34, 35]. This evidence concerns the gene SLC40A1 and metabolic syndrome.