In a population of mice with diet-induced obesity, toll-like receptor 4 (TLR-4), which expresses inflammation through the production of cytokines, has been observed to activate nuclear factor-κβ (NF-κβ), leading to a disruption of signaling to the satiety hormone, leptin, and insulin in the hypothalamus [20]. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.