LPS can induce metabolic endotoxemia and trigger downstream inflammation by interacting with CD14 cells and the co-receptor, Toll-like receptor 4 (TLR4), thus activating the nuclear factor κB (NF-κB) inflammatory pathway and leading to high transcription of several proinflammatory cytokines involved in the pathogenesis of chronic inflammation, which is a hallmark of obesity and other metabolic diseases [46]. Here, NFKB1 is linked to serum lipopolysaccharide activity.