LPS can activate TLR4 in macrophages, hepatocytes, adipocytes, and other cells, and activate NF-κB through MyD88 to induce adipose and hepatic inflammatory responses and promote lipid accumulation [121]; in addition, the activation of the NF-κB signaling pathway increases the ROS content, causing oxidative damage in the liver [122], and enteric-derived LPS is also capable of inducing insulin resistance, leading to disorders of glucose–lipid metabolism weight gain [123]. The gene discussed is NFKB1; the disease is Insulin resistance.