TP itself is hepatotoxic (Titov et al., 2011), and direct liver toxicity due to excessive exposure to TP, such as oxidative stress, excessive autophagy, apoptosis, metabolic disorders, etc. Cell damage caused by direct hepatotoxicity releases danger signals, such as DAMPs, which can activate the innate and adaptive immune systems, such as activation of NLRP3, recruitment of macrophages, Th17s, etc., and then a large number of pro-inflammatory factors will be released. Here, NLRP3 is linked to metabolic disease.