Thereby, Murphy et al. [245] demonstrated that the innate immune sensor NRLP1 is able to detect increases in the caloric content of the diet (either enriched in fat or in proteins) and activate the inflammasome mediated production of IL18 preventing obesity and metabolic syndrome, as shown in mice overexpressing NRLP1. The mechanism proposed for such effects, implied peripheral activation of AMPK, increased glucose uptake and lipid oxidation, leading to defective lipid accumulation in the AT and amelioration of IR. Here, IL18 is linked to metabolic syndrome.