NFKB1 and metabolic syndrome: For instance, sodium urate can stimulate NF-κB through TLR4 and TLR2, leading to the synthesis of pro-IL-1β and components of the inflammasome.361 Furthermore, sodium urate can induce renal inflammation in gouty nephropathy by activating tubular NF-κB signaling.362 Recent studies have also demonstrated the involvement of the pro-inflammatory NF-κB pathway in hypothalamic inflammation associated with metabolic syndrome.363,364