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- _4 wasQuotedFrom 15578112 provenance.
- _4 value "Recently, several studies have suggested that metabolic abnormalities are associated with polymorphisms in the human resistin gene [17,18]. Furthermore, several studies, though not all, have reported increased serum resistin levels in patients with obesity, insulin resistance, and/or type 2 diabetes [19,20,21,22,23,24,25,26]. However, the mechanism and importance of increased resistin levels in human metabolic disease are not known. Here we show that the endotoxin lipopolysaccharide (LPS), a potent inflammatory stimulant, dramatically increases resistin production by inducing secretion of inflammatory cytokines such as TNFa. This increase in resistin production is blocked by both aspirin and rosiglitazone, drugs that have dual anti-inflammatory and insulin-sensitizing actions and have been shown to antagonize NF-kB. Indeed, activation of NF-kB is sufficient to induce resistin expression, and loss of NF-kB function abolishes LPS induction of resistin." provenance.