These changes mimic those experienced in many chronic inflammatory diseases and predispose the mice to developing insulin resistance and metabolic disorders. An additional result of SIRT1 deletion is an increase in nuclear factor kappa beta (NF-kB) dependent proinflammatory cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and many others [18]. This evidence concerns the gene TNF and metabolic disease.