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Tumor necrosis factor (TNF) is a multifunctional proinflammatory cytokine secreted predominantly by monocytes/macrophages that has effects on lipid metabolism, coagulation, insulin resistance, and endothelial function.

Recent investigations have implicated the cytokine tumor necrosis factor (TNF)-α as a modulator of glucose metabolism. Particularly, TNF-α has been associated with the metabolic defects related to insulin resistance. Furthermore, increased TNF-α is associated with insulin resistance in obesity, sepsis, after muscle damage, and with age-associated muscle wasting. Interestingly, elevated plasma TNF-α levels have been observed in older men and women, and increased TNF-α protein expression has been reported in adipose tissue and skeletal muscle of obese and diabetic humans.

Aggarwal et al. (1985) presented evidence that TNF-alpha and TNF-beta share a common receptor on tumor cells and that the receptors are upregulated by gamma-interferon. Various interferons have been known to be synergistic with TNF in antitumor effects in vitro. Brenner et al. (1989) demonstrated that TNFa stimulates prolonged activation of the oncogene JUN expression; the JUN gene encodes transcription factor AP-1, which stimulates collagenase gene transcription. Thus, activation of JUN and collagenase gene expression may be one mechanism for mediating some of the biologic effects of TNFa.