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The possible role of TNF-α and IL-2 in inducing tumor-associated metabolic alterations

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Abstract

This study was conducted to investigate the role of tumor necrosis factor-α (TNF-α) and interleukin-2 (IL-2) in inducing cancer cachexia, and the results were compared with those obtained from our previous study on Fisher 344 rats with methylcholanthrene-induced sarcoma. Three groups of male Fisher 344 rats received one of the following regimens: 4×104 IU of human recombinant TNF-α per rat per day subcutaneously (sc) for 5 consecutive days (n=5), 3.5×105 U human recombinant IL-2 per rat per day sc for 14 consecutive days (n=5), or normal saline (n=5). The activities of both phosphoenolpyruvate carboxykinase (PEPCK) and malic enzyme (ME) were increased slightly in the IL-2 group. Furthermore, LPL activity was significantly increased in the adipose tissue of the TNF group and in the cardiac muscle of the IL-2 group, but not in that of the TNF group. These results show that there is a significant difference between the metabolic alterations seen in the tumor-bearing state and those induced by either TNF-α or IL-2 alone. Thus, it is unlikely that IL-2 or TNF-α is the sole mediator of cancer cachexia in this tumor and rat model.

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Noguchi, Y., Makino, T., Yoshikawa, T. et al. The possible role of TNF-α and IL-2 in inducing tumor-associated metabolic alterations. Surg Today 26, 36–41 (1996). https://doi.org/10.1007/BF00311989

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