INTERLEUKIN-1 RECEPTOR ANTAGONIST (IL-1RA) IS UNABLE TO REVERSE CACHEXIA IN RATS BEARING AN ASCITES HEPATOMA (YOSHIDA AH-130)

The mechanisms leading to the development of cancer cachexia are still poorly understood. Recently, cytokines such as interleukin 1 and tumo ur necrosis factor-alpha have been involved as mediators of the tissue wasting consequent to tumour growth, The rat ascites hepatoma Yoshida AH-130 is a highly anaplastic tumour that causes in the host an early and marked depletion of both the skeletal muscle and the adipose tiss ue, mainly accounted for by a hypercatabolic state. Profound hormonal alterations and the release of tumour necrosis factor-alpha and interl eukin 1 by the tumour cells likely concur in forcing the metabolic bal ance towards the catabolic side [1]. In order to possibly achieve the correction of this wasting condition, the AH-130 bearing rats were adm inistered a daily s.c, dose of interleukin 1 receptor antagonist (IL-1 ra; 2 mg/kg). This factor, however, was completely ineffective in eith er inhibiting tumour proliferation or in preventing the consequent tis sue depletion and protein hypercatabolism. These observations suggest that interleukin 1 is not important, at least in this model system, fo r either the development of cachexia or tumour growth.