Studies of the mechanism of carcass fat depletion in experimental cancer

Abstract

Loss of body fat is commonly associated with both experimental and human cancers. A direct effect of cancer upon free fatty acid mobilization from host adipose tissue could potentially explain this lipid depletion. Rates of free fatty acid (FFA) production were measured in epididymal adipose tissue removed from normal-control rats and rats bearing the Walker 256 carcinoma either intramuscularly (i.m.) or intraperitoneally (i.p.). By the 4th day after i.p. transplantation and by the time the i.m. tumor mass reached 4% of body weight (b.w.), basal lipolytic rates were 2–3 times higher in adipose tissue from tumor bearing than age matched control rats. Body neutral lipids were not yet significantly reduced at this early time. The high rates of adipose tissue lipolysis were maintained as the cancer progressed and body neutral lipids became significantly reduced once the i.m. tumor attained 6–7% of b.w. The mechanism by which cancer causes this increased fatty acid mobilization is yet unclear. The Walker 256 tumor might produce a lipolytic factor which directly stimulates adipose tissue lipolysis, since ascites serum from i.p. tumor bearing rats could stimulate adipose tissue lipolysis in vitro. However, blood serum from tumor bearing rats did not seem to stimulate adipose tissue lipolysis in vitro more than blood serum from control rats. Severe chronic stress seems an unlikely explanation for the early stimulated lipolysis in cancer, particularly the i.p. tumor. However, rats with even small i.m. tumors, although appearing stress free, possessed enlarged adrenal glands and somewhat atrophied thymus glands, classic markers for the presence of a stress situation. The cancer, in some unknown manner, might induce some special stress reaction.