An increased
glucose requirement by many solid
tumors produces an increased metabolic demand on the liver, resulting in an increased energy expenditure. In addition, several
cytokines and
tumor catabolic products have been suggested as being responsible for the depletion of adipose tissue and skeletal-muscle mass in
cachexia. A sulphated
glycoprotein of molecular mass 24 kDa, produced by
cachexia-inducing
tumors and present in the urine of
cancer patients actively losing weight, has been shown to be capable of inducing direct muscle catabolism in vitro and a state of
cachexia in vivo, with specific loss of the non-fat carcass mass. In vitro studies have shown the bioactivity of this proteolysis-inducing factor to be attenuated by the
polyunsaturated fatty acid,
eicosapentaenoic acid. Preliminary clinical studies have shown that
eicosapentaenoic acid stabilizes
body weight and
protein and fat reserves in patients with
pancreatic carcinoma. Further trials are required to confirm the efficacy of
eicosapentaenoic acid and to determine the anticachectic activity in other types of
cancer.