Tisdale M J
Pharmaceutical Sciences Research Institute, Aston University, Birmingham, UK.
Nutrition. 2000 Oct;16(10):1013-4. doi: 10.1016/s0899-9007(00)00409-3.
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.
许多实体瘤对葡萄糖需求的增加会导致肝脏的代谢需求增加，从而使能量消耗增加。此外，几种细胞因子和肿瘤分解代谢产物被认为是恶病质中脂肪组织和骨骼肌质量消耗的原因。一种由恶病质诱导肿瘤产生、分子量为24 kDa的硫酸化糖蛋白，存在于体重正在减轻的癌症患者尿液中，已被证明能够在体外诱导直接的肌肉分解代谢，并在体内诱导恶病质状态，伴有非脂肪胴体质量的特异性减少。体外研究表明，这种蛋白水解诱导因子的生物活性会被多不饱和脂肪酸二十碳五烯酸减弱。初步临床研究表明，二十碳五烯酸可稳定胰腺癌患者的体重以及蛋白质和脂肪储备。需要进一步试验来证实二十碳五烯酸的疗效，并确定其在其他类型癌症中的抗恶病质活性。
