Fearon K C, Tisdale M J, Preston T, Plumb J A, Calman K C
Br J Cancer. 1985 Jul;52(1):87-92. doi: 10.1038/bjc.1985.153.
The Walker 256 carcinosarcoma was shown to lack the enzyme 3-ketoacid CoA transferase. This suggests that ketone bodies cannot be used as a major substrate for the energy metabolism of this tumour. Systemic ketosis (1-2 mM acetoacetate plus 3-hydroxybutyrate) was induced both in tumour-bearing and in non-tumour-bearing rats with a diet containing 70% medium chain triglyceride. However, in rats bearing the Walker 256 tumour, this dietary ketosis did not reduce the tumour growth rate nor did it prevent the subsequent decrease in host body weight. Host body nitrogen losses were similarly unaffected. The ketosis induced in tumour bearing rats was shown to be abnormal since the blood glucose concentration of ketotic, tumour-bearing rats was significantly higher compared with that of ketotic non-tumour bearing rats (5.2 +/- 0.4 mM cf 3.4 +/- 0.6 mM, P less than 0.01). These results may partly explain why systemic ketosis failed to alter the growth and cachexia induced by the Walker 256 carcinosarcoma.
研究表明,Walker 256癌肉瘤缺乏3-酮酸辅酶A转移酶。这表明酮体不能作为该肿瘤能量代谢的主要底物。通过在含70%中链甘油三酯的饮食中饲养荷瘤大鼠和非荷瘤大鼠,诱导产生全身酮症(1-2 mM乙酰乙酸加3-羟基丁酸)。然而,在携带Walker 256肿瘤的大鼠中,这种饮食性酮症既没有降低肿瘤生长速率,也没有阻止随后宿主体重的下降。宿主身体的氮损失同样未受影响。结果显示,荷瘤大鼠诱导产生的酮症是异常的,因为酮症荷瘤大鼠的血糖浓度显著高于酮症非荷瘤大鼠(5.2±0.4 mM对3.4±0.6 mM,P<0.01)。这些结果可能部分解释了为什么全身酮症未能改变Walker 256癌肉瘤诱导的生长和恶病质。