Costelli P, Llovera M, García-Martínez C, Carbó N, López-Soriano F J, Argilés J M
Dipartimento di Medicina ed Oncologia Sperimentale, Università di Torino, Italy.
Cancer Lett. 1995 May 4;91(1):73-8. doi: 10.1016/0304-3835(94)03719-y.
The growth of the rat ascites hepatoma Yoshida AH-130 causes marked tissue protein hypercatabolism and alterations of the hormonal homeostasis in the host. After a single intravenous tracer dose of L-[1-14C]leucine in vivo, 14CO2 release by tumour-bearing rats is significantly elevated with respect to the controls. Treatment of the tumour hosts with a beta-adrenergic agonist (clenbuterol) is able to prevent either the depletion of the skeletal muscle mass or the enhanced whole-body leucine oxidation. Incubation of soleus muscles in the presence of L-[1-14C]leucine indicates an increased ability of the muscle obtained from the tumour hosts to utilize the amino acid for oxidation. Similarly to what is observed in vivo, clenbuterol administration exerts a protective effect reducing the rate of leucine oxidation to the control levels.
大鼠腹水型吉田AH - 130肝癌的生长会导致明显的组织蛋白分解代谢亢进以及宿主激素稳态的改变。在体内单次静脉注射示踪剂量的L - [1 - 14C]亮氨酸后，荷瘤大鼠的14CO2释放量相对于对照组显著升高。用β - 肾上腺素能激动剂（克伦特罗）治疗肿瘤宿主能够预防骨骼肌质量的减少或全身亮氨酸氧化的增强。在L - [1 - 14C]亮氨酸存在的情况下孵育比目鱼肌表明，从肿瘤宿主获得的肌肉利用氨基酸进行氧化的能力增强。与在体内观察到的情况类似，给予克伦特罗发挥保护作用，将亮氨酸氧化速率降低至对照水平。
