van Lammeren F M, Chance W T, Fischer J E
Peptides. 1984 Jan-Feb;5(1):97-101. doi: 10.1016/0196-9781(84)90058-5.
The interaction of cholecystokinin-induced hypophagia with cancer anorexia was investigated within both acute (Walker 256 carcinosarcoma) and chronic (methylcholanthrene-induced sarcoma) animal models of cancer anorexia. Cholecystokinin octapeptide (CCK8) effectively reduced feeding for at least one hour in both groups of rats. However, this peptide was no more effective in inducing hypophagia in tumor-bearing rats than in nontumor-bearing control rats when tested at a variety of doses (0.5, 5.0 and 50.0 microgram/kg; IP) both prior to and after the development of anorexia. Therefore, these data do not support a role of cholecystokinin in the mediation of experimental cancer anorexia, since no synergism of CCK8-induced hypophagia with the anorexia was observed.
在癌症恶病质的急性(Walker 256癌肉瘤)和慢性(甲基胆蒽诱导的肉瘤)动物模型中,研究了胆囊收缩素诱导的食欲减退与癌症恶病质的相互作用。在两组大鼠中,胆囊收缩素八肽(CCK8)有效地减少进食至少一小时。然而,当在厌食症发展之前和之后以多种剂量(0.5、5.0和50.0微克/千克;腹腔注射)进行测试时,该肽在诱导荷瘤大鼠食欲减退方面并不比未荷瘤对照大鼠更有效。因此,这些数据不支持胆囊收缩素在实验性癌症恶病质介导中的作用,因为未观察到CCK8诱导的食欲减退与厌食症之间的协同作用。