Chance W T, Balasubramaniam A, Sheriff S, Fischer J E
Department of Surgery, University of Cincinnati Medical Center, OH.
Adv Exp Med Biol. 1994;354:185-201. doi: 10.1007/978-1-4899-0939-8_14.
The efficacy of NPY to elicit feeding in TB rats was reduced prior to the onset of overt anorexia, with the feeding response decreasing further as anorexia developed. Hypothalamic concentration of NPY was reduced in TB rats, with the magnitude of the decrease paralleling the degree of anorexia. Binding affinity of NPY to hypothalamic membranes taken from TB rats suggested decreased binding affinity with no change in receptor number. Infusing ammonium salts at a concentration and rate necessary to increase blood ammonia levels to the degree observed in TB rats, produced anorexia and decreased NPY feeding. These results suggest that NPY feeding systems are abnormal in TB rats and that hyperammonemia may be of primary importance in this dysfunction.
在明显厌食症发作之前，神经肽Y（NPY）诱发结核（TB）大鼠进食的功效就已降低，随着厌食症的发展，进食反应进一步降低。TB大鼠下丘脑神经肽Y的浓度降低，其降低幅度与厌食程度平行。神经肽Y与取自TB大鼠的下丘脑膜的结合亲和力表明结合亲和力降低，而受体数量没有变化。以将血氨水平提高到在TB大鼠中观察到的程度所需的浓度和速率输注铵盐，会导致厌食症并减少神经肽Y诱导的进食。这些结果表明，TB大鼠中神经肽Y诱导进食的系统异常，高氨血症可能在这种功能障碍中起主要作用。
