Galbraith R A, Chua S C, Kappas A
Laboratory of Metabolism and Pharmacology, Rockefeller University Hospital, New York, NY 10021.
Brain Res Mol Brain Res. 1992 Oct;15(3-4):298-302. doi: 10.1016/0169-328x(92)90121-q.
The mechanism whereby neurally or peripherally administered cobalt-protoporphyrin (CoPP) leads to transient hypophagia and prolonged weight reduction in normal and genetically obese animals is unknown. Neuropeptide Y (NPY) is a known endogenous stimulator of feeding behavior and is elevated in the hypothalamus of food-deprived rats. Accordingly, we examined the interaction between CoPP and NPY in the central nervous system. Concentrations of NPY mRNA in the hypothalami of rats treated intracerebroventricularly with vehicle or CoPP responded to decreased food intake with comparable increases. However, intracerebroventricular infusions of NPY elicited increased intake of food in vehicle-treated rats but were without effect in CoPP-treated animals. The results suggest that CoPP acts, at least in part, by blocking the feeding response to NPY.
神经或外周给予钴原卟啉（CoPP）可使正常和遗传性肥胖动物出现短暂性摄食减少及体重长期减轻，但其机制尚不清楚。神经肽Y（NPY）是一种已知的进食行为内源性刺激物，在饥饿大鼠的下丘脑内水平升高。因此，我们研究了CoPP与NPY在中枢神经系统中的相互作用。经脑室注射溶剂或CoPP处理的大鼠下丘脑内，NPY mRNA浓度对食物摄入量减少的反应相当，均有类似程度的增加。然而，脑室注射NPY可使溶剂处理的大鼠食物摄入量增加，但对CoPP处理的动物没有影响。结果表明，CoPP至少部分通过阻断对NPY的进食反应发挥作用。
