Feeding induced by intracerebroventricular 2-deoxy-D-glucose in the rat.
Feeding induced by intracerebroventricular 2-deoxy-D-glucose in the rat.
复制标题
大鼠脑室内2-脱氧-D-葡萄糖诱导进食。
DOI：
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发表时间：
1975
影响因子：
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通讯作者：
A. N. Epstein
中科院分区：
文献类型：
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作者：
R. Miselis;A. N. Epstein
脑脑室（ICV）侧注射2-脱氧-d -葡萄糖（2-dg），这是一种葡萄糖类似物，可引起葡萄糖活化。ICV 2-DG（2.9或5.8 mg /只大鼠）后，摄食量平均增加2.6 g，但ICV d -葡萄糖或蔗糖后，摄食量没有增加。在相同剂量下，2-DG外周给药不增加摄食。外周给药后，2-DG剂量足以诱导进食时，核心温度呈剂量依赖性下降，但注射ICV时没有出现这种情况。当双侧注入下丘脑外侧、视前区或下丘脑前外侧时，2-DG（0.006—1.219 M）不刺激进食。在同样的大鼠身上，在同样的地方注射普鲁卡因HC1也不会产生摄食，而普鲁卡因HC1会导致摄食增加。因此，大脑在摄食控制中直接对葡萄糖活化敏感，仅葡萄糖活化就足以调动摄食行为。对葡糖苷化的具体敏感部位和葡糖苷化系统在大脑中的作用方式尚不清楚。
Feeding was induced with lateral intracerebroventricular (ICV) injections of 2-deoxy-D-glucose (2-dg), a glucose analogue causing glucoprivation. Feeding increased rapidly by an average of 2.6 g following ICV 2-DG (2.9 or 5.8 mg per rat), but did not increase after ICV D-glucose or sucrose. At the same doses, 2-DG did not increase feeding when given peripherally. Core temperature dropped in a dose-dependent manner with doses of 2-DG sufficient to induce feeding after peripheral administration, but did not occur with ICV injections. The 2-DG (0.006--1.219 M) did not stimulate feeding when infused bilaterally into the lateral hypothalamus, the preoptic area, or the anterior lateral hypothalamus. Nor did it produce feeding when injected into the ventromedial hypothalamus at the same sites and in the same rats in which procaine HC1 caused increased feeding. The brain, therefore, is directly sensitive to glucoprivation in the control of feeding, and glucoprivation alone is sufficient to mobilize feeding behavior. The specific site of sensitivity to glucoprivation and the mode of action of the glucoprivic system in the brain are unknown.