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脑室内注射2-脱氧葡萄糖会在没有其他糖剥夺迹象的情况下引发进食。

Intracerebroventricular 2-DG causes feeding in the absence of other signs of glucoprivation.

作者信息

Engeset R M, Ritter R C

出版信息

Brain Res. 1980 Nov 24;202(1):229-33.

PMID:7427740
Abstract

Intracerebroventricular (ICV) infusions of 2-deoxy-D-glucose (2-DG) elicited hyperglycemia and increased feeding at short latencies. If access to food was prevented for 6 h post-2-DG infusion, when blood glucose levels were normal and brain 2-DG concentrations were virtually zero, the rats still ate significantly more food than they did 6 h after control infusions. These data indicate that activation of brain glucoreceptors may mediate increased feeding even after other signs of cerebral glucoprivation have disappeared.

摘要

脑室内(ICV)注入2-脱氧-D-葡萄糖(2-DG)会引发高血糖,并在短时间内增加进食量。如果在注入2-DG后6小时内阻止大鼠获取食物,此时血糖水平正常且脑内2-DG浓度几乎为零,这些大鼠的进食量仍显著高于对照注入后6小时的进食量。这些数据表明,即使在脑内葡萄糖缺乏的其他迹象消失后,脑葡萄糖感受器的激活仍可能介导进食量增加。

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Intracerebroventricular 2-DG causes feeding in the absence of other signs of glucoprivation.脑室内注射2-脱氧葡萄糖会在没有其他糖剥夺迹象的情况下引发进食。
Brain Res. 1980 Nov 24;202(1):229-33.
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Feeding induced by intracerebroventricular 2-deoxy-D-glucose in the rat.脑室内注射2-脱氧-D-葡萄糖诱导大鼠进食。
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