Granneman J, Friedman M I
Am J Physiol. 1983 Mar;244(3):R383-8. doi: 10.1152/ajpregu.1983.244.3.R383.
Rats increased food intake 6 h after peripheral and intracerebroventricular injections of 2-deoxy-D-glucose (2-DG) when plasma glucose concentrations had returned to normal from elevated levels. Rats with adrenal demedullation did not become hyperglycemic after injection of 2-DG and increased food intake more than normal animals after peripheral, but not ventricular, injections of 2-DG. Peripheral injections of 2-DG inhibited gastric emptying in normal, but not adrenal demedullated, rats. Intravenous infusions of epinephrine into normal rats, which mimicked some of the physiological effects of peripheral 2-DG injection, did not increase food intake. The results indicate that a prior disruption of cerebral metabolism is sufficient to elicit feeding in the absence of an adrenomedullary response and that increased gastric fill may restrain the increase in food intake produced by a previous cerebral emergency.
在经外周和脑室内注射2-脱氧-D-葡萄糖（2-DG）6小时后，当血浆葡萄糖浓度从升高水平恢复正常时，大鼠的食物摄入量增加。肾上腺髓质切除的大鼠在注射2-DG后不会出现高血糖，并且在外周（而非脑室内）注射2-DG后，其食物摄入量比正常动物增加得更多。外周注射2-DG可抑制正常大鼠（而非肾上腺髓质切除大鼠）的胃排空。向正常大鼠静脉输注肾上腺素，模拟外周注射2-DG的一些生理效应，并不会增加食物摄入量。结果表明，在没有肾上腺髓质反应的情况下，先前的脑代谢紊乱足以引发进食，并且胃内充盈增加可能会抑制先前脑紧急情况所产生的食物摄入量增加。
