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葡萄糖缺乏减弱了肾上腺素在小鼠中诱导的摄食减少。

Glucoprivation attenuates the hypophagia induced by epinephrine in mice.

作者信息

Villanueva I, Racotta I S, Racotta R

机构信息

Departamento de Fisiología, Escuela Nacional de Ciencias Biológicas, IPN, Carpio y Plan de Ayala, México D.F., México.

出版信息

Physiol Behav. 1996 Nov;60(5):1383-6. doi: 10.1016/s0031-9384(96)00216-8.

DOI:10.1016/s0031-9384(96)00216-8
PMID:8916199
Abstract

It is well known that relatively high doses of epinephrine (E) injected intraperitoneally (IP) produce hypophagia, possibly by an action on liver metabolism. The purpose of the present experiment was to find out if lipoprivation with 2-mercaptoacetate (MA, 800 mumol/kg, IP) or glucoprivation with either 2-deoxy-D-glucose (2DG, 500 mg/kg, IP) or 2,5-anhydro-D-mannitol (2,5-AM, 400 mg/kg, IP) were able to modify the anorectic effect of E (300 micrograms/kg). At the onset of the dark period, mice received a first injection of saline (S) or one of the metabolic blockers mentioned above and, 30 min later, a second injection of S or E; then 30-min food intake was measured. E alone decreased feeding by 80% (p < 0.05); this effect was nearly the same when MA was previously injected. In contrast, in the presence of 2DG or 2,5-AM, E reduced food intake only by 22% and 24%, respectively (not significant). Attenuation of E-induced hypophagia by these blockers suggests the participation of glucose utilization pathways. Because it has been shown that 2,5-AM acts specifically on the liver, we could additionally suggest that E reduces feeding by an action on glucose hepatic metabolism.

摘要

众所周知,经腹腔注射(IP)相对高剂量的肾上腺素(E)会导致摄食减少,这可能是通过对肝脏代谢的作用实现的。本实验的目的是探究用2-巯基乙酸(MA,800 μmol/kg,腹腔注射)进行脂肪剥夺,或用2-脱氧-D-葡萄糖(2DG,500 mg/kg,腹腔注射)或2,5-脱水-D-甘露糖醇(2,5-AM,400 mg/kg,腹腔注射)进行糖剥夺是否能够改变E(300 μg/kg)的厌食作用。在黑暗期开始时,小鼠接受首次注射生理盐水(S)或上述代谢阻滞剂之一,30分钟后,进行第二次注射S或E;然后测量30分钟内的食物摄入量。单独注射E使摄食量减少了80%(p<0.05);预先注射MA时,这种作用几乎相同。相比之下,在存在2DG或2,5-AM的情况下,E分别仅使食物摄入量减少了22%和24%(无统计学意义)。这些阻滞剂对E诱导的厌食作用的减弱表明葡萄糖利用途径参与其中。因为已经表明2,5-AM特异性作用于肝脏,我们还可以推测E通过对肝脏葡萄糖代谢的作用来减少摄食量。

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