Glucagon-induced inhibition of feeding is impaired by hepatic portal alloxan injection.

Glucagon-induced inhibition of feeding is impaired by hepatic portal alloxan injection.
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肝门四氧嘧啶注射会损害胰高血糖素诱导的摄食抑制。

DOI:
10.1152/ajpregu.1986.250.4.r682
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发表时间:
1986
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Stone,SL
Stone,SL
中科院分区:
--
文献类型:
--
作者:
Ritter,S;Weatherford,SC;Stone,SL

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亚致糖尿病剂量的四氧嘧啶注射到大鼠的肝门静脉废除胰高血糖素诱导的抑制喂养(胰高血糖素饱腹感)在白天的测试中使用可口的食物,并在夜间测试中使用他们的标准颗粒饲料。与此相反,胆囊收缩素和肾上腺素对摄食的抑制作用以及2-脱氧-D-葡萄糖对摄食的刺激作用并未受到四氧嘧啶的损害。四氧嘧啶诱导的胰高血糖素饱腹感缺陷似乎不是由全身性肝细胞坏死引起的,因为饱腹感缺陷持续时间超过毒性的组织学体征,并且因为产生相似程度肝毒性的呋塞米不会损害胰高血糖素饱腹感。此外,四氧嘧啶的作用与受损的糖原储存或动员无关。一些动物的胰高血糖素饱腹感恢复,但直到四氧嘧啶后3-6个月才恢复。恢复程度与四氧嘧啶剂量呈负相关。我们的研究结果表明,当进入肝门静脉给药时,四氧嘧啶可能是一种相对特异性的毒素,用于介导胰高血糖素饱腹感的细胞。缺陷的特异性和恢复的时间过程表明,四氧嘧啶敏感细胞可能是肝迷走神经元。
Subdiabetogenic doses of alloxan injected into the hepatic portal vein of rats abolished glucagon-induced inhibition of feeding (glucagon satiety) both in daytime tests using a palatable food and in nighttime tests using their standard pelleted diet. In contrast, inhibition of food intake by cholecystokinin and epinephrine and stimulation of feeding by 2-deoxy-D-glucose were not impaired by alloxan. Alloxan-induced deficits in glucagon satiety did not appear to result from generalized hepatocellular necrosis, because satiety deficits outlasted histological signs of toxicity and because furosemide, which produced a similar degree of hepatotoxicity, did not impair glucagon satiety. In addition, alloxan's effects were not associated with impaired glycogen storage or mobilization. Recovery of glucagon satiety occurred in some animals but not until 3-6 mo after alloxan. The degree of recovery was inversely related to alloxan dose. Our results indicate that, when administered into the hepatic portal vein, alloxan may be a relatively specific toxin for cells involved in the mediation of glucagon satiety. The specificity of the deficit and the time course of recovery suggest that the alloxan-sensitive cells may be hepatic vagal neurons.
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