Geary N, Smith G P
Physiol Behav. 1983 Sep;31(3):391-4. doi: 10.1016/0031-9384(83)90207-x.
To test the hypothesis that hepatic vagal afferents mediate the satiety effect of pancreatic glucagon, we tested the effects of selective surgical and pharmacological lesions of the abdominal vagus on glucagon's potency to inhibit feeding. Surgical disconnection of only the hepatic branch of the abdominal vagus blocked glucagon's satiety effect as well as total abdominal vagotomy. However, abdominal vagotomy that spared the hepatic branch did not change glucagon's satiety effect. Glucagon also inhibited feeding after pharmacological blockade of peripheral postganglionic muscarinic receptors with atropine methylnitrate. All these results are consistent with the hypothesis that hepatic vagal afferents mediate the satiety effect of pancreatic glucagon.
为了验证肝迷走神经传入纤维介导胰高血糖素饱腹感效应的假说,我们测试了腹部迷走神经的选择性手术和药理学损伤对胰高血糖素抑制进食效力的影响。仅切断腹部迷走神经的肝支,与完全切断腹部迷走神经一样,均阻断了胰高血糖素的饱腹感效应。然而,保留肝支的腹部迷走神经切断术并未改变胰高血糖素的饱腹感效应。用硝酸甲基阿托品对节后外周毒蕈碱受体进行药理学阻断后,胰高血糖素仍能抑制进食。所有这些结果均与肝迷走神经传入纤维介导胰高血糖素饱腹感效应的假说一致。