Niijima A
Jpn J Physiol. 1986;36(5):827-41. doi: 10.2170/jjphysiol.36.827.
All of the experimental results described above can be categorized as follows: the relationship between glucose levels and pancreatic and adrenal nerve activities; innervations of the liver and their role in the regulation of blood glucose level; central integration of blood glucose level; glucose-sensitive afferent nerve fibers in the liver and regulation of blood glucose; oral and intestinal inputs involved in reflex control of blood glucose level. We showed that an increase in blood glucose content produced an increase in the activity of the pancreatic branch of the vagus nerve, whereas it induced a decrease in the activity of the adrenal nerve. It was also shown that a decrease in blood glucose activated the sympatho-adrenal system and suppressed the vago-pancreatic system. It seems rational that these responses are involved in the maintenance of blood glucose level. Studies on the innervation of the liver led us to a conclusion that sympathetic innervation of the liver might play a role in eliciting a prompt hyperglycemic response through liberation of norepinephrine from the nerve terminals, and that the vagal innervation synergically worked with the humoral factor (insulin) for glycogen synthesis in the hyperglycemic condition. The glucose-sensitive afferents from the liver seem to initiate a reflex control of blood glucose level. The gustatory information on EIR response, reported by STEFFENS, is supported by the electrophysiological observations. MEI's reports also indicated the importance of information from the intestinal glucoreceptors in the reflex control of insulin secretion. The role of integrative functions of the hypothalamus and brainstem through neuronal networks on neural control of blood glucose levels is also evident. A schematic diagram of the nervous networks involved in the regulation of the blood glucose levels is shown in Fig. 3.
血糖水平与胰腺和肾上腺神经活动之间的关系;肝脏的神经支配及其在血糖水平调节中的作用;血糖水平的中枢整合;肝脏中对葡萄糖敏感的传入神经纤维与血糖调节;参与血糖水平反射控制的口腔和肠道输入。我们发现血糖含量增加会使迷走神经胰腺分支的活动增加,而会导致肾上腺神经活动减少。还发现血糖降低会激活交感 - 肾上腺系统并抑制迷走 - 胰腺系统。这些反应参与血糖水平的维持似乎是合理的。对肝脏神经支配的研究使我们得出结论,肝脏的交感神经支配可能通过从神经末梢释放去甲肾上腺素在引发迅速的高血糖反应中起作用,并且迷走神经支配在高血糖状态下与体液因子(胰岛素)协同作用促进糖原合成。来自肝脏的对葡萄糖敏感的传入神经似乎启动了血糖水平的反射控制。斯特芬斯报道的关于EIR反应的味觉信息得到了电生理观察结果的支持。梅的报告也表明来自肠道葡萄糖感受器的信息在胰岛素分泌的反射控制中的重要性。下丘脑和脑干通过神经网络对血糖水平进行神经控制的整合功能的作用也很明显。图3显示了参与血糖水平调节的神经网络示意图。