Regulation of hepatic-mediated glucose release following hypoglycemic stress.

自主神经系统(ANS)在血糖循环水平降低(低血糖)时的血糖逆调节反应中起着关键作用。通过激活ANS的交感(SNS)、副交感(PNS)和交感-肾上腺(SNS-肾上腺)分支，刺激释放胰腺-胰高血糖素和肾上腺-肾上腺素，导致肝脏葡萄糖释放增加，随后恢复到正常血糖水平。有证据表明，必须存在额外的神经调节系统，其中，直接支配肝组织的SNS是最有可能的候选。ANS通过这种多方面的调节系统协调肝脏葡萄糖释放的神经机制还不是很清楚。此外，每种神经激素因子和肝脏中导致葡萄糖产生和释放的代谢信号通路的激活之间的分子联系尚未建立。阐明这些控制葡萄糖稳态的神经控制机制对于了解ANS活动的扰动，如在高血糖状态下，如何阻碍正常血糖对其他健康个体的低血糖逆调节反应至关重要。

The Autonomic Nervous System (ANS) plays a key role in the glucose counter-regulatory response to lowered circulating levels of blood glucose (hypoglycemia). Through the activation of the sympathetic (SNS), parasympathetic (PNS), and sympatho-adrenal (SNS-adrenal) branches of the ANS, the stimulated release of pancreatic-glucagon and adrenal-epinephrine leads to the increased release of hepatic glucose and a subsequent return to normal glucose levels. Evidence would suggest that additional neural regulatory systems must exist, of which, the direct SNS innervation to hepatic tissues is the most likely candidate. The neural mechanisms by which the ANS coordinates the release of hepatic glucose via this multi-faceted regulatory system are not well understood. Further, the molecular linkages between each neurohormonal factor and the activation of metabolic signalling pathways in the liver that lead to the production and release of glucose has not been made. The elucidation of these neural control mechanisms governing glucose homeostasis will prove paramount to the understanding of how perturbations in ANS activity, such as during states of hyperglycemia, can impede the normal glucose counter-regulatory response to hypoglycemia in otherwise healthy individuals.