Chun S J, Niijima A, Nagai N, Nagai K
Division of Protein Metabolism, Osaka University, Japan.
Brain Res. 1998 Nov 2;809(2):165-74. doi: 10.1016/s0006-8993(98)00854-3.
In mammals, the brain usually uses glucose as a sole energy source. Thus, under a central glucopenic condition after intracranial injection of 2-deoxy-D-glucose (2DG), an inhibitor of glucose utilization, it has been shown that rats elevate their blood glucose level through excitation of the sympathetic nerves. Experiments were conducted with rats to examine the role of the hypothalamic suprachiasmatic nucleus (SCN) in the hyperglycemic response to intracerebroventricular injection of either 2DG or vasoactive intestinal peptide (VIP). It was observed that, (1) intracerebroventricular injection of a VIP-antagonist inhibited the hyperglycemic and hyperglucagonemic responses to the intracranial injection of 2DG; (2) bilateral electrolytic lesioning of the SCN suppressed the hyperglycemic and hyperglucagonemic responses to intracranial injection of 2DG, and intracerebroventricular injection of VIP restored these responses to 2DG; and (3) bilateral electrolytic lesioning of the SCN also suppressed the hyperglycemic and hyperglucagonemic responses to the VIP injection, and additional intracerebroventricular injection of 2DG caused hyperglycemia. These findings indicate that in rats with bilateral lesions of the SCN intracranial injection of 2DG is able to elicit hyperglycemia when VIP was administered intracranially, and suggest that neurons containing VIP-like immunoreactive substance (VIP-neurons) in the SCN have an important role in the mechanism of hyperglycemia elicitation following intracranial injection of 2DG. Moreover, these findings show that 2DG and VIP are able to realize their functions through acting on the brain sites outside the SCN.
在哺乳动物中，大脑通常将葡萄糖作为唯一的能量来源。因此，在颅内注射葡萄糖利用抑制剂2-脱氧-D-葡萄糖（2DG）后出现中枢性低血糖的情况下，已表明大鼠通过交感神经兴奋来提高血糖水平。对大鼠进行了实验，以研究下丘脑视交叉上核（SCN）在对脑室内注射2DG或血管活性肠肽（VIP）的高血糖反应中的作用。观察到：（1）脑室内注射VIP拮抗剂可抑制对颅内注射2DG的高血糖和高胰高血糖素反应；（2）SCN的双侧电解损伤抑制了对颅内注射2DG的高血糖和高胰高血糖素反应，而脑室内注射VIP可使对2DG的这些反应恢复；（3）SCN的双侧电解损伤也抑制了对VIP注射的高血糖和高胰高血糖素反应，额外脑室内注射2DG会导致高血糖。这些发现表明，在SCN双侧损伤的大鼠中，当颅内给予VIP时，颅内注射2DG能够引发高血糖，并提示SCN中含有VIP样免疫反应物质的神经元（VIP神经元）在颅内注射2DG后的高血糖引发机制中起重要作用。此外，这些发现表明2DG和VIP能够通过作用于SCN以外的脑区来实现其功能。
